anti erbb2  (Danaher Inc)


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    Danaher Inc anti erbb2
    miR‐449c‐5p targeted <t>ERBB2.</t> (A) The predictive binding site of miR‐449c‐5p and ERBB2. (B) Luciferase activity of WT and MUT after co‐transfected with ERBB2 + miR‐449c‐5p into T47D cells. (C) Western blotting was used to investigate the expression level of ERBB2. (D) Relative expression of ERBB2 was evaluated in breast cancer tissues and normal tissues. (E) The distant metastasis survival curves with high or low ERBB2 expression. (F) The disease‐free survival curves with high or low ERBB2 expression. (G) The relapse survival curves with high or low ERBB2 expression.(H) The disease‐specific survival curves with high or low ERBB2 expression.(I) The overall survival curves with high or low ERBB2 expression. The results are presented as mean ± SD. n.s, not significant, *** P < .001, ** P < .01 and * P < .05. Statistical significance was analysed by two‐way ANOVA and t ‐test.
    Anti Erbb2, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti erbb2/product/Danaher Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti erbb2 - by Bioz Stars, 2024-02
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    Images

    1) Product Images from "miRNA ‐449c‐5p regulates the JAK‐STAT pathway in inhibiting cell proliferation and invasion in human breast cancer cells by targeting ERBB2"

    Article Title: miRNA ‐449c‐5p regulates the JAK‐STAT pathway in inhibiting cell proliferation and invasion in human breast cancer cells by targeting ERBB2

    Journal: Cancer Reports

    doi: 10.1002/cnr2.1974

    miR‐449c‐5p targeted ERBB2. (A) The predictive binding site of miR‐449c‐5p and ERBB2. (B) Luciferase activity of WT and MUT after co‐transfected with ERBB2 + miR‐449c‐5p into T47D cells. (C) Western blotting was used to investigate the expression level of ERBB2. (D) Relative expression of ERBB2 was evaluated in breast cancer tissues and normal tissues. (E) The distant metastasis survival curves with high or low ERBB2 expression. (F) The disease‐free survival curves with high or low ERBB2 expression. (G) The relapse survival curves with high or low ERBB2 expression.(H) The disease‐specific survival curves with high or low ERBB2 expression.(I) The overall survival curves with high or low ERBB2 expression. The results are presented as mean ± SD. n.s, not significant, *** P < .001, ** P < .01 and * P < .05. Statistical significance was analysed by two‐way ANOVA and t ‐test.
    Figure Legend Snippet: miR‐449c‐5p targeted ERBB2. (A) The predictive binding site of miR‐449c‐5p and ERBB2. (B) Luciferase activity of WT and MUT after co‐transfected with ERBB2 + miR‐449c‐5p into T47D cells. (C) Western blotting was used to investigate the expression level of ERBB2. (D) Relative expression of ERBB2 was evaluated in breast cancer tissues and normal tissues. (E) The distant metastasis survival curves with high or low ERBB2 expression. (F) The disease‐free survival curves with high or low ERBB2 expression. (G) The relapse survival curves with high or low ERBB2 expression.(H) The disease‐specific survival curves with high or low ERBB2 expression.(I) The overall survival curves with high or low ERBB2 expression. The results are presented as mean ± SD. n.s, not significant, *** P < .001, ** P < .01 and * P < .05. Statistical significance was analysed by two‐way ANOVA and t ‐test.

    Techniques Used: Binding Assay, Luciferase, Activity Assay, Transfection, Western Blot, Expressing

    Breast cancer cell proliferation, migration and invasion ability affected by miR‐449c‐5p and ERBB2. (A) Expression level of ERBB2 in three groups by Western blotting. (B) Colony formation was measured to detect the colony cells. (C) Cell viability was measured by CCK‐8. (D) The statistical results of migration area for Wound healing assay. (E) The statistical results of invasion cell number for Transwell assay. (F) Cell migration and invasion detected by Wound healing and Transwell. The mean ± SD is provided. n.s, not significant, **** P < .0001, *** P < .001, ** P < .01 and * P < .05, one‐way ANOVA and two‐way ANOVA.
    Figure Legend Snippet: Breast cancer cell proliferation, migration and invasion ability affected by miR‐449c‐5p and ERBB2. (A) Expression level of ERBB2 in three groups by Western blotting. (B) Colony formation was measured to detect the colony cells. (C) Cell viability was measured by CCK‐8. (D) The statistical results of migration area for Wound healing assay. (E) The statistical results of invasion cell number for Transwell assay. (F) Cell migration and invasion detected by Wound healing and Transwell. The mean ± SD is provided. n.s, not significant, **** P < .0001, *** P < .001, ** P < .01 and * P < .05, one‐way ANOVA and two‐way ANOVA.

    Techniques Used: Migration, Expressing, Western Blot, CCK-8 Assay, Wound Healing Assay, Transwell Assay

    The protein expression of JAK1, p‐JAK1, JAK2, p‐JAK2, STAT3, p‐STAT3, STAT5, and p‐STAT5 was measured by western blotting in T47D cells after transfection with pcDNA3.1‐NC, pcDNA3.1‐ERBB2, and miR‐449c‐5p mimic+pcDNA3.1‐ERBB2. (A) The protein expression level of JAK1, p‐JAK1, JAK2, p‐JAK2, STAT3, p‐STAT3, STAT5, and p‐STAT5 by western blotting assay. (B–I) The statistical results of western blotting assay. Results are presented as the mean ± SD. n.s, not significant, *** P < .001, ** P < .01 and * P < .05, according to one‐way ANOVA.
    Figure Legend Snippet: The protein expression of JAK1, p‐JAK1, JAK2, p‐JAK2, STAT3, p‐STAT3, STAT5, and p‐STAT5 was measured by western blotting in T47D cells after transfection with pcDNA3.1‐NC, pcDNA3.1‐ERBB2, and miR‐449c‐5p mimic+pcDNA3.1‐ERBB2. (A) The protein expression level of JAK1, p‐JAK1, JAK2, p‐JAK2, STAT3, p‐STAT3, STAT5, and p‐STAT5 by western blotting assay. (B–I) The statistical results of western blotting assay. Results are presented as the mean ± SD. n.s, not significant, *** P < .001, ** P < .01 and * P < .05, according to one‐way ANOVA.

    Techniques Used: Expressing, Western Blot, Transfection

    phospho erbb2 tyr1248  (Danaher Inc)


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    Danaher Inc phospho erbb2 tyr1248
    Effect of non‐SMC condensin I complex subunit H (NCAPH) expression on luminal <t>ERBB2‐positive</t> tumours in vivo. (A and B) Overexpression of NCAPH in patients with luminal ER‐positive HER2 + breast tumours was associated with a worse outcome (A), while this association was not seen in HER2 + ER‐negative tumours (B). Panels A and B were generated in the KM Plotter database. <xref ref-type= 59 Each graph displaying a Kaplan‐Meier curve panel specifies the number of patients it encompasses. Outcome (disease‐free survival [DFS] probability). Analysis using the KM plotter's optimal cutoff. (C) Scheme to generate double‐transgenic mice Mouse Mammary Tumor Virus (MMTV)‐ NCAPH ErBb2 . (D and E) Immunohistochemical proliferation assessment in non‐tumoural mammary glands: analysis of mammary glands from MMTV‐ ErbB2 (upper panels) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (D), with representative Ki67 immunohistochemistry images. Five mice per group were analysed, and field analysis results are shown in panel E, using the Mann–Whitney U ‐test. (F and G) Tumour development quantification: double‐transgenic mice exhibited significantly more tumours (F) and higher tumour multiplicity (G) compared to MMTV‐ ErbB2 mice. (H–J) Histopathological pattern analysis: this section assesses different histopathological patterns in the samples, focusing on nodular (H) and solid patterns (I). Notably, the solid pattern occurred more frequently in double‐transgenic mice compared to MMTV‐ ErbB2 mice (J). Ten mice per group were evaluated with a chi‐squared test. (K and L) Vascularisation variability in mouse tumours: the panels compare vascularisation in tumours from MMTV‐ ErbB2 and MMTV‐ NCAPH ErbB2 double‐transgenic mice. Haematoxylin–eosin staining is used to emphasise vascular differences between MMTV‐ ErbB2 (panel K) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (panel L). (M) Proliferative activity in tumour tissues: this section uses Ki67 immunohistochemical analysis to evaluate tumour proliferation in MMTV‐ ErbB2 (left) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (right). Quantitative results from this analysis are displayed below the corresponding images. (N) Mitotic index quantification using chi‐squared test. (O and P) Analysis of ERBB2 downstream signalling molecules via Western blot (O) with pAKT quantification (P). (Q and R) NCAPH induction increased genomic instability, evidenced by more micronuclei and chromosomal bridges (CIN). Micronuclei and chromosomal bridge images (Q) are accompanied by CIN quantification (R), analysed with Fisher's exact test. (S) Genomic stress linked to increased NCAPH is shown by elevated ɤH2AX levels post‐H 2 O 2 exposure and during 30‐ or 60‐min recovery. (T) pCHEK1 expression changes following NCAPH induction are displayed via Western blot. (U) RNA expression correlation in luminal breast cancer: this panel shows the correlation between NCAPH RNA and Ki67 , CHEK1 and H2AX in luminal breast cancer samples from The Cancer Genome Atlas (TCGA) database. It illustrates the correlation coefficients and patterns using CANCERTOOL. 62 SMC, structural chromosome maintenance. " width="250" height="auto" />
    Phospho Erbb2 Tyr1248, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phospho erbb2 tyr1248/product/Danaher Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    phospho erbb2 tyr1248 - by Bioz Stars, 2024-02
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    Images

    1) Product Images from "NCAPH drives breast cancer progression and identifies a gene signature that predicts luminal a tumour recurrence"

    Article Title: NCAPH drives breast cancer progression and identifies a gene signature that predicts luminal a tumour recurrence

    Journal: Clinical and Translational Medicine

    doi: 10.1002/ctm2.1554

    Effect of non‐SMC condensin I complex subunit H (NCAPH) expression on luminal ERBB2‐positive tumours in vivo. (A and B) Overexpression of NCAPH in patients with luminal ER‐positive HER2 + breast tumours was associated with a worse outcome (A), while this association was not seen in HER2 + ER‐negative tumours (B). Panels A and B were generated in the KM Plotter database. <xref ref-type= 59 Each graph displaying a Kaplan‐Meier curve panel specifies the number of patients it encompasses. Outcome (disease‐free survival [DFS] probability). Analysis using the KM plotter's optimal cutoff. (C) Scheme to generate double‐transgenic mice Mouse Mammary Tumor Virus (MMTV)‐ NCAPH ErBb2 . (D and E) Immunohistochemical proliferation assessment in non‐tumoural mammary glands: analysis of mammary glands from MMTV‐ ErbB2 (upper panels) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (D), with representative Ki67 immunohistochemistry images. Five mice per group were analysed, and field analysis results are shown in panel E, using the Mann–Whitney U ‐test. (F and G) Tumour development quantification: double‐transgenic mice exhibited significantly more tumours (F) and higher tumour multiplicity (G) compared to MMTV‐ ErbB2 mice. (H–J) Histopathological pattern analysis: this section assesses different histopathological patterns in the samples, focusing on nodular (H) and solid patterns (I). Notably, the solid pattern occurred more frequently in double‐transgenic mice compared to MMTV‐ ErbB2 mice (J). Ten mice per group were evaluated with a chi‐squared test. (K and L) Vascularisation variability in mouse tumours: the panels compare vascularisation in tumours from MMTV‐ ErbB2 and MMTV‐ NCAPH ErbB2 double‐transgenic mice. Haematoxylin–eosin staining is used to emphasise vascular differences between MMTV‐ ErbB2 (panel K) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (panel L). (M) Proliferative activity in tumour tissues: this section uses Ki67 immunohistochemical analysis to evaluate tumour proliferation in MMTV‐ ErbB2 (left) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (right). Quantitative results from this analysis are displayed below the corresponding images. (N) Mitotic index quantification using chi‐squared test. (O and P) Analysis of ERBB2 downstream signalling molecules via Western blot (O) with pAKT quantification (P). (Q and R) NCAPH induction increased genomic instability, evidenced by more micronuclei and chromosomal bridges (CIN). Micronuclei and chromosomal bridge images (Q) are accompanied by CIN quantification (R), analysed with Fisher's exact test. (S) Genomic stress linked to increased NCAPH is shown by elevated ɤH2AX levels post‐H 2 O 2 exposure and during 30‐ or 60‐min recovery. (T) pCHEK1 expression changes following NCAPH induction are displayed via Western blot. (U) RNA expression correlation in luminal breast cancer: this panel shows the correlation between NCAPH RNA and Ki67 , CHEK1 and H2AX in luminal breast cancer samples from The Cancer Genome Atlas (TCGA) database. It illustrates the correlation coefficients and patterns using CANCERTOOL. 62 SMC, structural chromosome maintenance. " title="... I complex subunit H (NCAPH) expression on luminal ERBB2‐positive tumours in vivo. (A and B) Overexpression of ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Effect of non‐SMC condensin I complex subunit H (NCAPH) expression on luminal ERBB2‐positive tumours in vivo. (A and B) Overexpression of NCAPH in patients with luminal ER‐positive HER2 + breast tumours was associated with a worse outcome (A), while this association was not seen in HER2 + ER‐negative tumours (B). Panels A and B were generated in the KM Plotter database. 59 Each graph displaying a Kaplan‐Meier curve panel specifies the number of patients it encompasses. Outcome (disease‐free survival [DFS] probability). Analysis using the KM plotter's optimal cutoff. (C) Scheme to generate double‐transgenic mice Mouse Mammary Tumor Virus (MMTV)‐ NCAPH ErBb2 . (D and E) Immunohistochemical proliferation assessment in non‐tumoural mammary glands: analysis of mammary glands from MMTV‐ ErbB2 (upper panels) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (D), with representative Ki67 immunohistochemistry images. Five mice per group were analysed, and field analysis results are shown in panel E, using the Mann–Whitney U ‐test. (F and G) Tumour development quantification: double‐transgenic mice exhibited significantly more tumours (F) and higher tumour multiplicity (G) compared to MMTV‐ ErbB2 mice. (H–J) Histopathological pattern analysis: this section assesses different histopathological patterns in the samples, focusing on nodular (H) and solid patterns (I). Notably, the solid pattern occurred more frequently in double‐transgenic mice compared to MMTV‐ ErbB2 mice (J). Ten mice per group were evaluated with a chi‐squared test. (K and L) Vascularisation variability in mouse tumours: the panels compare vascularisation in tumours from MMTV‐ ErbB2 and MMTV‐ NCAPH ErbB2 double‐transgenic mice. Haematoxylin–eosin staining is used to emphasise vascular differences between MMTV‐ ErbB2 (panel K) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (panel L). (M) Proliferative activity in tumour tissues: this section uses Ki67 immunohistochemical analysis to evaluate tumour proliferation in MMTV‐ ErbB2 (left) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (right). Quantitative results from this analysis are displayed below the corresponding images. (N) Mitotic index quantification using chi‐squared test. (O and P) Analysis of ERBB2 downstream signalling molecules via Western blot (O) with pAKT quantification (P). (Q and R) NCAPH induction increased genomic instability, evidenced by more micronuclei and chromosomal bridges (CIN). Micronuclei and chromosomal bridge images (Q) are accompanied by CIN quantification (R), analysed with Fisher's exact test. (S) Genomic stress linked to increased NCAPH is shown by elevated ɤH2AX levels post‐H 2 O 2 exposure and during 30‐ or 60‐min recovery. (T) pCHEK1 expression changes following NCAPH induction are displayed via Western blot. (U) RNA expression correlation in luminal breast cancer: this panel shows the correlation between NCAPH RNA and Ki67 , CHEK1 and H2AX in luminal breast cancer samples from The Cancer Genome Atlas (TCGA) database. It illustrates the correlation coefficients and patterns using CANCERTOOL. 62 SMC, structural chromosome maintenance.

    Techniques Used: Expressing, In Vivo, Over Expression, Generated, Transgenic Assay, Virus, Immunohistochemistry, MANN-WHITNEY, Staining, Activity Assay, Western Blot, RNA Expression

    Intratumoural levels of Ncaph were associated with a worse outcome and response to chemotherapy in a cohort of mice generated by backcrossing (BX‐ Neu + ). (A) Generation scheme for BX‐ Neu + cohort: the BX‐ Neu + cohort was created by backcrossing transgenic Mouse Mammary Tumor Virus (MMTV)‐ ErbB2 mice (FVB/N background) with C57BL/6 mice, which are resistant to breast cancer. The first‐generation offspring (F1) were further crossed with wild‐type FVB/N mice, producing the BX‐ Neu + cohort. This cohort is genetically diverse, displaying a range of phenotypic traits and intratumoural Ncaph gene expression. Mice from the highest and lowest tertiles of Ncaph expression were selected for evaluation, as shown in the schema. Gene expression was measured using robust multiarray analysis (RMA) log2. (B and C) Decrease in tumour latency probability (B) and survival probability (C) in BX‐ Neu + mice with elevated intratumoural levels of Ncaph . (D and E) Tumour growth velocity and final volume for tumours with high or low levels of Ncaph . Weekly tumour volume was measured in mm 3 using a digital caliper and calculated as (greater diameter × lesser diameter 2 )/2. Growth velocity was determined by (final volume – initial volume)/illness duration in weeks, expressed in mm 3 /week. (F) Diagram showing the allogeneic transplantation strategy, passing tumours generated in BX‐ Neu + mice into immunocompetent F1 mice. Assessments were conducted on mice selected from the top and bottom tertiles. (G–I) Docetaxel Impact on Tumour Growth Relative to Ncaph Levels. (G) This panel displays growth curve slopes at crucial docetaxel treatment stages: pre‐chemotherapy (S1) and during chemotherapy (S2, indicating peak response). Response during treatment (RDT) is derived as S1 minus S2, with a higher RDT signifying better response. (H) RDT comparison across tumours with different Ncaph levels, classified by external tertiles. (I) Post‐chemotherapy growth changes or Evolution Changes Induced by Chemotherapy (ECIC) are shown by comparing slopes pre‐chemotherapy (S1) and post‐chemotherapy (S3), with a greater ECIC value indicating improved treatment outcome (external tertiles). (J) Univariate Poisson regression analysis indicates a positive correlation between intratumoural Ncaph levels and post‐chemotherapy lung metastases, with higher Ncaph levels linked to increased metastases ( p ‐values < .05). A positive ‘Estimate’ indicates a correlation between higher Ncaph levels and an increased count of lung metastases. (K and L) Poisson GLM analysis further confirms this correlation in mice treated with docetaxel (K) and doxorubicin (L), where individual mouse data points display the relationship between Ncaph RNA levels and metastasis count. The model's red line illustrates the trend, underscoring Ncaph's role in lung metastasis after breast tumour treatment with these drugs.
    Figure Legend Snippet: Intratumoural levels of Ncaph were associated with a worse outcome and response to chemotherapy in a cohort of mice generated by backcrossing (BX‐ Neu + ). (A) Generation scheme for BX‐ Neu + cohort: the BX‐ Neu + cohort was created by backcrossing transgenic Mouse Mammary Tumor Virus (MMTV)‐ ErbB2 mice (FVB/N background) with C57BL/6 mice, which are resistant to breast cancer. The first‐generation offspring (F1) were further crossed with wild‐type FVB/N mice, producing the BX‐ Neu + cohort. This cohort is genetically diverse, displaying a range of phenotypic traits and intratumoural Ncaph gene expression. Mice from the highest and lowest tertiles of Ncaph expression were selected for evaluation, as shown in the schema. Gene expression was measured using robust multiarray analysis (RMA) log2. (B and C) Decrease in tumour latency probability (B) and survival probability (C) in BX‐ Neu + mice with elevated intratumoural levels of Ncaph . (D and E) Tumour growth velocity and final volume for tumours with high or low levels of Ncaph . Weekly tumour volume was measured in mm 3 using a digital caliper and calculated as (greater diameter × lesser diameter 2 )/2. Growth velocity was determined by (final volume – initial volume)/illness duration in weeks, expressed in mm 3 /week. (F) Diagram showing the allogeneic transplantation strategy, passing tumours generated in BX‐ Neu + mice into immunocompetent F1 mice. Assessments were conducted on mice selected from the top and bottom tertiles. (G–I) Docetaxel Impact on Tumour Growth Relative to Ncaph Levels. (G) This panel displays growth curve slopes at crucial docetaxel treatment stages: pre‐chemotherapy (S1) and during chemotherapy (S2, indicating peak response). Response during treatment (RDT) is derived as S1 minus S2, with a higher RDT signifying better response. (H) RDT comparison across tumours with different Ncaph levels, classified by external tertiles. (I) Post‐chemotherapy growth changes or Evolution Changes Induced by Chemotherapy (ECIC) are shown by comparing slopes pre‐chemotherapy (S1) and post‐chemotherapy (S3), with a greater ECIC value indicating improved treatment outcome (external tertiles). (J) Univariate Poisson regression analysis indicates a positive correlation between intratumoural Ncaph levels and post‐chemotherapy lung metastases, with higher Ncaph levels linked to increased metastases ( p ‐values < .05). A positive ‘Estimate’ indicates a correlation between higher Ncaph levels and an increased count of lung metastases. (K and L) Poisson GLM analysis further confirms this correlation in mice treated with docetaxel (K) and doxorubicin (L), where individual mouse data points display the relationship between Ncaph RNA levels and metastasis count. The model's red line illustrates the trend, underscoring Ncaph's role in lung metastasis after breast tumour treatment with these drugs.

    Techniques Used: Generated, Transgenic Assay, Virus, Expressing, Transplantation Assay, Derivative Assay, Comparison

    Identifying a gene signature associated with non‐SMC condensin I complex subunit H ( NCAPH ) in the Mouse Mammary Tumor Virus (MMTV)‐ ErbB2 cohort of mice generated by backcrossing (BX‐ Neu + ) recognises the poor outcome in mice and humans. (A) Heatmap showing the 64 differentially expressed genes between tumours with high or low intratumoural levels of Ncaph in BX‐ Neu + mice, of which 45 were shared with humans. Extreme tertiles of Ncaph expression were taken to define the high and low levels of Ncaph . The criteria for underexpressed and overexpressed genes were a ← twofold and a > twofold change, respectively, and a value of p < .05 (Table ). (B) Gene Ontology analysis shows the main biological functions in which the 45 genes of the signature participate (Table ). (C) Some of the genes in the 45‐gene signature were associated with the poor outcome of breast cancer in MMTV‐ ErbB2 mice generated by backcrossing. Correlation of the intratumoural levels of these genes with specific pathophenotypes of breast cancer in BX‐ Neu + mice: Pearson's test. The incidence of metastasis was evaluated with a chi‐squared test. (D–G) Least absolute shrinkage and selection operator (LASSO) regression model that defines poor outcome in BX‐ Neu + mice. The regression coefficient map of genes in the LASSO model, using cross‐validation to select the optimal tuning parameter ( λ ). The dotted vertical lines were drawn at the optimal values using the minimum criteria and 1 standard error (SE) of the minimum criteria (the 1 – SE criteria) (D). The graph shows the screening path of the LASSO regression model. Each curve represents a LASSO coefficient of the 45 prognostic genes, and the x‐axis indicates the regularisation penalty parameter. When the number of variables was 4, the partial likelihood deviation was at the minimum, corresponding to the minimum λ value (E). The LASSO regression model generated differentiates between low‐, intermediate‐ and high‐risk BX‐ Neu + mice in terms of survival probability and as defined by tertiles. Kaplan‒Meier curve and log‐rank test (F). Goodness‐of‐fit measures for the generated LASSO models in the BX‐ Neu + mouse cohort. Training, testing and global model results (G). (H) The heatmap represents the association of gene transcript levels with the prognosis of human luminal breast tumours, in relation to Ncaph levels in mouse breast tumours from the backcross cohort. Colour coding: Brown indicates genes where high transcript levels are statistically significantly associated with poor prognosis; green denotes genes where low transcript levels correlate with poor prognosis. The heatmap is supported by detailed data on patient count, expression values, and p ‐values in Table . SMC, structural chromosome maintenance.
    Figure Legend Snippet: Identifying a gene signature associated with non‐SMC condensin I complex subunit H ( NCAPH ) in the Mouse Mammary Tumor Virus (MMTV)‐ ErbB2 cohort of mice generated by backcrossing (BX‐ Neu + ) recognises the poor outcome in mice and humans. (A) Heatmap showing the 64 differentially expressed genes between tumours with high or low intratumoural levels of Ncaph in BX‐ Neu + mice, of which 45 were shared with humans. Extreme tertiles of Ncaph expression were taken to define the high and low levels of Ncaph . The criteria for underexpressed and overexpressed genes were a ← twofold and a > twofold change, respectively, and a value of p < .05 (Table ). (B) Gene Ontology analysis shows the main biological functions in which the 45 genes of the signature participate (Table ). (C) Some of the genes in the 45‐gene signature were associated with the poor outcome of breast cancer in MMTV‐ ErbB2 mice generated by backcrossing. Correlation of the intratumoural levels of these genes with specific pathophenotypes of breast cancer in BX‐ Neu + mice: Pearson's test. The incidence of metastasis was evaluated with a chi‐squared test. (D–G) Least absolute shrinkage and selection operator (LASSO) regression model that defines poor outcome in BX‐ Neu + mice. The regression coefficient map of genes in the LASSO model, using cross‐validation to select the optimal tuning parameter ( λ ). The dotted vertical lines were drawn at the optimal values using the minimum criteria and 1 standard error (SE) of the minimum criteria (the 1 – SE criteria) (D). The graph shows the screening path of the LASSO regression model. Each curve represents a LASSO coefficient of the 45 prognostic genes, and the x‐axis indicates the regularisation penalty parameter. When the number of variables was 4, the partial likelihood deviation was at the minimum, corresponding to the minimum λ value (E). The LASSO regression model generated differentiates between low‐, intermediate‐ and high‐risk BX‐ Neu + mice in terms of survival probability and as defined by tertiles. Kaplan‒Meier curve and log‐rank test (F). Goodness‐of‐fit measures for the generated LASSO models in the BX‐ Neu + mouse cohort. Training, testing and global model results (G). (H) The heatmap represents the association of gene transcript levels with the prognosis of human luminal breast tumours, in relation to Ncaph levels in mouse breast tumours from the backcross cohort. Colour coding: Brown indicates genes where high transcript levels are statistically significantly associated with poor prognosis; green denotes genes where low transcript levels correlate with poor prognosis. The heatmap is supported by detailed data on patient count, expression values, and p ‐values in Table . SMC, structural chromosome maintenance.

    Techniques Used: Virus, Generated, Expressing, Selection

    anti erbb2  (Danaher Inc)


    Bioz Verified Symbol Danaher Inc is a verified supplier
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    Danaher Inc anti erbb2
    Effect of non‐SMC condensin I complex subunit H (NCAPH) expression on luminal <t>ERBB2‐positive</t> tumours in vivo. (A and B) Overexpression of NCAPH in patients with luminal ER‐positive HER2 + breast tumours was associated with a worse outcome (A), while this association was not seen in HER2 + ER‐negative tumours (B). Panels A and B were generated in the KM Plotter database. <xref ref-type= 59 Each graph displaying a Kaplan‐Meier curve panel specifies the number of patients it encompasses. Outcome (disease‐free survival [DFS] probability). Analysis using the KM plotter's optimal cutoff. (C) Scheme to generate double‐transgenic mice Mouse Mammary Tumor Virus (MMTV)‐ NCAPH ErBb2 . (D and E) Immunohistochemical proliferation assessment in non‐tumoural mammary glands: analysis of mammary glands from MMTV‐ ErbB2 (upper panels) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (D), with representative Ki67 immunohistochemistry images. Five mice per group were analysed, and field analysis results are shown in panel E, using the Mann–Whitney U ‐test. (F and G) Tumour development quantification: double‐transgenic mice exhibited significantly more tumours (F) and higher tumour multiplicity (G) compared to MMTV‐ ErbB2 mice. (H–J) Histopathological pattern analysis: this section assesses different histopathological patterns in the samples, focusing on nodular (H) and solid patterns (I). Notably, the solid pattern occurred more frequently in double‐transgenic mice compared to MMTV‐ ErbB2 mice (J). Ten mice per group were evaluated with a chi‐squared test. (K and L) Vascularisation variability in mouse tumours: the panels compare vascularisation in tumours from MMTV‐ ErbB2 and MMTV‐ NCAPH ErbB2 double‐transgenic mice. Haematoxylin–eosin staining is used to emphasise vascular differences between MMTV‐ ErbB2 (panel K) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (panel L). (M) Proliferative activity in tumour tissues: this section uses Ki67 immunohistochemical analysis to evaluate tumour proliferation in MMTV‐ ErbB2 (left) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (right). Quantitative results from this analysis are displayed below the corresponding images. (N) Mitotic index quantification using chi‐squared test. (O and P) Analysis of ERBB2 downstream signalling molecules via Western blot (O) with pAKT quantification (P). (Q and R) NCAPH induction increased genomic instability, evidenced by more micronuclei and chromosomal bridges (CIN). Micronuclei and chromosomal bridge images (Q) are accompanied by CIN quantification (R), analysed with Fisher's exact test. (S) Genomic stress linked to increased NCAPH is shown by elevated ɤH2AX levels post‐H 2 O 2 exposure and during 30‐ or 60‐min recovery. (T) pCHEK1 expression changes following NCAPH induction are displayed via Western blot. (U) RNA expression correlation in luminal breast cancer: this panel shows the correlation between NCAPH RNA and Ki67 , CHEK1 and H2AX in luminal breast cancer samples from The Cancer Genome Atlas (TCGA) database. It illustrates the correlation coefficients and patterns using CANCERTOOL. 62 SMC, structural chromosome maintenance. " width="250" height="auto" />
    Anti Erbb2, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti erbb2/product/Danaher Inc
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    1) Product Images from "NCAPH drives breast cancer progression and identifies a gene signature that predicts luminal a tumour recurrence"

    Article Title: NCAPH drives breast cancer progression and identifies a gene signature that predicts luminal a tumour recurrence

    Journal: Clinical and Translational Medicine

    doi: 10.1002/ctm2.1554

    Effect of non‐SMC condensin I complex subunit H (NCAPH) expression on luminal ERBB2‐positive tumours in vivo. (A and B) Overexpression of NCAPH in patients with luminal ER‐positive HER2 + breast tumours was associated with a worse outcome (A), while this association was not seen in HER2 + ER‐negative tumours (B). Panels A and B were generated in the KM Plotter database. <xref ref-type= 59 Each graph displaying a Kaplan‐Meier curve panel specifies the number of patients it encompasses. Outcome (disease‐free survival [DFS] probability). Analysis using the KM plotter's optimal cutoff. (C) Scheme to generate double‐transgenic mice Mouse Mammary Tumor Virus (MMTV)‐ NCAPH ErBb2 . (D and E) Immunohistochemical proliferation assessment in non‐tumoural mammary glands: analysis of mammary glands from MMTV‐ ErbB2 (upper panels) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (D), with representative Ki67 immunohistochemistry images. Five mice per group were analysed, and field analysis results are shown in panel E, using the Mann–Whitney U ‐test. (F and G) Tumour development quantification: double‐transgenic mice exhibited significantly more tumours (F) and higher tumour multiplicity (G) compared to MMTV‐ ErbB2 mice. (H–J) Histopathological pattern analysis: this section assesses different histopathological patterns in the samples, focusing on nodular (H) and solid patterns (I). Notably, the solid pattern occurred more frequently in double‐transgenic mice compared to MMTV‐ ErbB2 mice (J). Ten mice per group were evaluated with a chi‐squared test. (K and L) Vascularisation variability in mouse tumours: the panels compare vascularisation in tumours from MMTV‐ ErbB2 and MMTV‐ NCAPH ErbB2 double‐transgenic mice. Haematoxylin–eosin staining is used to emphasise vascular differences between MMTV‐ ErbB2 (panel K) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (panel L). (M) Proliferative activity in tumour tissues: this section uses Ki67 immunohistochemical analysis to evaluate tumour proliferation in MMTV‐ ErbB2 (left) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (right). Quantitative results from this analysis are displayed below the corresponding images. (N) Mitotic index quantification using chi‐squared test. (O and P) Analysis of ERBB2 downstream signalling molecules via Western blot (O) with pAKT quantification (P). (Q and R) NCAPH induction increased genomic instability, evidenced by more micronuclei and chromosomal bridges (CIN). Micronuclei and chromosomal bridge images (Q) are accompanied by CIN quantification (R), analysed with Fisher's exact test. (S) Genomic stress linked to increased NCAPH is shown by elevated ɤH2AX levels post‐H 2 O 2 exposure and during 30‐ or 60‐min recovery. (T) pCHEK1 expression changes following NCAPH induction are displayed via Western blot. (U) RNA expression correlation in luminal breast cancer: this panel shows the correlation between NCAPH RNA and Ki67 , CHEK1 and H2AX in luminal breast cancer samples from The Cancer Genome Atlas (TCGA) database. It illustrates the correlation coefficients and patterns using CANCERTOOL. 62 SMC, structural chromosome maintenance. " title="... I complex subunit H (NCAPH) expression on luminal ERBB2‐positive tumours in vivo. (A and B) Overexpression of ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: Effect of non‐SMC condensin I complex subunit H (NCAPH) expression on luminal ERBB2‐positive tumours in vivo. (A and B) Overexpression of NCAPH in patients with luminal ER‐positive HER2 + breast tumours was associated with a worse outcome (A), while this association was not seen in HER2 + ER‐negative tumours (B). Panels A and B were generated in the KM Plotter database. 59 Each graph displaying a Kaplan‐Meier curve panel specifies the number of patients it encompasses. Outcome (disease‐free survival [DFS] probability). Analysis using the KM plotter's optimal cutoff. (C) Scheme to generate double‐transgenic mice Mouse Mammary Tumor Virus (MMTV)‐ NCAPH ErBb2 . (D and E) Immunohistochemical proliferation assessment in non‐tumoural mammary glands: analysis of mammary glands from MMTV‐ ErbB2 (upper panels) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (D), with representative Ki67 immunohistochemistry images. Five mice per group were analysed, and field analysis results are shown in panel E, using the Mann–Whitney U ‐test. (F and G) Tumour development quantification: double‐transgenic mice exhibited significantly more tumours (F) and higher tumour multiplicity (G) compared to MMTV‐ ErbB2 mice. (H–J) Histopathological pattern analysis: this section assesses different histopathological patterns in the samples, focusing on nodular (H) and solid patterns (I). Notably, the solid pattern occurred more frequently in double‐transgenic mice compared to MMTV‐ ErbB2 mice (J). Ten mice per group were evaluated with a chi‐squared test. (K and L) Vascularisation variability in mouse tumours: the panels compare vascularisation in tumours from MMTV‐ ErbB2 and MMTV‐ NCAPH ErbB2 double‐transgenic mice. Haematoxylin–eosin staining is used to emphasise vascular differences between MMTV‐ ErbB2 (panel K) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (panel L). (M) Proliferative activity in tumour tissues: this section uses Ki67 immunohistochemical analysis to evaluate tumour proliferation in MMTV‐ ErbB2 (left) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (right). Quantitative results from this analysis are displayed below the corresponding images. (N) Mitotic index quantification using chi‐squared test. (O and P) Analysis of ERBB2 downstream signalling molecules via Western blot (O) with pAKT quantification (P). (Q and R) NCAPH induction increased genomic instability, evidenced by more micronuclei and chromosomal bridges (CIN). Micronuclei and chromosomal bridge images (Q) are accompanied by CIN quantification (R), analysed with Fisher's exact test. (S) Genomic stress linked to increased NCAPH is shown by elevated ɤH2AX levels post‐H 2 O 2 exposure and during 30‐ or 60‐min recovery. (T) pCHEK1 expression changes following NCAPH induction are displayed via Western blot. (U) RNA expression correlation in luminal breast cancer: this panel shows the correlation between NCAPH RNA and Ki67 , CHEK1 and H2AX in luminal breast cancer samples from The Cancer Genome Atlas (TCGA) database. It illustrates the correlation coefficients and patterns using CANCERTOOL. 62 SMC, structural chromosome maintenance.

    Techniques Used: Expressing, In Vivo, Over Expression, Generated, Transgenic Assay, Virus, Immunohistochemistry, MANN-WHITNEY, Staining, Activity Assay, Western Blot, RNA Expression

    Intratumoural levels of Ncaph were associated with a worse outcome and response to chemotherapy in a cohort of mice generated by backcrossing (BX‐ Neu + ). (A) Generation scheme for BX‐ Neu + cohort: the BX‐ Neu + cohort was created by backcrossing transgenic Mouse Mammary Tumor Virus (MMTV)‐ ErbB2 mice (FVB/N background) with C57BL/6 mice, which are resistant to breast cancer. The first‐generation offspring (F1) were further crossed with wild‐type FVB/N mice, producing the BX‐ Neu + cohort. This cohort is genetically diverse, displaying a range of phenotypic traits and intratumoural Ncaph gene expression. Mice from the highest and lowest tertiles of Ncaph expression were selected for evaluation, as shown in the schema. Gene expression was measured using robust multiarray analysis (RMA) log2. (B and C) Decrease in tumour latency probability (B) and survival probability (C) in BX‐ Neu + mice with elevated intratumoural levels of Ncaph . (D and E) Tumour growth velocity and final volume for tumours with high or low levels of Ncaph . Weekly tumour volume was measured in mm 3 using a digital caliper and calculated as (greater diameter × lesser diameter 2 )/2. Growth velocity was determined by (final volume – initial volume)/illness duration in weeks, expressed in mm 3 /week. (F) Diagram showing the allogeneic transplantation strategy, passing tumours generated in BX‐ Neu + mice into immunocompetent F1 mice. Assessments were conducted on mice selected from the top and bottom tertiles. (G–I) Docetaxel Impact on Tumour Growth Relative to Ncaph Levels. (G) This panel displays growth curve slopes at crucial docetaxel treatment stages: pre‐chemotherapy (S1) and during chemotherapy (S2, indicating peak response). Response during treatment (RDT) is derived as S1 minus S2, with a higher RDT signifying better response. (H) RDT comparison across tumours with different Ncaph levels, classified by external tertiles. (I) Post‐chemotherapy growth changes or Evolution Changes Induced by Chemotherapy (ECIC) are shown by comparing slopes pre‐chemotherapy (S1) and post‐chemotherapy (S3), with a greater ECIC value indicating improved treatment outcome (external tertiles). (J) Univariate Poisson regression analysis indicates a positive correlation between intratumoural Ncaph levels and post‐chemotherapy lung metastases, with higher Ncaph levels linked to increased metastases ( p ‐values < .05). A positive ‘Estimate’ indicates a correlation between higher Ncaph levels and an increased count of lung metastases. (K and L) Poisson GLM analysis further confirms this correlation in mice treated with docetaxel (K) and doxorubicin (L), where individual mouse data points display the relationship between Ncaph RNA levels and metastasis count. The model's red line illustrates the trend, underscoring Ncaph's role in lung metastasis after breast tumour treatment with these drugs.
    Figure Legend Snippet: Intratumoural levels of Ncaph were associated with a worse outcome and response to chemotherapy in a cohort of mice generated by backcrossing (BX‐ Neu + ). (A) Generation scheme for BX‐ Neu + cohort: the BX‐ Neu + cohort was created by backcrossing transgenic Mouse Mammary Tumor Virus (MMTV)‐ ErbB2 mice (FVB/N background) with C57BL/6 mice, which are resistant to breast cancer. The first‐generation offspring (F1) were further crossed with wild‐type FVB/N mice, producing the BX‐ Neu + cohort. This cohort is genetically diverse, displaying a range of phenotypic traits and intratumoural Ncaph gene expression. Mice from the highest and lowest tertiles of Ncaph expression were selected for evaluation, as shown in the schema. Gene expression was measured using robust multiarray analysis (RMA) log2. (B and C) Decrease in tumour latency probability (B) and survival probability (C) in BX‐ Neu + mice with elevated intratumoural levels of Ncaph . (D and E) Tumour growth velocity and final volume for tumours with high or low levels of Ncaph . Weekly tumour volume was measured in mm 3 using a digital caliper and calculated as (greater diameter × lesser diameter 2 )/2. Growth velocity was determined by (final volume – initial volume)/illness duration in weeks, expressed in mm 3 /week. (F) Diagram showing the allogeneic transplantation strategy, passing tumours generated in BX‐ Neu + mice into immunocompetent F1 mice. Assessments were conducted on mice selected from the top and bottom tertiles. (G–I) Docetaxel Impact on Tumour Growth Relative to Ncaph Levels. (G) This panel displays growth curve slopes at crucial docetaxel treatment stages: pre‐chemotherapy (S1) and during chemotherapy (S2, indicating peak response). Response during treatment (RDT) is derived as S1 minus S2, with a higher RDT signifying better response. (H) RDT comparison across tumours with different Ncaph levels, classified by external tertiles. (I) Post‐chemotherapy growth changes or Evolution Changes Induced by Chemotherapy (ECIC) are shown by comparing slopes pre‐chemotherapy (S1) and post‐chemotherapy (S3), with a greater ECIC value indicating improved treatment outcome (external tertiles). (J) Univariate Poisson regression analysis indicates a positive correlation between intratumoural Ncaph levels and post‐chemotherapy lung metastases, with higher Ncaph levels linked to increased metastases ( p ‐values < .05). A positive ‘Estimate’ indicates a correlation between higher Ncaph levels and an increased count of lung metastases. (K and L) Poisson GLM analysis further confirms this correlation in mice treated with docetaxel (K) and doxorubicin (L), where individual mouse data points display the relationship between Ncaph RNA levels and metastasis count. The model's red line illustrates the trend, underscoring Ncaph's role in lung metastasis after breast tumour treatment with these drugs.

    Techniques Used: Generated, Transgenic Assay, Virus, Expressing, Transplantation Assay, Derivative Assay, Comparison

    Identifying a gene signature associated with non‐SMC condensin I complex subunit H ( NCAPH ) in the Mouse Mammary Tumor Virus (MMTV)‐ ErbB2 cohort of mice generated by backcrossing (BX‐ Neu + ) recognises the poor outcome in mice and humans. (A) Heatmap showing the 64 differentially expressed genes between tumours with high or low intratumoural levels of Ncaph in BX‐ Neu + mice, of which 45 were shared with humans. Extreme tertiles of Ncaph expression were taken to define the high and low levels of Ncaph . The criteria for underexpressed and overexpressed genes were a ← twofold and a > twofold change, respectively, and a value of p < .05 (Table ). (B) Gene Ontology analysis shows the main biological functions in which the 45 genes of the signature participate (Table ). (C) Some of the genes in the 45‐gene signature were associated with the poor outcome of breast cancer in MMTV‐ ErbB2 mice generated by backcrossing. Correlation of the intratumoural levels of these genes with specific pathophenotypes of breast cancer in BX‐ Neu + mice: Pearson's test. The incidence of metastasis was evaluated with a chi‐squared test. (D–G) Least absolute shrinkage and selection operator (LASSO) regression model that defines poor outcome in BX‐ Neu + mice. The regression coefficient map of genes in the LASSO model, using cross‐validation to select the optimal tuning parameter ( λ ). The dotted vertical lines were drawn at the optimal values using the minimum criteria and 1 standard error (SE) of the minimum criteria (the 1 – SE criteria) (D). The graph shows the screening path of the LASSO regression model. Each curve represents a LASSO coefficient of the 45 prognostic genes, and the x‐axis indicates the regularisation penalty parameter. When the number of variables was 4, the partial likelihood deviation was at the minimum, corresponding to the minimum λ value (E). The LASSO regression model generated differentiates between low‐, intermediate‐ and high‐risk BX‐ Neu + mice in terms of survival probability and as defined by tertiles. Kaplan‒Meier curve and log‐rank test (F). Goodness‐of‐fit measures for the generated LASSO models in the BX‐ Neu + mouse cohort. Training, testing and global model results (G). (H) The heatmap represents the association of gene transcript levels with the prognosis of human luminal breast tumours, in relation to Ncaph levels in mouse breast tumours from the backcross cohort. Colour coding: Brown indicates genes where high transcript levels are statistically significantly associated with poor prognosis; green denotes genes where low transcript levels correlate with poor prognosis. The heatmap is supported by detailed data on patient count, expression values, and p ‐values in Table . SMC, structural chromosome maintenance.
    Figure Legend Snippet: Identifying a gene signature associated with non‐SMC condensin I complex subunit H ( NCAPH ) in the Mouse Mammary Tumor Virus (MMTV)‐ ErbB2 cohort of mice generated by backcrossing (BX‐ Neu + ) recognises the poor outcome in mice and humans. (A) Heatmap showing the 64 differentially expressed genes between tumours with high or low intratumoural levels of Ncaph in BX‐ Neu + mice, of which 45 were shared with humans. Extreme tertiles of Ncaph expression were taken to define the high and low levels of Ncaph . The criteria for underexpressed and overexpressed genes were a ← twofold and a > twofold change, respectively, and a value of p < .05 (Table ). (B) Gene Ontology analysis shows the main biological functions in which the 45 genes of the signature participate (Table ). (C) Some of the genes in the 45‐gene signature were associated with the poor outcome of breast cancer in MMTV‐ ErbB2 mice generated by backcrossing. Correlation of the intratumoural levels of these genes with specific pathophenotypes of breast cancer in BX‐ Neu + mice: Pearson's test. The incidence of metastasis was evaluated with a chi‐squared test. (D–G) Least absolute shrinkage and selection operator (LASSO) regression model that defines poor outcome in BX‐ Neu + mice. The regression coefficient map of genes in the LASSO model, using cross‐validation to select the optimal tuning parameter ( λ ). The dotted vertical lines were drawn at the optimal values using the minimum criteria and 1 standard error (SE) of the minimum criteria (the 1 – SE criteria) (D). The graph shows the screening path of the LASSO regression model. Each curve represents a LASSO coefficient of the 45 prognostic genes, and the x‐axis indicates the regularisation penalty parameter. When the number of variables was 4, the partial likelihood deviation was at the minimum, corresponding to the minimum λ value (E). The LASSO regression model generated differentiates between low‐, intermediate‐ and high‐risk BX‐ Neu + mice in terms of survival probability and as defined by tertiles. Kaplan‒Meier curve and log‐rank test (F). Goodness‐of‐fit measures for the generated LASSO models in the BX‐ Neu + mouse cohort. Training, testing and global model results (G). (H) The heatmap represents the association of gene transcript levels with the prognosis of human luminal breast tumours, in relation to Ncaph levels in mouse breast tumours from the backcross cohort. Colour coding: Brown indicates genes where high transcript levels are statistically significantly associated with poor prognosis; green denotes genes where low transcript levels correlate with poor prognosis. The heatmap is supported by detailed data on patient count, expression values, and p ‐values in Table . SMC, structural chromosome maintenance.

    Techniques Used: Virus, Generated, Expressing, Selection

    anti erbb2  (Danaher Inc)


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    Danaher Inc anti erbb2
    Sequences of all Primers.
    Anti Erbb2, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Clinical significance and immune characteristics analysis of miR-221-3p and its key target genes related to epithelial-mesenchymal transition in breast cancer"

    Article Title: Clinical significance and immune characteristics analysis of miR-221-3p and its key target genes related to epithelial-mesenchymal transition in breast cancer

    Journal: Aging (Albany NY)

    doi: 10.18632/aging.205370

    Sequences of all Primers.
    Figure Legend Snippet: Sequences of all Primers.

    Techniques Used: Sequencing

    Analysis of genetic alteration of 10 ETGs ( A ). The KM survival curves show the OS and DSS between the ETGs altered group and the unaltered group ( B , C ). The KM survival curve shows the OS of the ETGs-unaltered group and the ETGs-altered groups of EGFR, ERBB2 and FGFR1 ( D ).
    Figure Legend Snippet: Analysis of genetic alteration of 10 ETGs ( A ). The KM survival curves show the OS and DSS between the ETGs altered group and the unaltered group ( B , C ). The KM survival curve shows the OS of the ETGs-unaltered group and the ETGs-altered groups of EGFR, ERBB2 and FGFR1 ( D ).

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    anti her 2  (Danaher Inc)


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    Danaher Inc anti her 2
    Anti Her 2, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti her 2  (Danaher Inc)


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    Danaher Inc anti her 2
    Anti Her 2, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti erbb2 antibody  (Danaher Inc)


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    Danaher Inc anti erbb2 antibody
    Determination <t>of</t> <t>Her-2,</t> MutP53, Ki67, and Mismatch repair (MMR) proteins immunohistochemical staining results. Her-2 protein expression levels of negative (A) , 1+ (B) , 2+ (C) , 3+ (D) . MutP53 proteins expression levels of 10%+ (E) , 30%+ (F) , 50%+ (G) , 70%+ (H) , 90%+ (I) . Ki67 protein expression levels of 10%+ (J) , 30%+ (K) , 50%+ (L) , 70%+ (M) , 90%+ (N) . MLH1 protein negative (O) and positive (P) expression. MSH2 protein negative (Q) and positive (R) expression. MSH6 protein negative (S) and positive (T) expression. PSM2 protein negative (U) and positive (V) expression.
    Anti Erbb2 Antibody, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Exploration and validation of the Ki67, Her-2, and mutant P53 protein-based risk model, nomogram and lymph node metastasis model for predicting colorectal cancer progression and prognosis"

    Article Title: Exploration and validation of the Ki67, Her-2, and mutant P53 protein-based risk model, nomogram and lymph node metastasis model for predicting colorectal cancer progression and prognosis

    Journal: Frontiers in Oncology

    doi: 10.3389/fonc.2023.1236441

    Determination of Her-2, MutP53, Ki67, and Mismatch repair (MMR) proteins immunohistochemical staining results. Her-2 protein expression levels of negative (A) , 1+ (B) , 2+ (C) , 3+ (D) . MutP53 proteins expression levels of 10%+ (E) , 30%+ (F) , 50%+ (G) , 70%+ (H) , 90%+ (I) . Ki67 protein expression levels of 10%+ (J) , 30%+ (K) , 50%+ (L) , 70%+ (M) , 90%+ (N) . MLH1 protein negative (O) and positive (P) expression. MSH2 protein negative (Q) and positive (R) expression. MSH6 protein negative (S) and positive (T) expression. PSM2 protein negative (U) and positive (V) expression.
    Figure Legend Snippet: Determination of Her-2, MutP53, Ki67, and Mismatch repair (MMR) proteins immunohistochemical staining results. Her-2 protein expression levels of negative (A) , 1+ (B) , 2+ (C) , 3+ (D) . MutP53 proteins expression levels of 10%+ (E) , 30%+ (F) , 50%+ (G) , 70%+ (H) , 90%+ (I) . Ki67 protein expression levels of 10%+ (J) , 30%+ (K) , 50%+ (L) , 70%+ (M) , 90%+ (N) . MLH1 protein negative (O) and positive (P) expression. MSH2 protein negative (Q) and positive (R) expression. MSH6 protein negative (S) and positive (T) expression. PSM2 protein negative (U) and positive (V) expression.

    Techniques Used: Immunohistochemistry, Staining, Expressing

    Overall pathological characteristics of patients with CRC and the relationship between Ki67, Her-2, and MutP53 expression. Relationship between Ki67, Her-2, and MutP53 protein expression (A) . General situation of Ki67, Her-2 and MutP53 protein expression in 755 CRC patients with different pathological characteristics (B) .
    Figure Legend Snippet: Overall pathological characteristics of patients with CRC and the relationship between Ki67, Her-2, and MutP53 expression. Relationship between Ki67, Her-2, and MutP53 protein expression (A) . General situation of Ki67, Her-2 and MutP53 protein expression in 755 CRC patients with different pathological characteristics (B) .

    Techniques Used: Expressing

    Determination of Ki67, Her-2 and MutP53 proteins immunohistochemical staining results. Determination of Ki67 (A) , Her-2 (B) and MutP53 (C) proteins immunohistochemical staining results.
    Figure Legend Snippet: Determination of Ki67, Her-2 and MutP53 proteins immunohistochemical staining results. Determination of Ki67 (A) , Her-2 (B) and MutP53 (C) proteins immunohistochemical staining results.

    Techniques Used: Immunohistochemistry, Staining

    Comparisons between Her-2 protein expression and the pathological features of CRC. Comparisons between Her-2 protein expression and age (A) , sex (B) , mucinous carcinoma component (C) , MMR (D) , Signet ring cell component (E) , adenoma carcinogenesis (F) , perineural invasion (G) , vascular invasion (H) , organization differentiation (I) , T stage (J) , N stage (K) , TNM stage (L) , tumor location (M) . *P < 0.05; ***P < 0.001; ns, not significant.
    Figure Legend Snippet: Comparisons between Her-2 protein expression and the pathological features of CRC. Comparisons between Her-2 protein expression and age (A) , sex (B) , mucinous carcinoma component (C) , MMR (D) , Signet ring cell component (E) , adenoma carcinogenesis (F) , perineural invasion (G) , vascular invasion (H) , organization differentiation (I) , T stage (J) , N stage (K) , TNM stage (L) , tumor location (M) . *P < 0.05; ***P < 0.001; ns, not significant.

    Techniques Used: Expressing

    Analysis of survival differences based on the expression of Ki67, Her-2, and MutP53, and various pathological features in patients with colorectal cancer (CRC). The Kaplan–Meier curves demonstrate differences in prognosis based on Her-2 expression (A) , Ki67 expression (B) , MutP53 expression (C) , T-stage (D) , N-stage (E) , signet ring cell carcinoma component (F) , perineural invasion (G) , vascular invasion (H) , adenoma carcinogenesis (I) , MMR (J) , sex (K) , age (L) , TNM stage (M) , organization differentiation (N) , and tumor location (O) .
    Figure Legend Snippet: Analysis of survival differences based on the expression of Ki67, Her-2, and MutP53, and various pathological features in patients with colorectal cancer (CRC). The Kaplan–Meier curves demonstrate differences in prognosis based on Her-2 expression (A) , Ki67 expression (B) , MutP53 expression (C) , T-stage (D) , N-stage (E) , signet ring cell carcinoma component (F) , perineural invasion (G) , vascular invasion (H) , adenoma carcinogenesis (I) , MMR (J) , sex (K) , age (L) , TNM stage (M) , organization differentiation (N) , and tumor location (O) .

    Techniques Used: Expressing

    Establishment and prognostic evaluation of the risk model. (A) Interaction network of Ki67, Her-2, and P53 protein expression and other related proteins. (B) Establishment of the risk model using the multivariate Cox proportional hazards regression analysis. (C) Alluvial plot showing the relationship between TNM stage, risk groups, and survival status. Survival (D) and cumulative hazard (E) differences between high and low risk groups. Predictive efficacy of the risk model (F) , Ki67 protein expression (G) , Her-2 protein expression (H) , and MutP53 protein expression (I) for survival at 12, 36, and 60 months. (J) Risk factor plot of the risk model. (K) PCA plot testing the discrimination between the high-risk and low-risk groups. (L) Prognostic calibration curve for the risk model.
    Figure Legend Snippet: Establishment and prognostic evaluation of the risk model. (A) Interaction network of Ki67, Her-2, and P53 protein expression and other related proteins. (B) Establishment of the risk model using the multivariate Cox proportional hazards regression analysis. (C) Alluvial plot showing the relationship between TNM stage, risk groups, and survival status. Survival (D) and cumulative hazard (E) differences between high and low risk groups. Predictive efficacy of the risk model (F) , Ki67 protein expression (G) , Her-2 protein expression (H) , and MutP53 protein expression (I) for survival at 12, 36, and 60 months. (J) Risk factor plot of the risk model. (K) PCA plot testing the discrimination between the high-risk and low-risk groups. (L) Prognostic calibration curve for the risk model.

    Techniques Used: Expressing

    recombinant human erbb2 her2 ab60866  (Danaher Inc)


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    Danaher Inc recombinant human erbb2 her2 ab60866
    Recombinant Human Erbb2 Her2 Ab60866, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    erbb2  (Danaher Inc)


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    Danaher Inc erbb2
    Erbb2, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    erbb2  (Danaher Inc)


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    Structured Review

    Danaher Inc erbb2
    ATM is involved in vascular injury in T2D through the ErbB signaling pathway. (A, B) GSEA was used to screen the genes related to T2D occurrence in the GSE26168 dataset. (C) The matrix correlation calculation tool was used to analyze the correlation between genes regulating the ErbB signaling pathway and T2D-related genes. (D) The PPI network for the regulation of ATM on the ErbB signaling pathway. (E) The expression of ATM in the GSE26168 dataset. (F) The ChIPBase website validated the co-expression relationship between ATM and the ErbB1, <t>ErbB2,</t> and ErbB4 genes in vascular tissues.
    Erbb2, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "miR-135a-5p overexpression in peripheral blood-derived exosomes mediates vascular injury in type 2 diabetes patients"

    Article Title: miR-135a-5p overexpression in peripheral blood-derived exosomes mediates vascular injury in type 2 diabetes patients

    Journal: Frontiers in Endocrinology

    doi: 10.3389/fendo.2023.1035029

    ATM is involved in vascular injury in T2D through the ErbB signaling pathway. (A, B) GSEA was used to screen the genes related to T2D occurrence in the GSE26168 dataset. (C) The matrix correlation calculation tool was used to analyze the correlation between genes regulating the ErbB signaling pathway and T2D-related genes. (D) The PPI network for the regulation of ATM on the ErbB signaling pathway. (E) The expression of ATM in the GSE26168 dataset. (F) The ChIPBase website validated the co-expression relationship between ATM and the ErbB1, ErbB2, and ErbB4 genes in vascular tissues.
    Figure Legend Snippet: ATM is involved in vascular injury in T2D through the ErbB signaling pathway. (A, B) GSEA was used to screen the genes related to T2D occurrence in the GSE26168 dataset. (C) The matrix correlation calculation tool was used to analyze the correlation between genes regulating the ErbB signaling pathway and T2D-related genes. (D) The PPI network for the regulation of ATM on the ErbB signaling pathway. (E) The expression of ATM in the GSE26168 dataset. (F) The ChIPBase website validated the co-expression relationship between ATM and the ErbB1, ErbB2, and ErbB4 genes in vascular tissues.

    Techniques Used: Expressing

    Peripheral blood-derived Exos from T2D patients carrying miR-135a-3p alleviate vascular injury in T2D by regulating the ATM/ErbB axis. (A) Dual-luciferase gene reporter assay verified the targeting relationship between miR-135a-3p and ATM. (B) The transwell assay was used to detect the migration ability of HVSMCs. (C) The expression of miR-135a-3p in HVSMCs was determined by RT-qPCR. (D) The expression of ATM, ErbB2, Bcl-2, VEGF, and Bax was determined by Western blot. * p < 0.05 vs. hC-Exos. # p < 0.05 vs. hT2D-Exos.
    Figure Legend Snippet: Peripheral blood-derived Exos from T2D patients carrying miR-135a-3p alleviate vascular injury in T2D by regulating the ATM/ErbB axis. (A) Dual-luciferase gene reporter assay verified the targeting relationship between miR-135a-3p and ATM. (B) The transwell assay was used to detect the migration ability of HVSMCs. (C) The expression of miR-135a-3p in HVSMCs was determined by RT-qPCR. (D) The expression of ATM, ErbB2, Bcl-2, VEGF, and Bax was determined by Western blot. * p < 0.05 vs. hC-Exos. # p < 0.05 vs. hT2D-Exos.

    Techniques Used: Derivative Assay, Luciferase, Reporter Assay, Transwell Assay, Migration, Expressing, Quantitative RT-PCR, Western Blot

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    Danaher Inc anti erbb2
    miR‐449c‐5p targeted <t>ERBB2.</t> (A) The predictive binding site of miR‐449c‐5p and ERBB2. (B) Luciferase activity of WT and MUT after co‐transfected with ERBB2 + miR‐449c‐5p into T47D cells. (C) Western blotting was used to investigate the expression level of ERBB2. (D) Relative expression of ERBB2 was evaluated in breast cancer tissues and normal tissues. (E) The distant metastasis survival curves with high or low ERBB2 expression. (F) The disease‐free survival curves with high or low ERBB2 expression. (G) The relapse survival curves with high or low ERBB2 expression.(H) The disease‐specific survival curves with high or low ERBB2 expression.(I) The overall survival curves with high or low ERBB2 expression. The results are presented as mean ± SD. n.s, not significant, *** P < .001, ** P < .01 and * P < .05. Statistical significance was analysed by two‐way ANOVA and t ‐test.
    Anti Erbb2, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Danaher Inc phospho erbb2 tyr1248
    Effect of non‐SMC condensin I complex subunit H (NCAPH) expression on luminal <t>ERBB2‐positive</t> tumours in vivo. (A and B) Overexpression of NCAPH in patients with luminal ER‐positive HER2 + breast tumours was associated with a worse outcome (A), while this association was not seen in HER2 + ER‐negative tumours (B). Panels A and B were generated in the KM Plotter database. <xref ref-type= 59 Each graph displaying a Kaplan‐Meier curve panel specifies the number of patients it encompasses. Outcome (disease‐free survival [DFS] probability). Analysis using the KM plotter's optimal cutoff. (C) Scheme to generate double‐transgenic mice Mouse Mammary Tumor Virus (MMTV)‐ NCAPH ErBb2 . (D and E) Immunohistochemical proliferation assessment in non‐tumoural mammary glands: analysis of mammary glands from MMTV‐ ErbB2 (upper panels) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (D), with representative Ki67 immunohistochemistry images. Five mice per group were analysed, and field analysis results are shown in panel E, using the Mann–Whitney U ‐test. (F and G) Tumour development quantification: double‐transgenic mice exhibited significantly more tumours (F) and higher tumour multiplicity (G) compared to MMTV‐ ErbB2 mice. (H–J) Histopathological pattern analysis: this section assesses different histopathological patterns in the samples, focusing on nodular (H) and solid patterns (I). Notably, the solid pattern occurred more frequently in double‐transgenic mice compared to MMTV‐ ErbB2 mice (J). Ten mice per group were evaluated with a chi‐squared test. (K and L) Vascularisation variability in mouse tumours: the panels compare vascularisation in tumours from MMTV‐ ErbB2 and MMTV‐ NCAPH ErbB2 double‐transgenic mice. Haematoxylin–eosin staining is used to emphasise vascular differences between MMTV‐ ErbB2 (panel K) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (panel L). (M) Proliferative activity in tumour tissues: this section uses Ki67 immunohistochemical analysis to evaluate tumour proliferation in MMTV‐ ErbB2 (left) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (right). Quantitative results from this analysis are displayed below the corresponding images. (N) Mitotic index quantification using chi‐squared test. (O and P) Analysis of ERBB2 downstream signalling molecules via Western blot (O) with pAKT quantification (P). (Q and R) NCAPH induction increased genomic instability, evidenced by more micronuclei and chromosomal bridges (CIN). Micronuclei and chromosomal bridge images (Q) are accompanied by CIN quantification (R), analysed with Fisher's exact test. (S) Genomic stress linked to increased NCAPH is shown by elevated ɤH2AX levels post‐H 2 O 2 exposure and during 30‐ or 60‐min recovery. (T) pCHEK1 expression changes following NCAPH induction are displayed via Western blot. (U) RNA expression correlation in luminal breast cancer: this panel shows the correlation between NCAPH RNA and Ki67 , CHEK1 and H2AX in luminal breast cancer samples from The Cancer Genome Atlas (TCGA) database. It illustrates the correlation coefficients and patterns using CANCERTOOL. 62 SMC, structural chromosome maintenance. " width="250" height="auto" />
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    Danaher Inc anti her 2
    Effect of non‐SMC condensin I complex subunit H (NCAPH) expression on luminal <t>ERBB2‐positive</t> tumours in vivo. (A and B) Overexpression of NCAPH in patients with luminal ER‐positive HER2 + breast tumours was associated with a worse outcome (A), while this association was not seen in HER2 + ER‐negative tumours (B). Panels A and B were generated in the KM Plotter database. <xref ref-type= 59 Each graph displaying a Kaplan‐Meier curve panel specifies the number of patients it encompasses. Outcome (disease‐free survival [DFS] probability). Analysis using the KM plotter's optimal cutoff. (C) Scheme to generate double‐transgenic mice Mouse Mammary Tumor Virus (MMTV)‐ NCAPH ErBb2 . (D and E) Immunohistochemical proliferation assessment in non‐tumoural mammary glands: analysis of mammary glands from MMTV‐ ErbB2 (upper panels) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (D), with representative Ki67 immunohistochemistry images. Five mice per group were analysed, and field analysis results are shown in panel E, using the Mann–Whitney U ‐test. (F and G) Tumour development quantification: double‐transgenic mice exhibited significantly more tumours (F) and higher tumour multiplicity (G) compared to MMTV‐ ErbB2 mice. (H–J) Histopathological pattern analysis: this section assesses different histopathological patterns in the samples, focusing on nodular (H) and solid patterns (I). Notably, the solid pattern occurred more frequently in double‐transgenic mice compared to MMTV‐ ErbB2 mice (J). Ten mice per group were evaluated with a chi‐squared test. (K and L) Vascularisation variability in mouse tumours: the panels compare vascularisation in tumours from MMTV‐ ErbB2 and MMTV‐ NCAPH ErbB2 double‐transgenic mice. Haematoxylin–eosin staining is used to emphasise vascular differences between MMTV‐ ErbB2 (panel K) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (panel L). (M) Proliferative activity in tumour tissues: this section uses Ki67 immunohistochemical analysis to evaluate tumour proliferation in MMTV‐ ErbB2 (left) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (right). Quantitative results from this analysis are displayed below the corresponding images. (N) Mitotic index quantification using chi‐squared test. (O and P) Analysis of ERBB2 downstream signalling molecules via Western blot (O) with pAKT quantification (P). (Q and R) NCAPH induction increased genomic instability, evidenced by more micronuclei and chromosomal bridges (CIN). Micronuclei and chromosomal bridge images (Q) are accompanied by CIN quantification (R), analysed with Fisher's exact test. (S) Genomic stress linked to increased NCAPH is shown by elevated ɤH2AX levels post‐H 2 O 2 exposure and during 30‐ or 60‐min recovery. (T) pCHEK1 expression changes following NCAPH induction are displayed via Western blot. (U) RNA expression correlation in luminal breast cancer: this panel shows the correlation between NCAPH RNA and Ki67 , CHEK1 and H2AX in luminal breast cancer samples from The Cancer Genome Atlas (TCGA) database. It illustrates the correlation coefficients and patterns using CANCERTOOL. 62 SMC, structural chromosome maintenance. " width="250" height="auto" />
    Anti Her 2, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Danaher Inc anti erbb2 antibody
    Determination <t>of</t> <t>Her-2,</t> MutP53, Ki67, and Mismatch repair (MMR) proteins immunohistochemical staining results. Her-2 protein expression levels of negative (A) , 1+ (B) , 2+ (C) , 3+ (D) . MutP53 proteins expression levels of 10%+ (E) , 30%+ (F) , 50%+ (G) , 70%+ (H) , 90%+ (I) . Ki67 protein expression levels of 10%+ (J) , 30%+ (K) , 50%+ (L) , 70%+ (M) , 90%+ (N) . MLH1 protein negative (O) and positive (P) expression. MSH2 protein negative (Q) and positive (R) expression. MSH6 protein negative (S) and positive (T) expression. PSM2 protein negative (U) and positive (V) expression.
    Anti Erbb2 Antibody, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Danaher Inc recombinant human erbb2 her2 ab60866
    Determination <t>of</t> <t>Her-2,</t> MutP53, Ki67, and Mismatch repair (MMR) proteins immunohistochemical staining results. Her-2 protein expression levels of negative (A) , 1+ (B) , 2+ (C) , 3+ (D) . MutP53 proteins expression levels of 10%+ (E) , 30%+ (F) , 50%+ (G) , 70%+ (H) , 90%+ (I) . Ki67 protein expression levels of 10%+ (J) , 30%+ (K) , 50%+ (L) , 70%+ (M) , 90%+ (N) . MLH1 protein negative (O) and positive (P) expression. MSH2 protein negative (Q) and positive (R) expression. MSH6 protein negative (S) and positive (T) expression. PSM2 protein negative (U) and positive (V) expression.
    Recombinant Human Erbb2 Her2 Ab60866, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    recombinant human erbb2 her2 ab60866 - by Bioz Stars, 2024-02
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    Danaher Inc erbb2
    Determination <t>of</t> <t>Her-2,</t> MutP53, Ki67, and Mismatch repair (MMR) proteins immunohistochemical staining results. Her-2 protein expression levels of negative (A) , 1+ (B) , 2+ (C) , 3+ (D) . MutP53 proteins expression levels of 10%+ (E) , 30%+ (F) , 50%+ (G) , 70%+ (H) , 90%+ (I) . Ki67 protein expression levels of 10%+ (J) , 30%+ (K) , 50%+ (L) , 70%+ (M) , 90%+ (N) . MLH1 protein negative (O) and positive (P) expression. MSH2 protein negative (Q) and positive (R) expression. MSH6 protein negative (S) and positive (T) expression. PSM2 protein negative (U) and positive (V) expression.
    Erbb2, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    miR‐449c‐5p targeted ERBB2. (A) The predictive binding site of miR‐449c‐5p and ERBB2. (B) Luciferase activity of WT and MUT after co‐transfected with ERBB2 + miR‐449c‐5p into T47D cells. (C) Western blotting was used to investigate the expression level of ERBB2. (D) Relative expression of ERBB2 was evaluated in breast cancer tissues and normal tissues. (E) The distant metastasis survival curves with high or low ERBB2 expression. (F) The disease‐free survival curves with high or low ERBB2 expression. (G) The relapse survival curves with high or low ERBB2 expression.(H) The disease‐specific survival curves with high or low ERBB2 expression.(I) The overall survival curves with high or low ERBB2 expression. The results are presented as mean ± SD. n.s, not significant, *** P < .001, ** P < .01 and * P < .05. Statistical significance was analysed by two‐way ANOVA and t ‐test.

    Journal: Cancer Reports

    Article Title: miRNA ‐449c‐5p regulates the JAK‐STAT pathway in inhibiting cell proliferation and invasion in human breast cancer cells by targeting ERBB2

    doi: 10.1002/cnr2.1974

    Figure Lengend Snippet: miR‐449c‐5p targeted ERBB2. (A) The predictive binding site of miR‐449c‐5p and ERBB2. (B) Luciferase activity of WT and MUT after co‐transfected with ERBB2 + miR‐449c‐5p into T47D cells. (C) Western blotting was used to investigate the expression level of ERBB2. (D) Relative expression of ERBB2 was evaluated in breast cancer tissues and normal tissues. (E) The distant metastasis survival curves with high or low ERBB2 expression. (F) The disease‐free survival curves with high or low ERBB2 expression. (G) The relapse survival curves with high or low ERBB2 expression.(H) The disease‐specific survival curves with high or low ERBB2 expression.(I) The overall survival curves with high or low ERBB2 expression. The results are presented as mean ± SD. n.s, not significant, *** P < .001, ** P < .01 and * P < .05. Statistical significance was analysed by two‐way ANOVA and t ‐test.

    Article Snippet: Primary antibodies were provided from Abcam company, anti‐ERBB2 (1:1000, ab134182), anti‐JAK1 (1:1000, ab138005), anti‐JAK2 (1:1000, ab267373), anti‐STAT3 (1:1000, ab68153), anti‐STAT5 (1:1000, ab32364), anti‐GAPDH (1:1000, ab8245).

    Techniques: Binding Assay, Luciferase, Activity Assay, Transfection, Western Blot, Expressing

    Breast cancer cell proliferation, migration and invasion ability affected by miR‐449c‐5p and ERBB2. (A) Expression level of ERBB2 in three groups by Western blotting. (B) Colony formation was measured to detect the colony cells. (C) Cell viability was measured by CCK‐8. (D) The statistical results of migration area for Wound healing assay. (E) The statistical results of invasion cell number for Transwell assay. (F) Cell migration and invasion detected by Wound healing and Transwell. The mean ± SD is provided. n.s, not significant, **** P < .0001, *** P < .001, ** P < .01 and * P < .05, one‐way ANOVA and two‐way ANOVA.

    Journal: Cancer Reports

    Article Title: miRNA ‐449c‐5p regulates the JAK‐STAT pathway in inhibiting cell proliferation and invasion in human breast cancer cells by targeting ERBB2

    doi: 10.1002/cnr2.1974

    Figure Lengend Snippet: Breast cancer cell proliferation, migration and invasion ability affected by miR‐449c‐5p and ERBB2. (A) Expression level of ERBB2 in three groups by Western blotting. (B) Colony formation was measured to detect the colony cells. (C) Cell viability was measured by CCK‐8. (D) The statistical results of migration area for Wound healing assay. (E) The statistical results of invasion cell number for Transwell assay. (F) Cell migration and invasion detected by Wound healing and Transwell. The mean ± SD is provided. n.s, not significant, **** P < .0001, *** P < .001, ** P < .01 and * P < .05, one‐way ANOVA and two‐way ANOVA.

    Article Snippet: Primary antibodies were provided from Abcam company, anti‐ERBB2 (1:1000, ab134182), anti‐JAK1 (1:1000, ab138005), anti‐JAK2 (1:1000, ab267373), anti‐STAT3 (1:1000, ab68153), anti‐STAT5 (1:1000, ab32364), anti‐GAPDH (1:1000, ab8245).

    Techniques: Migration, Expressing, Western Blot, CCK-8 Assay, Wound Healing Assay, Transwell Assay

    The protein expression of JAK1, p‐JAK1, JAK2, p‐JAK2, STAT3, p‐STAT3, STAT5, and p‐STAT5 was measured by western blotting in T47D cells after transfection with pcDNA3.1‐NC, pcDNA3.1‐ERBB2, and miR‐449c‐5p mimic+pcDNA3.1‐ERBB2. (A) The protein expression level of JAK1, p‐JAK1, JAK2, p‐JAK2, STAT3, p‐STAT3, STAT5, and p‐STAT5 by western blotting assay. (B–I) The statistical results of western blotting assay. Results are presented as the mean ± SD. n.s, not significant, *** P < .001, ** P < .01 and * P < .05, according to one‐way ANOVA.

    Journal: Cancer Reports

    Article Title: miRNA ‐449c‐5p regulates the JAK‐STAT pathway in inhibiting cell proliferation and invasion in human breast cancer cells by targeting ERBB2

    doi: 10.1002/cnr2.1974

    Figure Lengend Snippet: The protein expression of JAK1, p‐JAK1, JAK2, p‐JAK2, STAT3, p‐STAT3, STAT5, and p‐STAT5 was measured by western blotting in T47D cells after transfection with pcDNA3.1‐NC, pcDNA3.1‐ERBB2, and miR‐449c‐5p mimic+pcDNA3.1‐ERBB2. (A) The protein expression level of JAK1, p‐JAK1, JAK2, p‐JAK2, STAT3, p‐STAT3, STAT5, and p‐STAT5 by western blotting assay. (B–I) The statistical results of western blotting assay. Results are presented as the mean ± SD. n.s, not significant, *** P < .001, ** P < .01 and * P < .05, according to one‐way ANOVA.

    Article Snippet: Primary antibodies were provided from Abcam company, anti‐ERBB2 (1:1000, ab134182), anti‐JAK1 (1:1000, ab138005), anti‐JAK2 (1:1000, ab267373), anti‐STAT3 (1:1000, ab68153), anti‐STAT5 (1:1000, ab32364), anti‐GAPDH (1:1000, ab8245).

    Techniques: Expressing, Western Blot, Transfection

    Effect of non‐SMC condensin I complex subunit H (NCAPH) expression on luminal ERBB2‐positive tumours in vivo. (A and B) Overexpression of NCAPH in patients with luminal ER‐positive HER2 + breast tumours was associated with a worse outcome (A), while this association was not seen in HER2 + ER‐negative tumours (B). Panels A and B were generated in the KM Plotter database. <xref ref-type= 59 Each graph displaying a Kaplan‐Meier curve panel specifies the number of patients it encompasses. Outcome (disease‐free survival [DFS] probability). Analysis using the KM plotter's optimal cutoff. (C) Scheme to generate double‐transgenic mice Mouse Mammary Tumor Virus (MMTV)‐ NCAPH ErBb2 . (D and E) Immunohistochemical proliferation assessment in non‐tumoural mammary glands: analysis of mammary glands from MMTV‐ ErbB2 (upper panels) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (D), with representative Ki67 immunohistochemistry images. Five mice per group were analysed, and field analysis results are shown in panel E, using the Mann–Whitney U ‐test. (F and G) Tumour development quantification: double‐transgenic mice exhibited significantly more tumours (F) and higher tumour multiplicity (G) compared to MMTV‐ ErbB2 mice. (H–J) Histopathological pattern analysis: this section assesses different histopathological patterns in the samples, focusing on nodular (H) and solid patterns (I). Notably, the solid pattern occurred more frequently in double‐transgenic mice compared to MMTV‐ ErbB2 mice (J). Ten mice per group were evaluated with a chi‐squared test. (K and L) Vascularisation variability in mouse tumours: the panels compare vascularisation in tumours from MMTV‐ ErbB2 and MMTV‐ NCAPH ErbB2 double‐transgenic mice. Haematoxylin–eosin staining is used to emphasise vascular differences between MMTV‐ ErbB2 (panel K) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (panel L). (M) Proliferative activity in tumour tissues: this section uses Ki67 immunohistochemical analysis to evaluate tumour proliferation in MMTV‐ ErbB2 (left) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (right). Quantitative results from this analysis are displayed below the corresponding images. (N) Mitotic index quantification using chi‐squared test. (O and P) Analysis of ERBB2 downstream signalling molecules via Western blot (O) with pAKT quantification (P). (Q and R) NCAPH induction increased genomic instability, evidenced by more micronuclei and chromosomal bridges (CIN). Micronuclei and chromosomal bridge images (Q) are accompanied by CIN quantification (R), analysed with Fisher's exact test. (S) Genomic stress linked to increased NCAPH is shown by elevated ɤH2AX levels post‐H 2 O 2 exposure and during 30‐ or 60‐min recovery. (T) pCHEK1 expression changes following NCAPH induction are displayed via Western blot. (U) RNA expression correlation in luminal breast cancer: this panel shows the correlation between NCAPH RNA and Ki67 , CHEK1 and H2AX in luminal breast cancer samples from The Cancer Genome Atlas (TCGA) database. It illustrates the correlation coefficients and patterns using CANCERTOOL. 62 SMC, structural chromosome maintenance. " width="100%" height="100%">

    Journal: Clinical and Translational Medicine

    Article Title: NCAPH drives breast cancer progression and identifies a gene signature that predicts luminal a tumour recurrence

    doi: 10.1002/ctm2.1554

    Figure Lengend Snippet: Effect of non‐SMC condensin I complex subunit H (NCAPH) expression on luminal ERBB2‐positive tumours in vivo. (A and B) Overexpression of NCAPH in patients with luminal ER‐positive HER2 + breast tumours was associated with a worse outcome (A), while this association was not seen in HER2 + ER‐negative tumours (B). Panels A and B were generated in the KM Plotter database. 59 Each graph displaying a Kaplan‐Meier curve panel specifies the number of patients it encompasses. Outcome (disease‐free survival [DFS] probability). Analysis using the KM plotter's optimal cutoff. (C) Scheme to generate double‐transgenic mice Mouse Mammary Tumor Virus (MMTV)‐ NCAPH ErBb2 . (D and E) Immunohistochemical proliferation assessment in non‐tumoural mammary glands: analysis of mammary glands from MMTV‐ ErbB2 (upper panels) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (D), with representative Ki67 immunohistochemistry images. Five mice per group were analysed, and field analysis results are shown in panel E, using the Mann–Whitney U ‐test. (F and G) Tumour development quantification: double‐transgenic mice exhibited significantly more tumours (F) and higher tumour multiplicity (G) compared to MMTV‐ ErbB2 mice. (H–J) Histopathological pattern analysis: this section assesses different histopathological patterns in the samples, focusing on nodular (H) and solid patterns (I). Notably, the solid pattern occurred more frequently in double‐transgenic mice compared to MMTV‐ ErbB2 mice (J). Ten mice per group were evaluated with a chi‐squared test. (K and L) Vascularisation variability in mouse tumours: the panels compare vascularisation in tumours from MMTV‐ ErbB2 and MMTV‐ NCAPH ErbB2 double‐transgenic mice. Haematoxylin–eosin staining is used to emphasise vascular differences between MMTV‐ ErbB2 (panel K) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (panel L). (M) Proliferative activity in tumour tissues: this section uses Ki67 immunohistochemical analysis to evaluate tumour proliferation in MMTV‐ ErbB2 (left) and MMTV‐ NCAPH ErbB2 double‐transgenic mice (right). Quantitative results from this analysis are displayed below the corresponding images. (N) Mitotic index quantification using chi‐squared test. (O and P) Analysis of ERBB2 downstream signalling molecules via Western blot (O) with pAKT quantification (P). (Q and R) NCAPH induction increased genomic instability, evidenced by more micronuclei and chromosomal bridges (CIN). Micronuclei and chromosomal bridge images (Q) are accompanied by CIN quantification (R), analysed with Fisher's exact test. (S) Genomic stress linked to increased NCAPH is shown by elevated ɤH2AX levels post‐H 2 O 2 exposure and during 30‐ or 60‐min recovery. (T) pCHEK1 expression changes following NCAPH induction are displayed via Western blot. (U) RNA expression correlation in luminal breast cancer: this panel shows the correlation between NCAPH RNA and Ki67 , CHEK1 and H2AX in luminal breast cancer samples from The Cancer Genome Atlas (TCGA) database. It illustrates the correlation coefficients and patterns using CANCERTOOL. 62 SMC, structural chromosome maintenance.

    Article Snippet: The membranes were probed with the following primary antibodies raised against NCAPH (1:10000, #TA303239: OriGene), cyclin D1 (1:1000, #sc8396: Santa Cruz Biotechnology), γH2AX (1:200, Ser139 #05‐636: Millipore), pCHK1 (1:200, Ser345 #2348: Cell Signalling), tubulin (1:1000, DM1A; Sigma‒Aldrich; #T6199), HSP90 (1:1000, #515081: Santa Cruz Biotechnology), actin (1:1000, #A5441: Sigma‒Aldrich), pERK1/2 (1:1000, #9101: Cell Signalling), total ERK1/2 (1:1000, #4696: Cell Signalling), pAKT S473 (1:1000, #32581: Elabscience), total AKT (1:1000, #30471: Elabscience), cleaved Caspase‐3 (Cell Signalling #9661), anti‐ERBB2 (1:1000, #ab2428: Abcam) and anti‐phospho‐ERBB2 (Tyr1248) (1:1000, #ab47755: Abcam).

    Techniques: Expressing, In Vivo, Over Expression, Generated, Transgenic Assay, Virus, Immunohistochemistry, MANN-WHITNEY, Staining, Activity Assay, Western Blot, RNA Expression

    Intratumoural levels of Ncaph were associated with a worse outcome and response to chemotherapy in a cohort of mice generated by backcrossing (BX‐ Neu + ). (A) Generation scheme for BX‐ Neu + cohort: the BX‐ Neu + cohort was created by backcrossing transgenic Mouse Mammary Tumor Virus (MMTV)‐ ErbB2 mice (FVB/N background) with C57BL/6 mice, which are resistant to breast cancer. The first‐generation offspring (F1) were further crossed with wild‐type FVB/N mice, producing the BX‐ Neu + cohort. This cohort is genetically diverse, displaying a range of phenotypic traits and intratumoural Ncaph gene expression. Mice from the highest and lowest tertiles of Ncaph expression were selected for evaluation, as shown in the schema. Gene expression was measured using robust multiarray analysis (RMA) log2. (B and C) Decrease in tumour latency probability (B) and survival probability (C) in BX‐ Neu + mice with elevated intratumoural levels of Ncaph . (D and E) Tumour growth velocity and final volume for tumours with high or low levels of Ncaph . Weekly tumour volume was measured in mm 3 using a digital caliper and calculated as (greater diameter × lesser diameter 2 )/2. Growth velocity was determined by (final volume – initial volume)/illness duration in weeks, expressed in mm 3 /week. (F) Diagram showing the allogeneic transplantation strategy, passing tumours generated in BX‐ Neu + mice into immunocompetent F1 mice. Assessments were conducted on mice selected from the top and bottom tertiles. (G–I) Docetaxel Impact on Tumour Growth Relative to Ncaph Levels. (G) This panel displays growth curve slopes at crucial docetaxel treatment stages: pre‐chemotherapy (S1) and during chemotherapy (S2, indicating peak response). Response during treatment (RDT) is derived as S1 minus S2, with a higher RDT signifying better response. (H) RDT comparison across tumours with different Ncaph levels, classified by external tertiles. (I) Post‐chemotherapy growth changes or Evolution Changes Induced by Chemotherapy (ECIC) are shown by comparing slopes pre‐chemotherapy (S1) and post‐chemotherapy (S3), with a greater ECIC value indicating improved treatment outcome (external tertiles). (J) Univariate Poisson regression analysis indicates a positive correlation between intratumoural Ncaph levels and post‐chemotherapy lung metastases, with higher Ncaph levels linked to increased metastases ( p ‐values < .05). A positive ‘Estimate’ indicates a correlation between higher Ncaph levels and an increased count of lung metastases. (K and L) Poisson GLM analysis further confirms this correlation in mice treated with docetaxel (K) and doxorubicin (L), where individual mouse data points display the relationship between Ncaph RNA levels and metastasis count. The model's red line illustrates the trend, underscoring Ncaph's role in lung metastasis after breast tumour treatment with these drugs.

    Journal: Clinical and Translational Medicine

    Article Title: NCAPH drives breast cancer progression and identifies a gene signature that predicts luminal a tumour recurrence

    doi: 10.1002/ctm2.1554

    Figure Lengend Snippet: Intratumoural levels of Ncaph were associated with a worse outcome and response to chemotherapy in a cohort of mice generated by backcrossing (BX‐ Neu + ). (A) Generation scheme for BX‐ Neu + cohort: the BX‐ Neu + cohort was created by backcrossing transgenic Mouse Mammary Tumor Virus (MMTV)‐ ErbB2 mice (FVB/N background) with C57BL/6 mice, which are resistant to breast cancer. The first‐generation offspring (F1) were further crossed with wild‐type FVB/N mice, producing the BX‐ Neu + cohort. This cohort is genetically diverse, displaying a range of phenotypic traits and intratumoural Ncaph gene expression. Mice from the highest and lowest tertiles of Ncaph expression were selected for evaluation, as shown in the schema. Gene expression was measured using robust multiarray analysis (RMA) log2. (B and C) Decrease in tumour latency probability (B) and survival probability (C) in BX‐ Neu + mice with elevated intratumoural levels of Ncaph . (D and E) Tumour growth velocity and final volume for tumours with high or low levels of Ncaph . Weekly tumour volume was measured in mm 3 using a digital caliper and calculated as (greater diameter × lesser diameter 2 )/2. Growth velocity was determined by (final volume – initial volume)/illness duration in weeks, expressed in mm 3 /week. (F) Diagram showing the allogeneic transplantation strategy, passing tumours generated in BX‐ Neu + mice into immunocompetent F1 mice. Assessments were conducted on mice selected from the top and bottom tertiles. (G–I) Docetaxel Impact on Tumour Growth Relative to Ncaph Levels. (G) This panel displays growth curve slopes at crucial docetaxel treatment stages: pre‐chemotherapy (S1) and during chemotherapy (S2, indicating peak response). Response during treatment (RDT) is derived as S1 minus S2, with a higher RDT signifying better response. (H) RDT comparison across tumours with different Ncaph levels, classified by external tertiles. (I) Post‐chemotherapy growth changes or Evolution Changes Induced by Chemotherapy (ECIC) are shown by comparing slopes pre‐chemotherapy (S1) and post‐chemotherapy (S3), with a greater ECIC value indicating improved treatment outcome (external tertiles). (J) Univariate Poisson regression analysis indicates a positive correlation between intratumoural Ncaph levels and post‐chemotherapy lung metastases, with higher Ncaph levels linked to increased metastases ( p ‐values < .05). A positive ‘Estimate’ indicates a correlation between higher Ncaph levels and an increased count of lung metastases. (K and L) Poisson GLM analysis further confirms this correlation in mice treated with docetaxel (K) and doxorubicin (L), where individual mouse data points display the relationship between Ncaph RNA levels and metastasis count. The model's red line illustrates the trend, underscoring Ncaph's role in lung metastasis after breast tumour treatment with these drugs.

    Article Snippet: The membranes were probed with the following primary antibodies raised against NCAPH (1:10000, #TA303239: OriGene), cyclin D1 (1:1000, #sc8396: Santa Cruz Biotechnology), γH2AX (1:200, Ser139 #05‐636: Millipore), pCHK1 (1:200, Ser345 #2348: Cell Signalling), tubulin (1:1000, DM1A; Sigma‒Aldrich; #T6199), HSP90 (1:1000, #515081: Santa Cruz Biotechnology), actin (1:1000, #A5441: Sigma‒Aldrich), pERK1/2 (1:1000, #9101: Cell Signalling), total ERK1/2 (1:1000, #4696: Cell Signalling), pAKT S473 (1:1000, #32581: Elabscience), total AKT (1:1000, #30471: Elabscience), cleaved Caspase‐3 (Cell Signalling #9661), anti‐ERBB2 (1:1000, #ab2428: Abcam) and anti‐phospho‐ERBB2 (Tyr1248) (1:1000, #ab47755: Abcam).

    Techniques: Generated, Transgenic Assay, Virus, Expressing, Transplantation Assay, Derivative Assay, Comparison

    Identifying a gene signature associated with non‐SMC condensin I complex subunit H ( NCAPH ) in the Mouse Mammary Tumor Virus (MMTV)‐ ErbB2 cohort of mice generated by backcrossing (BX‐ Neu + ) recognises the poor outcome in mice and humans. (A) Heatmap showing the 64 differentially expressed genes between tumours with high or low intratumoural levels of Ncaph in BX‐ Neu + mice, of which 45 were shared with humans. Extreme tertiles of Ncaph expression were taken to define the high and low levels of Ncaph . The criteria for underexpressed and overexpressed genes were a ← twofold and a > twofold change, respectively, and a value of p < .05 (Table ). (B) Gene Ontology analysis shows the main biological functions in which the 45 genes of the signature participate (Table ). (C) Some of the genes in the 45‐gene signature were associated with the poor outcome of breast cancer in MMTV‐ ErbB2 mice generated by backcrossing. Correlation of the intratumoural levels of these genes with specific pathophenotypes of breast cancer in BX‐ Neu + mice: Pearson's test. The incidence of metastasis was evaluated with a chi‐squared test. (D–G) Least absolute shrinkage and selection operator (LASSO) regression model that defines poor outcome in BX‐ Neu + mice. The regression coefficient map of genes in the LASSO model, using cross‐validation to select the optimal tuning parameter ( λ ). The dotted vertical lines were drawn at the optimal values using the minimum criteria and 1 standard error (SE) of the minimum criteria (the 1 – SE criteria) (D). The graph shows the screening path of the LASSO regression model. Each curve represents a LASSO coefficient of the 45 prognostic genes, and the x‐axis indicates the regularisation penalty parameter. When the number of variables was 4, the partial likelihood deviation was at the minimum, corresponding to the minimum λ value (E). The LASSO regression model generated differentiates between low‐, intermediate‐ and high‐risk BX‐ Neu + mice in terms of survival probability and as defined by tertiles. Kaplan‒Meier curve and log‐rank test (F). Goodness‐of‐fit measures for the generated LASSO models in the BX‐ Neu + mouse cohort. Training, testing and global model results (G). (H) The heatmap represents the association of gene transcript levels with the prognosis of human luminal breast tumours, in relation to Ncaph levels in mouse breast tumours from the backcross cohort. Colour coding: Brown indicates genes where high transcript levels are statistically significantly associated with poor prognosis; green denotes genes where low transcript levels correlate with poor prognosis. The heatmap is supported by detailed data on patient count, expression values, and p ‐values in Table . SMC, structural chromosome maintenance.

    Journal: Clinical and Translational Medicine

    Article Title: NCAPH drives breast cancer progression and identifies a gene signature that predicts luminal a tumour recurrence

    doi: 10.1002/ctm2.1554

    Figure Lengend Snippet: Identifying a gene signature associated with non‐SMC condensin I complex subunit H ( NCAPH ) in the Mouse Mammary Tumor Virus (MMTV)‐ ErbB2 cohort of mice generated by backcrossing (BX‐ Neu + ) recognises the poor outcome in mice and humans. (A) Heatmap showing the 64 differentially expressed genes between tumours with high or low intratumoural levels of Ncaph in BX‐ Neu + mice, of which 45 were shared with humans. Extreme tertiles of Ncaph expression were taken to define the high and low levels of Ncaph . The criteria for underexpressed and overexpressed genes were a ← twofold and a > twofold change, respectively, and a value of p < .05 (Table ). (B) Gene Ontology analysis shows the main biological functions in which the 45 genes of the signature participate (Table ). (C) Some of the genes in the 45‐gene signature were associated with the poor outcome of breast cancer in MMTV‐ ErbB2 mice generated by backcrossing. Correlation of the intratumoural levels of these genes with specific pathophenotypes of breast cancer in BX‐ Neu + mice: Pearson's test. The incidence of metastasis was evaluated with a chi‐squared test. (D–G) Least absolute shrinkage and selection operator (LASSO) regression model that defines poor outcome in BX‐ Neu + mice. The regression coefficient map of genes in the LASSO model, using cross‐validation to select the optimal tuning parameter ( λ ). The dotted vertical lines were drawn at the optimal values using the minimum criteria and 1 standard error (SE) of the minimum criteria (the 1 – SE criteria) (D). The graph shows the screening path of the LASSO regression model. Each curve represents a LASSO coefficient of the 45 prognostic genes, and the x‐axis indicates the regularisation penalty parameter. When the number of variables was 4, the partial likelihood deviation was at the minimum, corresponding to the minimum λ value (E). The LASSO regression model generated differentiates between low‐, intermediate‐ and high‐risk BX‐ Neu + mice in terms of survival probability and as defined by tertiles. Kaplan‒Meier curve and log‐rank test (F). Goodness‐of‐fit measures for the generated LASSO models in the BX‐ Neu + mouse cohort. Training, testing and global model results (G). (H) The heatmap represents the association of gene transcript levels with the prognosis of human luminal breast tumours, in relation to Ncaph levels in mouse breast tumours from the backcross cohort. Colour coding: Brown indicates genes where high transcript levels are statistically significantly associated with poor prognosis; green denotes genes where low transcript levels correlate with poor prognosis. The heatmap is supported by detailed data on patient count, expression values, and p ‐values in Table . SMC, structural chromosome maintenance.

    Article Snippet: The membranes were probed with the following primary antibodies raised against NCAPH (1:10000, #TA303239: OriGene), cyclin D1 (1:1000, #sc8396: Santa Cruz Biotechnology), γH2AX (1:200, Ser139 #05‐636: Millipore), pCHK1 (1:200, Ser345 #2348: Cell Signalling), tubulin (1:1000, DM1A; Sigma‒Aldrich; #T6199), HSP90 (1:1000, #515081: Santa Cruz Biotechnology), actin (1:1000, #A5441: Sigma‒Aldrich), pERK1/2 (1:1000, #9101: Cell Signalling), total ERK1/2 (1:1000, #4696: Cell Signalling), pAKT S473 (1:1000, #32581: Elabscience), total AKT (1:1000, #30471: Elabscience), cleaved Caspase‐3 (Cell Signalling #9661), anti‐ERBB2 (1:1000, #ab2428: Abcam) and anti‐phospho‐ERBB2 (Tyr1248) (1:1000, #ab47755: Abcam).

    Techniques: Virus, Generated, Expressing, Selection

    Determination of Her-2, MutP53, Ki67, and Mismatch repair (MMR) proteins immunohistochemical staining results. Her-2 protein expression levels of negative (A) , 1+ (B) , 2+ (C) , 3+ (D) . MutP53 proteins expression levels of 10%+ (E) , 30%+ (F) , 50%+ (G) , 70%+ (H) , 90%+ (I) . Ki67 protein expression levels of 10%+ (J) , 30%+ (K) , 50%+ (L) , 70%+ (M) , 90%+ (N) . MLH1 protein negative (O) and positive (P) expression. MSH2 protein negative (Q) and positive (R) expression. MSH6 protein negative (S) and positive (T) expression. PSM2 protein negative (U) and positive (V) expression.

    Journal: Frontiers in Oncology

    Article Title: Exploration and validation of the Ki67, Her-2, and mutant P53 protein-based risk model, nomogram and lymph node metastasis model for predicting colorectal cancer progression and prognosis

    doi: 10.3389/fonc.2023.1236441

    Figure Lengend Snippet: Determination of Her-2, MutP53, Ki67, and Mismatch repair (MMR) proteins immunohistochemical staining results. Her-2 protein expression levels of negative (A) , 1+ (B) , 2+ (C) , 3+ (D) . MutP53 proteins expression levels of 10%+ (E) , 30%+ (F) , 50%+ (G) , 70%+ (H) , 90%+ (I) . Ki67 protein expression levels of 10%+ (J) , 30%+ (K) , 50%+ (L) , 70%+ (M) , 90%+ (N) . MLH1 protein negative (O) and positive (P) expression. MSH2 protein negative (Q) and positive (R) expression. MSH6 protein negative (S) and positive (T) expression. PSM2 protein negative (U) and positive (V) expression.

    Article Snippet: Subsequently, goat serum blocking solution was added and incubated for 15 minutes, and primary antibodies against Ki67 [Abcam Anti-Ki67 antibody (ab15580)], Her-2 [Abcam Anti-ErbB2 antibody (ab16901)], and MutP53 [Abcam Anti-P53 antibody (ab1101)] were added and incubated for 4 hours at 37°C.

    Techniques: Immunohistochemistry, Staining, Expressing

    Overall pathological characteristics of patients with CRC and the relationship between Ki67, Her-2, and MutP53 expression. Relationship between Ki67, Her-2, and MutP53 protein expression (A) . General situation of Ki67, Her-2 and MutP53 protein expression in 755 CRC patients with different pathological characteristics (B) .

    Journal: Frontiers in Oncology

    Article Title: Exploration and validation of the Ki67, Her-2, and mutant P53 protein-based risk model, nomogram and lymph node metastasis model for predicting colorectal cancer progression and prognosis

    doi: 10.3389/fonc.2023.1236441

    Figure Lengend Snippet: Overall pathological characteristics of patients with CRC and the relationship between Ki67, Her-2, and MutP53 expression. Relationship between Ki67, Her-2, and MutP53 protein expression (A) . General situation of Ki67, Her-2 and MutP53 protein expression in 755 CRC patients with different pathological characteristics (B) .

    Article Snippet: Subsequently, goat serum blocking solution was added and incubated for 15 minutes, and primary antibodies against Ki67 [Abcam Anti-Ki67 antibody (ab15580)], Her-2 [Abcam Anti-ErbB2 antibody (ab16901)], and MutP53 [Abcam Anti-P53 antibody (ab1101)] were added and incubated for 4 hours at 37°C.

    Techniques: Expressing

    Determination of Ki67, Her-2 and MutP53 proteins immunohistochemical staining results. Determination of Ki67 (A) , Her-2 (B) and MutP53 (C) proteins immunohistochemical staining results.

    Journal: Frontiers in Oncology

    Article Title: Exploration and validation of the Ki67, Her-2, and mutant P53 protein-based risk model, nomogram and lymph node metastasis model for predicting colorectal cancer progression and prognosis

    doi: 10.3389/fonc.2023.1236441

    Figure Lengend Snippet: Determination of Ki67, Her-2 and MutP53 proteins immunohistochemical staining results. Determination of Ki67 (A) , Her-2 (B) and MutP53 (C) proteins immunohistochemical staining results.

    Article Snippet: Subsequently, goat serum blocking solution was added and incubated for 15 minutes, and primary antibodies against Ki67 [Abcam Anti-Ki67 antibody (ab15580)], Her-2 [Abcam Anti-ErbB2 antibody (ab16901)], and MutP53 [Abcam Anti-P53 antibody (ab1101)] were added and incubated for 4 hours at 37°C.

    Techniques: Immunohistochemistry, Staining

    Comparisons between Her-2 protein expression and the pathological features of CRC. Comparisons between Her-2 protein expression and age (A) , sex (B) , mucinous carcinoma component (C) , MMR (D) , Signet ring cell component (E) , adenoma carcinogenesis (F) , perineural invasion (G) , vascular invasion (H) , organization differentiation (I) , T stage (J) , N stage (K) , TNM stage (L) , tumor location (M) . *P < 0.05; ***P < 0.001; ns, not significant.

    Journal: Frontiers in Oncology

    Article Title: Exploration and validation of the Ki67, Her-2, and mutant P53 protein-based risk model, nomogram and lymph node metastasis model for predicting colorectal cancer progression and prognosis

    doi: 10.3389/fonc.2023.1236441

    Figure Lengend Snippet: Comparisons between Her-2 protein expression and the pathological features of CRC. Comparisons between Her-2 protein expression and age (A) , sex (B) , mucinous carcinoma component (C) , MMR (D) , Signet ring cell component (E) , adenoma carcinogenesis (F) , perineural invasion (G) , vascular invasion (H) , organization differentiation (I) , T stage (J) , N stage (K) , TNM stage (L) , tumor location (M) . *P < 0.05; ***P < 0.001; ns, not significant.

    Article Snippet: Subsequently, goat serum blocking solution was added and incubated for 15 minutes, and primary antibodies against Ki67 [Abcam Anti-Ki67 antibody (ab15580)], Her-2 [Abcam Anti-ErbB2 antibody (ab16901)], and MutP53 [Abcam Anti-P53 antibody (ab1101)] were added and incubated for 4 hours at 37°C.

    Techniques: Expressing

    Analysis of survival differences based on the expression of Ki67, Her-2, and MutP53, and various pathological features in patients with colorectal cancer (CRC). The Kaplan–Meier curves demonstrate differences in prognosis based on Her-2 expression (A) , Ki67 expression (B) , MutP53 expression (C) , T-stage (D) , N-stage (E) , signet ring cell carcinoma component (F) , perineural invasion (G) , vascular invasion (H) , adenoma carcinogenesis (I) , MMR (J) , sex (K) , age (L) , TNM stage (M) , organization differentiation (N) , and tumor location (O) .

    Journal: Frontiers in Oncology

    Article Title: Exploration and validation of the Ki67, Her-2, and mutant P53 protein-based risk model, nomogram and lymph node metastasis model for predicting colorectal cancer progression and prognosis

    doi: 10.3389/fonc.2023.1236441

    Figure Lengend Snippet: Analysis of survival differences based on the expression of Ki67, Her-2, and MutP53, and various pathological features in patients with colorectal cancer (CRC). The Kaplan–Meier curves demonstrate differences in prognosis based on Her-2 expression (A) , Ki67 expression (B) , MutP53 expression (C) , T-stage (D) , N-stage (E) , signet ring cell carcinoma component (F) , perineural invasion (G) , vascular invasion (H) , adenoma carcinogenesis (I) , MMR (J) , sex (K) , age (L) , TNM stage (M) , organization differentiation (N) , and tumor location (O) .

    Article Snippet: Subsequently, goat serum blocking solution was added and incubated for 15 minutes, and primary antibodies against Ki67 [Abcam Anti-Ki67 antibody (ab15580)], Her-2 [Abcam Anti-ErbB2 antibody (ab16901)], and MutP53 [Abcam Anti-P53 antibody (ab1101)] were added and incubated for 4 hours at 37°C.

    Techniques: Expressing

    Establishment and prognostic evaluation of the risk model. (A) Interaction network of Ki67, Her-2, and P53 protein expression and other related proteins. (B) Establishment of the risk model using the multivariate Cox proportional hazards regression analysis. (C) Alluvial plot showing the relationship between TNM stage, risk groups, and survival status. Survival (D) and cumulative hazard (E) differences between high and low risk groups. Predictive efficacy of the risk model (F) , Ki67 protein expression (G) , Her-2 protein expression (H) , and MutP53 protein expression (I) for survival at 12, 36, and 60 months. (J) Risk factor plot of the risk model. (K) PCA plot testing the discrimination between the high-risk and low-risk groups. (L) Prognostic calibration curve for the risk model.

    Journal: Frontiers in Oncology

    Article Title: Exploration and validation of the Ki67, Her-2, and mutant P53 protein-based risk model, nomogram and lymph node metastasis model for predicting colorectal cancer progression and prognosis

    doi: 10.3389/fonc.2023.1236441

    Figure Lengend Snippet: Establishment and prognostic evaluation of the risk model. (A) Interaction network of Ki67, Her-2, and P53 protein expression and other related proteins. (B) Establishment of the risk model using the multivariate Cox proportional hazards regression analysis. (C) Alluvial plot showing the relationship between TNM stage, risk groups, and survival status. Survival (D) and cumulative hazard (E) differences between high and low risk groups. Predictive efficacy of the risk model (F) , Ki67 protein expression (G) , Her-2 protein expression (H) , and MutP53 protein expression (I) for survival at 12, 36, and 60 months. (J) Risk factor plot of the risk model. (K) PCA plot testing the discrimination between the high-risk and low-risk groups. (L) Prognostic calibration curve for the risk model.

    Article Snippet: Subsequently, goat serum blocking solution was added and incubated for 15 minutes, and primary antibodies against Ki67 [Abcam Anti-Ki67 antibody (ab15580)], Her-2 [Abcam Anti-ErbB2 antibody (ab16901)], and MutP53 [Abcam Anti-P53 antibody (ab1101)] were added and incubated for 4 hours at 37°C.

    Techniques: Expressing