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Keygen Biotech sw48 cancer cell lines
Knockdown of RPS4X expression reduced tumor stemness. (A) The RPS4X gene expression level was assessed by qPCR. GAPDH served as an internal parameter (n = 3). (B) The cell proliferation ability of <t>SW48</t> was determined using the CCK-8 assay (n = 3). (C–D) Cell migration and invasion ability of SW48 were evaluated (n = 3). Data are presented as mean ± SD. *P < 0.05 (E–F) Cell apoptotic rate of SW48 was evaluated (n = 3). Data are presented as mean ± SD. **P < 0.01. (G) Tumor growth curve and RPS4X down-regulation in tumors from mice (n = 5 per group). Data are presented as mean ± SD. *P < 0.05 **P < 0.01 ***P < 0.001. (H) Representative images showing the tumors harvested from SW48-bearing mice (n = 5 per group). (I)Weight of the harvested tumors from tumor-bearing mice (n = 5 per group). Data are presented as mean ± SD. **P < 0.01.
Sw48 Cancer Cell Lines, supplied by Keygen Biotech, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Exercise potentially prevents colorectal cancer liver metastases by suppressing tumor epithelial cell stemness via RPS4X downregulation"

Article Title: Exercise potentially prevents colorectal cancer liver metastases by suppressing tumor epithelial cell stemness via RPS4X downregulation

Journal: Heliyon

doi: 10.1016/j.heliyon.2024.e26604

Knockdown of RPS4X expression reduced tumor stemness. (A) The RPS4X gene expression level was assessed by qPCR. GAPDH served as an internal parameter (n = 3). (B) The cell proliferation ability of SW48 was determined using the CCK-8 assay (n = 3). (C–D) Cell migration and invasion ability of SW48 were evaluated (n = 3). Data are presented as mean ± SD. *P < 0.05 (E–F) Cell apoptotic rate of SW48 was evaluated (n = 3). Data are presented as mean ± SD. **P < 0.01. (G) Tumor growth curve and RPS4X down-regulation in tumors from mice (n = 5 per group). Data are presented as mean ± SD. *P < 0.05 **P < 0.01 ***P < 0.001. (H) Representative images showing the tumors harvested from SW48-bearing mice (n = 5 per group). (I)Weight of the harvested tumors from tumor-bearing mice (n = 5 per group). Data are presented as mean ± SD. **P < 0.01.
Figure Legend Snippet: Knockdown of RPS4X expression reduced tumor stemness. (A) The RPS4X gene expression level was assessed by qPCR. GAPDH served as an internal parameter (n = 3). (B) The cell proliferation ability of SW48 was determined using the CCK-8 assay (n = 3). (C–D) Cell migration and invasion ability of SW48 were evaluated (n = 3). Data are presented as mean ± SD. *P < 0.05 (E–F) Cell apoptotic rate of SW48 was evaluated (n = 3). Data are presented as mean ± SD. **P < 0.01. (G) Tumor growth curve and RPS4X down-regulation in tumors from mice (n = 5 per group). Data are presented as mean ± SD. *P < 0.05 **P < 0.01 ***P < 0.001. (H) Representative images showing the tumors harvested from SW48-bearing mice (n = 5 per group). (I)Weight of the harvested tumors from tumor-bearing mice (n = 5 per group). Data are presented as mean ± SD. **P < 0.01.

Techniques Used: Knockdown, Expressing, Gene Expression, CCK-8 Assay, Migration



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Knockdown of PRMT6 significantly inhibits colorectal tumor proliferation in vivo. ( A ) Representative images of tumors from mice injected with <t>SW48</t> cells stably expressing shNC or shPRMT6. (B) Tumor growth curves showing the growth rates of tumors derived from mice injected with shNC or shPRMT6 cells. (C) Scatter plot of tumor weights from mice injected with shNC or shPRMT6 cells. (D) Kaplan-Meier survival curves for mice bearing tumors from the three experimental groups. (E) Representative images of immunohistochemistry (IHC) assays showing PRMT6, c-MYC, and Ki-67 expression in tumors. (F) Western blot analysis to detect the expression levels of intratumoral PRMT6, c-MYC, and Ki-67. (G) Working model: PRMT6 mono-methylated c-MYC at arginine 371 site, which suppressed the poly-ubiquitin level of c-MYC, and then promoted colorectal cancer progress. Student’s t-test was employed for statistical analysis, and all Western blot experiments were performed in triplicate
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Knockdown of RPS4X expression reduced tumor stemness. (A) The RPS4X gene expression level was assessed by qPCR. GAPDH served as an internal parameter (n = 3). (B) The cell proliferation ability of <t>SW48</t> was determined using the CCK-8 assay (n = 3). (C–D) Cell migration and invasion ability of SW48 were evaluated (n = 3). Data are presented as mean ± SD. *P < 0.05 (E–F) Cell apoptotic rate of SW48 was evaluated (n = 3). Data are presented as mean ± SD. **P < 0.01. (G) Tumor growth curve and RPS4X down-regulation in tumors from mice (n = 5 per group). Data are presented as mean ± SD. *P < 0.05 **P < 0.01 ***P < 0.001. (H) Representative images showing the tumors harvested from SW48-bearing mice (n = 5 per group). (I)Weight of the harvested tumors from tumor-bearing mice (n = 5 per group). Data are presented as mean ± SD. **P < 0.01.
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Tumor volume of xenografted HCT 116 ( a ) and <t>SW48</t> ( b ) human <t>colorectal</t> tumors. Mice were randomized according to tumor volume on day 0. For mice with HCT 116 xenografts, control mice (○) were not treated; mice treated with FTD/TPI alone (days 1–5, 8–12, and 15–19 at 200 mg/kg, p.o., •), fruquintinib alone (days 1–21 at 10 mg/kg, p.o., □) or FTD/TPI plus fruquintinib (■). For mice with SW48 xenografts, control mice (○) were not treated; mice treated with FTD/TPI alone (days 1–5, 8–12, and 15 at 200 mg/kg, p.o., •), fruquintinib alone (days 1–15, at 10 mg/kg, p.o., □) or FTD/TPI plus fruquintinib (■). Values are the mean and SE. *, **: p < 0.05 and 0.01, respectively versus Control, Dunnett test. ## p < 0.01 versus FTD/TPI alone, Aspin-Welch t test. § p < 0.05 versus fruquintinib alone, Aspin-Welch t test.
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HRMA derivative plot for KRAS mutation detection . (A1) Derivative plot generated after ARMS amplification for the detection of KRAS G12V and (B1) KRAS G12D mutations. (A2) Average intensity of the melting peak generated after ARMS-HRMA reaction for the detection of G12V and (B2) G12D mutations in G12V/G12V (SW480) (green line), wt/wt <t>(SW48)</t> (gray line), and G12D/wt (LS174T) (yellow line). **** P value < 0.0001 using Mann–Whitney test. Error bars represent the standard error mean of the average result of at least 8 replicates
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HRMA derivative plot for KRAS mutation detection . (A1) Derivative plot generated after ARMS amplification for the detection of KRAS G12V and (B1) KRAS G12D mutations. (A2) Average intensity of the melting peak generated after ARMS-HRMA reaction for the detection of G12V and (B2) G12D mutations in G12V/G12V (SW480) (green line), wt/wt <t>(SW48)</t> (gray line), and G12D/wt (LS174T) (yellow line). **** P value < 0.0001 using Mann–Whitney test. Error bars represent the standard error mean of the average result of at least 8 replicates
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Image Search Results


Knockdown of PRMT6 significantly inhibits colorectal tumor proliferation in vivo. ( A ) Representative images of tumors from mice injected with SW48 cells stably expressing shNC or shPRMT6. (B) Tumor growth curves showing the growth rates of tumors derived from mice injected with shNC or shPRMT6 cells. (C) Scatter plot of tumor weights from mice injected with shNC or shPRMT6 cells. (D) Kaplan-Meier survival curves for mice bearing tumors from the three experimental groups. (E) Representative images of immunohistochemistry (IHC) assays showing PRMT6, c-MYC, and Ki-67 expression in tumors. (F) Western blot analysis to detect the expression levels of intratumoral PRMT6, c-MYC, and Ki-67. (G) Working model: PRMT6 mono-methylated c-MYC at arginine 371 site, which suppressed the poly-ubiquitin level of c-MYC, and then promoted colorectal cancer progress. Student’s t-test was employed for statistical analysis, and all Western blot experiments were performed in triplicate

Journal: Journal of Translational Medicine

Article Title: PRMT6 promotes colorectal cancer progress via activating MYC signaling

doi: 10.1186/s12967-025-06097-y

Figure Lengend Snippet: Knockdown of PRMT6 significantly inhibits colorectal tumor proliferation in vivo. ( A ) Representative images of tumors from mice injected with SW48 cells stably expressing shNC or shPRMT6. (B) Tumor growth curves showing the growth rates of tumors derived from mice injected with shNC or shPRMT6 cells. (C) Scatter plot of tumor weights from mice injected with shNC or shPRMT6 cells. (D) Kaplan-Meier survival curves for mice bearing tumors from the three experimental groups. (E) Representative images of immunohistochemistry (IHC) assays showing PRMT6, c-MYC, and Ki-67 expression in tumors. (F) Western blot analysis to detect the expression levels of intratumoral PRMT6, c-MYC, and Ki-67. (G) Working model: PRMT6 mono-methylated c-MYC at arginine 371 site, which suppressed the poly-ubiquitin level of c-MYC, and then promoted colorectal cancer progress. Student’s t-test was employed for statistical analysis, and all Western blot experiments were performed in triplicate

Article Snippet: RKO and SW48 cancer cell lines were acquired from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Knockdown, In Vivo, Injection, Stable Transfection, Expressing, Derivative Assay, Immunohistochemistry, Western Blot, Methylation, Ubiquitin Proteomics

Knockdown of RPS4X expression reduced tumor stemness. (A) The RPS4X gene expression level was assessed by qPCR. GAPDH served as an internal parameter (n = 3). (B) The cell proliferation ability of SW48 was determined using the CCK-8 assay (n = 3). (C–D) Cell migration and invasion ability of SW48 were evaluated (n = 3). Data are presented as mean ± SD. *P < 0.05 (E–F) Cell apoptotic rate of SW48 was evaluated (n = 3). Data are presented as mean ± SD. **P < 0.01. (G) Tumor growth curve and RPS4X down-regulation in tumors from mice (n = 5 per group). Data are presented as mean ± SD. *P < 0.05 **P < 0.01 ***P < 0.001. (H) Representative images showing the tumors harvested from SW48-bearing mice (n = 5 per group). (I)Weight of the harvested tumors from tumor-bearing mice (n = 5 per group). Data are presented as mean ± SD. **P < 0.01.

Journal: Heliyon

Article Title: Exercise potentially prevents colorectal cancer liver metastases by suppressing tumor epithelial cell stemness via RPS4X downregulation

doi: 10.1016/j.heliyon.2024.e26604

Figure Lengend Snippet: Knockdown of RPS4X expression reduced tumor stemness. (A) The RPS4X gene expression level was assessed by qPCR. GAPDH served as an internal parameter (n = 3). (B) The cell proliferation ability of SW48 was determined using the CCK-8 assay (n = 3). (C–D) Cell migration and invasion ability of SW48 were evaluated (n = 3). Data are presented as mean ± SD. *P < 0.05 (E–F) Cell apoptotic rate of SW48 was evaluated (n = 3). Data are presented as mean ± SD. **P < 0.01. (G) Tumor growth curve and RPS4X down-regulation in tumors from mice (n = 5 per group). Data are presented as mean ± SD. *P < 0.05 **P < 0.01 ***P < 0.001. (H) Representative images showing the tumors harvested from SW48-bearing mice (n = 5 per group). (I)Weight of the harvested tumors from tumor-bearing mice (n = 5 per group). Data are presented as mean ± SD. **P < 0.01.

Article Snippet: SW48 (catalog KG536) cancer cell lines were purchased from KeyGEN.

Techniques: Knockdown, Expressing, Gene Expression, CCK-8 Assay, Migration

Tumor volume of xenografted HCT 116 ( a ) and SW48 ( b ) human colorectal tumors. Mice were randomized according to tumor volume on day 0. For mice with HCT 116 xenografts, control mice (○) were not treated; mice treated with FTD/TPI alone (days 1–5, 8–12, and 15–19 at 200 mg/kg, p.o., •), fruquintinib alone (days 1–21 at 10 mg/kg, p.o., □) or FTD/TPI plus fruquintinib (■). For mice with SW48 xenografts, control mice (○) were not treated; mice treated with FTD/TPI alone (days 1–5, 8–12, and 15 at 200 mg/kg, p.o., •), fruquintinib alone (days 1–15, at 10 mg/kg, p.o., □) or FTD/TPI plus fruquintinib (■). Values are the mean and SE. *, **: p < 0.05 and 0.01, respectively versus Control, Dunnett test. ## p < 0.01 versus FTD/TPI alone, Aspin-Welch t test. § p < 0.05 versus fruquintinib alone, Aspin-Welch t test.

Journal: Chemotherapy

Article Title: Evaluation of a Novel Combination Therapy, Based on Trifluridine/Tipiracil and Fruquintinib, against Colorectal Cancer

doi: 10.1159/000528867

Figure Lengend Snippet: Tumor volume of xenografted HCT 116 ( a ) and SW48 ( b ) human colorectal tumors. Mice were randomized according to tumor volume on day 0. For mice with HCT 116 xenografts, control mice (○) were not treated; mice treated with FTD/TPI alone (days 1–5, 8–12, and 15–19 at 200 mg/kg, p.o., •), fruquintinib alone (days 1–21 at 10 mg/kg, p.o., □) or FTD/TPI plus fruquintinib (■). For mice with SW48 xenografts, control mice (○) were not treated; mice treated with FTD/TPI alone (days 1–5, 8–12, and 15 at 200 mg/kg, p.o., •), fruquintinib alone (days 1–15, at 10 mg/kg, p.o., □) or FTD/TPI plus fruquintinib (■). Values are the mean and SE. *, **: p < 0.05 and 0.01, respectively versus Control, Dunnett test. ## p < 0.01 versus FTD/TPI alone, Aspin-Welch t test. § p < 0.05 versus fruquintinib alone, Aspin-Welch t test.

Article Snippet: The human colorectal cancer cell line SW48, derived from Dukes' type C, grade IV, colon adenocarcinoma, and colon carcinoma, and HCT 116 were purchased from American Type Culture Collection (Rockville, MD).

Techniques: Control

Body weight changes of nude mice with HCT 116 ( a ) and SW48 ( b ) xenografts. Mice were randomized according to tumor volume on day 0. For mice with HCT 116 xenografts, control mice (○) were not treated; mice treated with FTD/TPI alone (days 1–5, 8–12, and 15–19 at 200 mg/kg, p.o., •), fruquintinib alone (days 1–21 at 10 mg/kg, p.o., □) or FTD/TPI plus fruquintinib (■). For mice with SW48 xenografts, control mice (○) were not treated; mice treated with FTD/TPI alone (days 1–5, 8–12, and 15 at 200 mg/kg, p.o., •), fruquintinib alone (days 1–15, at 10 mg/kg, p.o., □) or FTD/TPI plus fruquintinib (■). Values are the mean and SE.

Journal: Chemotherapy

Article Title: Evaluation of a Novel Combination Therapy, Based on Trifluridine/Tipiracil and Fruquintinib, against Colorectal Cancer

doi: 10.1159/000528867

Figure Lengend Snippet: Body weight changes of nude mice with HCT 116 ( a ) and SW48 ( b ) xenografts. Mice were randomized according to tumor volume on day 0. For mice with HCT 116 xenografts, control mice (○) were not treated; mice treated with FTD/TPI alone (days 1–5, 8–12, and 15–19 at 200 mg/kg, p.o., •), fruquintinib alone (days 1–21 at 10 mg/kg, p.o., □) or FTD/TPI plus fruquintinib (■). For mice with SW48 xenografts, control mice (○) were not treated; mice treated with FTD/TPI alone (days 1–5, 8–12, and 15 at 200 mg/kg, p.o., •), fruquintinib alone (days 1–15, at 10 mg/kg, p.o., □) or FTD/TPI plus fruquintinib (■). Values are the mean and SE.

Article Snippet: The human colorectal cancer cell line SW48, derived from Dukes' type C, grade IV, colon adenocarcinoma, and colon carcinoma, and HCT 116 were purchased from American Type Culture Collection (Rockville, MD).

Techniques: Control

Typical images of hematoxylin-and-eosin-stained tissue in HCT 116 (upper part) and SW48 (lower part) xenografts. a Control. b FTD/TPI. c Fruquintinib. d FTD/TPI plus fruquintinib. The white triangles (Δ) indicate swollen nuclei, and the black triangles (▴) indicate condensed chromosomes and karyorrhexis. The original magnification was ×400; the scale bar indicates 100 μm.

Journal: Chemotherapy

Article Title: Evaluation of a Novel Combination Therapy, Based on Trifluridine/Tipiracil and Fruquintinib, against Colorectal Cancer

doi: 10.1159/000528867

Figure Lengend Snippet: Typical images of hematoxylin-and-eosin-stained tissue in HCT 116 (upper part) and SW48 (lower part) xenografts. a Control. b FTD/TPI. c Fruquintinib. d FTD/TPI plus fruquintinib. The white triangles (Δ) indicate swollen nuclei, and the black triangles (▴) indicate condensed chromosomes and karyorrhexis. The original magnification was ×400; the scale bar indicates 100 μm.

Article Snippet: The human colorectal cancer cell line SW48, derived from Dukes' type C, grade IV, colon adenocarcinoma, and colon carcinoma, and HCT 116 were purchased from American Type Culture Collection (Rockville, MD).

Techniques: Staining, Control

Typical images of immunohistochemical visualization of FTD using anti-BrdU antibody in HCT 116 (upper part) and SW48 (lower part) xenografts. a Control. b FTD/TPI. c Fruquintinib. d FTD/TPI plus fruquintinib. The original magnification was ×400; and the scale bar indicates 100 μm.

Journal: Chemotherapy

Article Title: Evaluation of a Novel Combination Therapy, Based on Trifluridine/Tipiracil and Fruquintinib, against Colorectal Cancer

doi: 10.1159/000528867

Figure Lengend Snippet: Typical images of immunohistochemical visualization of FTD using anti-BrdU antibody in HCT 116 (upper part) and SW48 (lower part) xenografts. a Control. b FTD/TPI. c Fruquintinib. d FTD/TPI plus fruquintinib. The original magnification was ×400; and the scale bar indicates 100 μm.

Article Snippet: The human colorectal cancer cell line SW48, derived from Dukes' type C, grade IV, colon adenocarcinoma, and colon carcinoma, and HCT 116 were purchased from American Type Culture Collection (Rockville, MD).

Techniques: Immunohistochemical staining, Control

Typical images of immunohistochemical visualization of tumor vessels using anti-CD31 antibody in HCT 116 (upper part) and SW48 (lower part) xenografts. a Control. b FTD/TPI. c Fruquintinib. d FTD/TPI plus fruquintinib. The original magnification was approximately ×200, and the scale bar indicates 250 μm.

Journal: Chemotherapy

Article Title: Evaluation of a Novel Combination Therapy, Based on Trifluridine/Tipiracil and Fruquintinib, against Colorectal Cancer

doi: 10.1159/000528867

Figure Lengend Snippet: Typical images of immunohistochemical visualization of tumor vessels using anti-CD31 antibody in HCT 116 (upper part) and SW48 (lower part) xenografts. a Control. b FTD/TPI. c Fruquintinib. d FTD/TPI plus fruquintinib. The original magnification was approximately ×200, and the scale bar indicates 250 μm.

Article Snippet: The human colorectal cancer cell line SW48, derived from Dukes' type C, grade IV, colon adenocarcinoma, and colon carcinoma, and HCT 116 were purchased from American Type Culture Collection (Rockville, MD).

Techniques: Immunohistochemical staining, Control

HRMA derivative plot for KRAS mutation detection . (A1) Derivative plot generated after ARMS amplification for the detection of KRAS G12V and (B1) KRAS G12D mutations. (A2) Average intensity of the melting peak generated after ARMS-HRMA reaction for the detection of G12V and (B2) G12D mutations in G12V/G12V (SW480) (green line), wt/wt (SW48) (gray line), and G12D/wt (LS174T) (yellow line). **** P value < 0.0001 using Mann–Whitney test. Error bars represent the standard error mean of the average result of at least 8 replicates

Journal: Analytical and Bioanalytical Chemistry

Article Title: Combining the amplification refractory mutation system and high-resolution melting analysis for KRAS mutation detection in clinical samples

doi: 10.1007/s00216-023-04696-6

Figure Lengend Snippet: HRMA derivative plot for KRAS mutation detection . (A1) Derivative plot generated after ARMS amplification for the detection of KRAS G12V and (B1) KRAS G12D mutations. (A2) Average intensity of the melting peak generated after ARMS-HRMA reaction for the detection of G12V and (B2) G12D mutations in G12V/G12V (SW480) (green line), wt/wt (SW48) (gray line), and G12D/wt (LS174T) (yellow line). **** P value < 0.0001 using Mann–Whitney test. Error bars represent the standard error mean of the average result of at least 8 replicates

Article Snippet: Control DNA was extracted from colorectal cancer cell lines SW48 – wildtype genotype (American Type Culture Collection [ATCC]® reference no. CCL-231), SW480 – G12V mutation (ATCC® reference no. CCL-228), and LS174T – G12D mutation (ATCC® reference no. CL-188) as previously described [ ].

Techniques: Mutagenesis, Generated, Amplification, MANN-WHITNEY

ARMS-HRMA for the detection of KRAS G12V mutation . A HRMA derivative plot for KRAS G12V mutation analysis for the tumor samples T1 (blue green line), T2 (yellow line), T3 (blue line), and T4 (dark gray line). Cell lines SW480 (turquoise line) and SW48 (gray line) as G12V positive and negative controls, respectively. B Difference plot. The difference plot shows the melting curve of each tumor sample subtracted from the SW48 cell line. C Chromograms for SS results for KRAS codon 12 (wt: GGT). Sequence obtained with forward primer. Arrows indicate the mutations at positions 2 of codon 12 of KRAS . Sanger sequencing showed a G to T transversion at position 2 of codon 2 (G12V: GGT > GTT) in tumors T1 and T3, and a G to A transition (G12D: GGT > GAT) in tumor T2. T4 has a wt KRAS codon 12

Journal: Analytical and Bioanalytical Chemistry

Article Title: Combining the amplification refractory mutation system and high-resolution melting analysis for KRAS mutation detection in clinical samples

doi: 10.1007/s00216-023-04696-6

Figure Lengend Snippet: ARMS-HRMA for the detection of KRAS G12V mutation . A HRMA derivative plot for KRAS G12V mutation analysis for the tumor samples T1 (blue green line), T2 (yellow line), T3 (blue line), and T4 (dark gray line). Cell lines SW480 (turquoise line) and SW48 (gray line) as G12V positive and negative controls, respectively. B Difference plot. The difference plot shows the melting curve of each tumor sample subtracted from the SW48 cell line. C Chromograms for SS results for KRAS codon 12 (wt: GGT). Sequence obtained with forward primer. Arrows indicate the mutations at positions 2 of codon 12 of KRAS . Sanger sequencing showed a G to T transversion at position 2 of codon 2 (G12V: GGT > GTT) in tumors T1 and T3, and a G to A transition (G12D: GGT > GAT) in tumor T2. T4 has a wt KRAS codon 12

Article Snippet: Control DNA was extracted from colorectal cancer cell lines SW48 – wildtype genotype (American Type Culture Collection [ATCC]® reference no. CCL-231), SW480 – G12V mutation (ATCC® reference no. CCL-228), and LS174T – G12D mutation (ATCC® reference no. CL-188) as previously described [ ].

Techniques: Mutagenesis, Sequencing

ARMS-HRMA for the detection of KRAS G12V mutation in tumor samples. A G12V mutation scoring for the set of 30 tumor samples, based on the intensity of the melting peak at 79.5 °C. The dark blue bars represent tumor samples scored as G12V non-mutated. B Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. The blue green bar represents tumor samples scored as G12V mutated; the light gray bar represents the SW48 cell line as the control for G12V non-mutated samples; the turquoise bar represents the SW480 cell line as the control for G12V mutated samples. The dagger represents samples scored as G12V mutated with non-concordant result based on SS. Error bars represent the standard error mean of the average result of at least 4 replicates

Journal: Analytical and Bioanalytical Chemistry

Article Title: Combining the amplification refractory mutation system and high-resolution melting analysis for KRAS mutation detection in clinical samples

doi: 10.1007/s00216-023-04696-6

Figure Lengend Snippet: ARMS-HRMA for the detection of KRAS G12V mutation in tumor samples. A G12V mutation scoring for the set of 30 tumor samples, based on the intensity of the melting peak at 79.5 °C. The dark blue bars represent tumor samples scored as G12V non-mutated. B Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. The blue green bar represents tumor samples scored as G12V mutated; the light gray bar represents the SW48 cell line as the control for G12V non-mutated samples; the turquoise bar represents the SW480 cell line as the control for G12V mutated samples. The dagger represents samples scored as G12V mutated with non-concordant result based on SS. Error bars represent the standard error mean of the average result of at least 4 replicates

Article Snippet: Control DNA was extracted from colorectal cancer cell lines SW48 – wildtype genotype (American Type Culture Collection [ATCC]® reference no. CCL-231), SW480 – G12V mutation (ATCC® reference no. CCL-228), and LS174T – G12D mutation (ATCC® reference no. CL-188) as previously described [ ].

Techniques: Mutagenesis, MANN-WHITNEY, Control

ARMS-HRMA for KRAS G12D mutation detection. A Derivative plot generated after ARMS amplification for the detection of KRAS G12D mutation in LS174T (wt/G12D) (yellow line) and SW48 (wt/wt) (gray line) cell lines and four tumor samples (T2 (dark yellow line), T3 (blue line), T4 (dark blue line), and T5 (brown line)). B G12D mutation scoring for the set of 30 tumor samples, based on the intensity of the melting peak at 79.5 °C; the dagger represents samples scored as G12D mutated with non-concordant result based on SS, and the asterisk represents samples with non-concordant results by both ddPCR and SS. C Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. The dark gray bar represents tumor samples scored as G12D non-mutated; the dark yellow bar represents tumor samples scored as G12D mutated; the light gray SW48 cell line as control for G12D non-mutated samples; the light yellow bar represents the LS174T cell line as the control for G12D mutated samples. Error bars represent the standard error mean of the average result of at least 4 replicates

Journal: Analytical and Bioanalytical Chemistry

Article Title: Combining the amplification refractory mutation system and high-resolution melting analysis for KRAS mutation detection in clinical samples

doi: 10.1007/s00216-023-04696-6

Figure Lengend Snippet: ARMS-HRMA for KRAS G12D mutation detection. A Derivative plot generated after ARMS amplification for the detection of KRAS G12D mutation in LS174T (wt/G12D) (yellow line) and SW48 (wt/wt) (gray line) cell lines and four tumor samples (T2 (dark yellow line), T3 (blue line), T4 (dark blue line), and T5 (brown line)). B G12D mutation scoring for the set of 30 tumor samples, based on the intensity of the melting peak at 79.5 °C; the dagger represents samples scored as G12D mutated with non-concordant result based on SS, and the asterisk represents samples with non-concordant results by both ddPCR and SS. C Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. The dark gray bar represents tumor samples scored as G12D non-mutated; the dark yellow bar represents tumor samples scored as G12D mutated; the light gray SW48 cell line as control for G12D non-mutated samples; the light yellow bar represents the LS174T cell line as the control for G12D mutated samples. Error bars represent the standard error mean of the average result of at least 4 replicates

Article Snippet: Control DNA was extracted from colorectal cancer cell lines SW48 – wildtype genotype (American Type Culture Collection [ATCC]® reference no. CCL-231), SW480 – G12V mutation (ATCC® reference no. CCL-228), and LS174T – G12D mutation (ATCC® reference no. CL-188) as previously described [ ].

Techniques: Mutagenesis, Generated, Amplification, MANN-WHITNEY, Control

ARMS-HRMA detection of KRAS G12V mutation in plasma samples. A G12V mutation scoring for the set of 30 plasma samples, based on the intensity of the melting peak at 79.5 °C. The dark blue bars represent tumor samples scored as G12V non-mutated. B Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. The dark blue bar represents plasma samples scored as G12V mutated; the dark gray bar represents the SW48 cell line as the control for G12V non-mutated samples; the blue bar represents the SW480 cell line as the control for G12V mutated samples. The dagger represents samples scored as G12V mutated with non-concordant result based on SS. Error bars represent the standard error mean of the average result of at least 4 replicates

Journal: Analytical and Bioanalytical Chemistry

Article Title: Combining the amplification refractory mutation system and high-resolution melting analysis for KRAS mutation detection in clinical samples

doi: 10.1007/s00216-023-04696-6

Figure Lengend Snippet: ARMS-HRMA detection of KRAS G12V mutation in plasma samples. A G12V mutation scoring for the set of 30 plasma samples, based on the intensity of the melting peak at 79.5 °C. The dark blue bars represent tumor samples scored as G12V non-mutated. B Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. The dark blue bar represents plasma samples scored as G12V mutated; the dark gray bar represents the SW48 cell line as the control for G12V non-mutated samples; the blue bar represents the SW480 cell line as the control for G12V mutated samples. The dagger represents samples scored as G12V mutated with non-concordant result based on SS. Error bars represent the standard error mean of the average result of at least 4 replicates

Article Snippet: Control DNA was extracted from colorectal cancer cell lines SW48 – wildtype genotype (American Type Culture Collection [ATCC]® reference no. CCL-231), SW480 – G12V mutation (ATCC® reference no. CCL-228), and LS174T – G12D mutation (ATCC® reference no. CL-188) as previously described [ ].

Techniques: Mutagenesis, Clinical Proteomics, MANN-WHITNEY, Control

ARMS-HRMA for KRAS G12D mutation detection on plasma samples. A Derivative plot generated after ARMS amplification for the detection of KRAS G12D mutation in plasma sample P7. B Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. C Mutation scoring for the set of 24 plasma samples, based on the average intensity of the melting peak at 79.5 °C/80 °C. The dark gray bar represents plasma samples scored as G12D non-mutated; the dark yellow bar represents plasma samples scored as G12D mutated; the light gray bar represents the SW48 cell line as the control for G12D non-mutated samples; the yellow bar represents the LS174T cell line as the control for G12D mutated samples. The asterisk represents samples scored as G12D mutated with non-concordant result based on SS and ddPCR

Journal: Analytical and Bioanalytical Chemistry

Article Title: Combining the amplification refractory mutation system and high-resolution melting analysis for KRAS mutation detection in clinical samples

doi: 10.1007/s00216-023-04696-6

Figure Lengend Snippet: ARMS-HRMA for KRAS G12D mutation detection on plasma samples. A Derivative plot generated after ARMS amplification for the detection of KRAS G12D mutation in plasma sample P7. B Statistical analysis of the average intensity of the melting peak in each sample group. Four asterisks, P value < 0.0001 using Mann–Whitney test. C Mutation scoring for the set of 24 plasma samples, based on the average intensity of the melting peak at 79.5 °C/80 °C. The dark gray bar represents plasma samples scored as G12D non-mutated; the dark yellow bar represents plasma samples scored as G12D mutated; the light gray bar represents the SW48 cell line as the control for G12D non-mutated samples; the yellow bar represents the LS174T cell line as the control for G12D mutated samples. The asterisk represents samples scored as G12D mutated with non-concordant result based on SS and ddPCR

Article Snippet: Control DNA was extracted from colorectal cancer cell lines SW48 – wildtype genotype (American Type Culture Collection [ATCC]® reference no. CCL-231), SW480 – G12V mutation (ATCC® reference no. CCL-228), and LS174T – G12D mutation (ATCC® reference no. CL-188) as previously described [ ].

Techniques: Mutagenesis, Clinical Proteomics, Generated, Amplification, MANN-WHITNEY, Control