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  • 99
    Millipore crc aom
    Crc Aom, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    crc aom - by Bioz Stars, 2020-04
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    92
    Brinkmann Instruments crcs
    Crcs, supplied by Brinkmann Instruments, used in various techniques. Bioz Stars score: 92/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Folio Biosciences crcs
    Crcs, supplied by Folio Biosciences, used in various techniques. Bioz Stars score: 88/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Coltene Whaledent crcs
    Crcs, supplied by Coltene Whaledent, used in various techniques. Bioz Stars score: 91/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    97
    Thermo Fisher crcs
    Crcs, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 97/100, based on 88 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Preiser Scientific crcs
    Crcs, supplied by Preiser Scientific, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Human Protein Atlas crcs
    Crcs, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Targeted Cell Therapies LLC crcs
    Clinical significance of FRA1 and FRA1 <t>EMT</t> genes in CRC. (A) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients according to expression of the FRA1 gene ( FOSL1 ). (B) Unsupervised clustering of stage B and stage C <t>CRCs</t> based on FRA1 EMT genes encompassing concordant probesets exhibiting significant expression differences between the two main groups. Clustering divides cancers into groups with mesenchymal and epithelial profiles. Samples are arranged along the X-axis and genes along the Y-axis. Genes are grouped into those downregulated (blue) or upregulated (orange) upon FRA1 knockdown in BE cells relative to the mean- and sample-centered scaled expression. (C) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients based on expression of both FOSL1 (low vs high) and mesenchymal (Mes, dark green) or epithelial (Epi, light green) subsets of FRA1 EMT genes. The log-rank test was used for comparisons.
    Crcs, supplied by Targeted Cell Therapies LLC, used in various techniques. Bioz Stars score: 86/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Allscripts crcs
    Clinical significance of FRA1 and FRA1 <t>EMT</t> genes in CRC. (A) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients according to expression of the FRA1 gene ( FOSL1 ). (B) Unsupervised clustering of stage B and stage C <t>CRCs</t> based on FRA1 EMT genes encompassing concordant probesets exhibiting significant expression differences between the two main groups. Clustering divides cancers into groups with mesenchymal and epithelial profiles. Samples are arranged along the X-axis and genes along the Y-axis. Genes are grouped into those downregulated (blue) or upregulated (orange) upon FRA1 knockdown in BE cells relative to the mean- and sample-centered scaled expression. (C) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients based on expression of both FOSL1 (low vs high) and mesenchymal (Mes, dark green) or epithelial (Epi, light green) subsets of FRA1 EMT genes. The log-rank test was used for comparisons.
    Crcs, supplied by Allscripts, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    CellSearch metastatic crcs
    Clinical significance of FRA1 and FRA1 <t>EMT</t> genes in CRC. (A) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients according to expression of the FRA1 gene ( FOSL1 ). (B) Unsupervised clustering of stage B and stage C <t>CRCs</t> based on FRA1 EMT genes encompassing concordant probesets exhibiting significant expression differences between the two main groups. Clustering divides cancers into groups with mesenchymal and epithelial profiles. Samples are arranged along the X-axis and genes along the Y-axis. Genes are grouped into those downregulated (blue) or upregulated (orange) upon FRA1 knockdown in BE cells relative to the mean- and sample-centered scaled expression. (C) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients based on expression of both FOSL1 (low vs high) and mesenchymal (Mes, dark green) or epithelial (Epi, light green) subsets of FRA1 EMT genes. The log-rank test was used for comparisons.
    Metastatic Crcs, supplied by CellSearch, used in various techniques. Bioz Stars score: 91/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Indivumed pretreatment crcs
    Clinical significance of FRA1 and FRA1 <t>EMT</t> genes in CRC. (A) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients according to expression of the FRA1 gene ( FOSL1 ). (B) Unsupervised clustering of stage B and stage C <t>CRCs</t> based on FRA1 EMT genes encompassing concordant probesets exhibiting significant expression differences between the two main groups. Clustering divides cancers into groups with mesenchymal and epithelial profiles. Samples are arranged along the X-axis and genes along the Y-axis. Genes are grouped into those downregulated (blue) or upregulated (orange) upon FRA1 knockdown in BE cells relative to the mean- and sample-centered scaled expression. (C) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients based on expression of both FOSL1 (low vs high) and mesenchymal (Mes, dark green) or epithelial (Epi, light green) subsets of FRA1 EMT genes. The log-rank test was used for comparisons.
    Pretreatment Crcs, supplied by Indivumed, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    84
    Johnson & Johnson tma crcs
    Clinical significance of FRA1 and FRA1 <t>EMT</t> genes in CRC. (A) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients according to expression of the FRA1 gene ( FOSL1 ). (B) Unsupervised clustering of stage B and stage C <t>CRCs</t> based on FRA1 EMT genes encompassing concordant probesets exhibiting significant expression differences between the two main groups. Clustering divides cancers into groups with mesenchymal and epithelial profiles. Samples are arranged along the X-axis and genes along the Y-axis. Genes are grouped into those downregulated (blue) or upregulated (orange) upon FRA1 knockdown in BE cells relative to the mean- and sample-centered scaled expression. (C) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients based on expression of both FOSL1 (low vs high) and mesenchymal (Mes, dark green) or epithelial (Epi, light green) subsets of FRA1 EMT genes. The log-rank test was used for comparisons.
    Tma Crcs, supplied by Johnson & Johnson, used in various techniques. Bioz Stars score: 84/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Showa Gloves t1 crcs
    Clinical significance of FRA1 and FRA1 <t>EMT</t> genes in CRC. (A) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients according to expression of the FRA1 gene ( FOSL1 ). (B) Unsupervised clustering of stage B and stage C <t>CRCs</t> based on FRA1 EMT genes encompassing concordant probesets exhibiting significant expression differences between the two main groups. Clustering divides cancers into groups with mesenchymal and epithelial profiles. Samples are arranged along the X-axis and genes along the Y-axis. Genes are grouped into those downregulated (blue) or upregulated (orange) upon FRA1 knockdown in BE cells relative to the mean- and sample-centered scaled expression. (C) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients based on expression of both FOSL1 (low vs high) and mesenchymal (Mes, dark green) or epithelial (Epi, light green) subsets of FRA1 EMT genes. The log-rank test was used for comparisons.
    T1 Crcs, supplied by Showa Gloves, used in various techniques. Bioz Stars score: 92/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Hamamatsu crcs resected
    Clinical significance of FRA1 and FRA1 <t>EMT</t> genes in CRC. (A) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients according to expression of the FRA1 gene ( FOSL1 ). (B) Unsupervised clustering of stage B and stage C <t>CRCs</t> based on FRA1 EMT genes encompassing concordant probesets exhibiting significant expression differences between the two main groups. Clustering divides cancers into groups with mesenchymal and epithelial profiles. Samples are arranged along the X-axis and genes along the Y-axis. Genes are grouped into those downregulated (blue) or upregulated (orange) upon FRA1 knockdown in BE cells relative to the mean- and sample-centered scaled expression. (C) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients based on expression of both FOSL1 (low vs high) and mesenchymal (Mes, dark green) or epithelial (Epi, light green) subsets of FRA1 EMT genes. The log-rank test was used for comparisons.
    Crcs Resected, supplied by Hamamatsu, used in various techniques. Bioz Stars score: 92/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Randox crcs multiplex array biochip
    Clinical significance of FRA1 and FRA1 <t>EMT</t> genes in CRC. (A) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients according to expression of the FRA1 gene ( FOSL1 ). (B) Unsupervised clustering of stage B and stage C <t>CRCs</t> based on FRA1 EMT genes encompassing concordant probesets exhibiting significant expression differences between the two main groups. Clustering divides cancers into groups with mesenchymal and epithelial profiles. Samples are arranged along the X-axis and genes along the Y-axis. Genes are grouped into those downregulated (blue) or upregulated (orange) upon FRA1 knockdown in BE cells relative to the mean- and sample-centered scaled expression. (C) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients based on expression of both FOSL1 (low vs high) and mesenchymal (Mes, dark green) or epithelial (Epi, light green) subsets of FRA1 EMT genes. The log-rank test was used for comparisons.
    Crcs Multiplex Array Biochip, supplied by Randox, used in various techniques. Bioz Stars score: 86/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    Caris Life Sciences 558 non msi h crcs
    MLH1 and MSH2 protein domains annotated with somatic non-synonymous alterations observed in <t>MSI-H</t> <t>CRCs</t> from the COSMIC database A . MLH1 domains and variants. Three known domains are shown in the protein structure. The alterations including missense, nonsense and frameshift mutations are mapped with respect to known domains. Different numbers and colors of triangles in the same positions are representatives of frequency and diversity of mutations in the same spot, respectively. Red triangles represent the truncated mutations, while missense variants are shown in blue, brown and green. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle as well as red/orange rectangle. Red rectangles are representative of damaging mutations with high probability ( > 90%) and orange rectangles outline the mutations with possibility ( > 50%). B . MSH2 domains and variants.
    558 Non Msi H Crcs, supplied by Caris Life Sciences, used in various techniques. Bioz Stars score: 91/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Caris Life Sciences discovery cohort msi h crcs
    MLH1 and MSH2 protein domains annotated with somatic non-synonymous alterations observed in <t>MSI-H</t> <t>CRCs</t> from the COSMIC database A . MLH1 domains and variants. Three known domains are shown in the protein structure. The alterations including missense, nonsense and frameshift mutations are mapped with respect to known domains. Different numbers and colors of triangles in the same positions are representatives of frequency and diversity of mutations in the same spot, respectively. Red triangles represent the truncated mutations, while missense variants are shown in blue, brown and green. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle as well as red/orange rectangle. Red rectangles are representative of damaging mutations with high probability ( > 90%) and orange rectangles outline the mutations with possibility ( > 50%). B . MSH2 domains and variants.
    Discovery Cohort Msi H Crcs, supplied by Caris Life Sciences, used in various techniques. Bioz Stars score: 92/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Taylor & Francis crc taylor
    MLH1 and MSH2 protein domains annotated with somatic non-synonymous alterations observed in <t>MSI-H</t> <t>CRCs</t> from the COSMIC database A . MLH1 domains and variants. Three known domains are shown in the protein structure. The alterations including missense, nonsense and frameshift mutations are mapped with respect to known domains. Different numbers and colors of triangles in the same positions are representatives of frequency and diversity of mutations in the same spot, respectively. Red triangles represent the truncated mutations, while missense variants are shown in blue, brown and green. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle as well as red/orange rectangle. Red rectangles are representative of damaging mutations with high probability ( > 90%) and orange rectangles outline the mutations with possibility ( > 50%). B . MSH2 domains and variants.
    Crc Taylor, supplied by Taylor & Francis, used in various techniques. Bioz Stars score: 93/100, based on 37 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Taylor & Francis crc press
    MLH1 and MSH2 protein domains annotated with somatic non-synonymous alterations observed in <t>MSI-H</t> <t>CRCs</t> from the COSMIC database A . MLH1 domains and variants. Three known domains are shown in the protein structure. The alterations including missense, nonsense and frameshift mutations are mapped with respect to known domains. Different numbers and colors of triangles in the same positions are representatives of frequency and diversity of mutations in the same spot, respectively. Red triangles represent the truncated mutations, while missense variants are shown in blue, brown and green. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle as well as red/orange rectangle. Red rectangles are representative of damaging mutations with high probability ( > 90%) and orange rectangles outline the mutations with possibility ( > 50%). B . MSH2 domains and variants.
    Crc Press, supplied by Taylor & Francis, used in various techniques. Bioz Stars score: 94/100, based on 121 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Capintec crc 15r
    Plot of photon energy versus sensitivity for a <t>Capintec</t> <t>CRC-15R</t> dose calibrator. (Reprinted with permission of Capintec Inc. from the CRC-15R Owner's Manual).
    Crc 15r, supplied by Capintec, used in various techniques. Bioz Stars score: 85/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    87
    Taylor & Francis uk crc press
    Plot of photon energy versus sensitivity for a <t>Capintec</t> <t>CRC-15R</t> dose calibrator. (Reprinted with permission of Capintec Inc. from the CRC-15R Owner's Manual).
    Uk Crc Press, supplied by Taylor & Francis, used in various techniques. Bioz Stars score: 87/100, based on 17 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    87
    VANGL2 LTD scrib crc
    Triply heterozygous PCP mutant embryos have no more severe phenotypes than double heterozygotes. Embryos at E10.5 generated from intercross of a Celsr1 Crsh /+ female with a <t>Vangl2</t> Lp /+ ; <t>Scrib</t> Crc /+ male. (A) Triple mutant Vangl2 Lp /+ ; Scrib Crc /+ ; Celsr1 Crsh /+ with craniorachischisis. (B) Triple mutant Vangl2 Lp /+ ; Scrib Crc /+ ; Celsr1 Crsh /+ with hindbrain exencephaly. (C) Double mutant Vangl2 Lp /+ ; Scrib + / + ; Celsr1 Crsh /+ with craniorachischisis. (D) Double mutant Vangl2 Lp /+ ; Scrib Crc /+ ; Celsr1 +/+ with a looped-tail phenotype. (E) Double mutant Vangl2 +/+ ; Scrib Crc /+ ; Celsr1 Crsh /+ with no overt phenotype. Arrows in A, B and C indicate the cranial and caudal ends of the open region, in each embryo. Scale bar: 1 mm.
    Scrib Crc, supplied by VANGL2 LTD, used in various techniques. Bioz Stars score: 87/100, based on 44 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Capintec crc 15r calibrator
    Plot of photon energy versus sensitivity for a Capintec <t>CRC-15R</t> dose calibrator. (Reprinted with permission of Capintec Inc. from the CRC-15R Owner's Manual).
    Crc 15r Calibrator, supplied by Capintec, used in various techniques. Bioz Stars score: 86/100, based on 55 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    94
    Genomictree Inc earlytect crc test
    Plot of photon energy versus sensitivity for a Capintec <t>CRC-15R</t> dose calibrator. (Reprinted with permission of Capintec Inc. from the CRC-15R Owner's Manual).
    Earlytect Crc Test, supplied by Genomictree Inc, used in various techniques. Bioz Stars score: 94/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Exosome Diagnostics crc exosomes
    Colorectal cancer <t>exosomes</t> induce changes in colonic MSC morphology and growth rate ( A ) Transmission electron microscopy image of SW480 primary <t>CRC</t> derived exosomes (pCRCexo). Arrows indicate different size nanovesicles. Scale bar, 0.2 μM. ( B ) Western blot analysis of sucrose gradient fractions of pCRCexo blotted for the detection of carcinoembryonic antigen (CEA), tsg101 and CD81 (ubiquitous exosome markers) molecules. The density in which exosomes float corresponds to the tsg101- and CD81-positive fractions, and it is comprised between 0.90 and 1.22 g/ml. Total protein extracts of pCRC cells and their purified exosomes (pCRCexo) were loaded as control. M is the weight molecular protein marker; 1–12 correspond to the twelve fractions from sucrose density gradient. ( C ) Phase contrast microscopy (left panels) and scanning electron microscopy (SEM, right panels) images of colonic MSCs (cMSCs) treated for 6 days with pCRCexo. Arrows, asterisks and dotted circle indicate pseudopods, microvilli and vesicles respectively. 20X magnification in contrast microscopy; in SEM scale bar, 20 μM. Inserts represent a 2X magnification. Representative images of two independent experiments are reported. ( D ) Cell proliferation of cMSCs exposed to pCRCexo or cMSCs derived exosomes (cMSCexo) for 6 and 12 days; arrow indicates the exosomes re-feeding at day 9; proliferation was measured at day 6 and 12. ( E ) Cell proliferation of cMSCs incubated with pCRCexo or cMSCexo for 9 days and then replated in fresh medium without exosomes for other 7 days; proliferation was measured at day 9 and 16. ( F ) Cell proliferation of cMSCs or SW480 primary CRC (pCRC) cells incubated with pCRCexo or cMSCexo for 6 days at 1% FCS and pH 6.5 culture conditions. Results in D, E and F are expressed as optical density (mean ± SD, n = at least three independent sets of experiments (** p ≤ 0.005; (*** p ≤ 0.001;), compared to untreated cMSCs (CTR).
    Crc Exosomes, supplied by Exosome Diagnostics, used in various techniques. Bioz Stars score: 93/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Taylor & Francis crc press balkema
    Colorectal cancer <t>exosomes</t> induce changes in colonic MSC morphology and growth rate ( A ) Transmission electron microscopy image of SW480 primary <t>CRC</t> derived exosomes (pCRCexo). Arrows indicate different size nanovesicles. Scale bar, 0.2 μM. ( B ) Western blot analysis of sucrose gradient fractions of pCRCexo blotted for the detection of carcinoembryonic antigen (CEA), tsg101 and CD81 (ubiquitous exosome markers) molecules. The density in which exosomes float corresponds to the tsg101- and CD81-positive fractions, and it is comprised between 0.90 and 1.22 g/ml. Total protein extracts of pCRC cells and their purified exosomes (pCRCexo) were loaded as control. M is the weight molecular protein marker; 1–12 correspond to the twelve fractions from sucrose density gradient. ( C ) Phase contrast microscopy (left panels) and scanning electron microscopy (SEM, right panels) images of colonic MSCs (cMSCs) treated for 6 days with pCRCexo. Arrows, asterisks and dotted circle indicate pseudopods, microvilli and vesicles respectively. 20X magnification in contrast microscopy; in SEM scale bar, 20 μM. Inserts represent a 2X magnification. Representative images of two independent experiments are reported. ( D ) Cell proliferation of cMSCs exposed to pCRCexo or cMSCs derived exosomes (cMSCexo) for 6 and 12 days; arrow indicates the exosomes re-feeding at day 9; proliferation was measured at day 6 and 12. ( E ) Cell proliferation of cMSCs incubated with pCRCexo or cMSCexo for 9 days and then replated in fresh medium without exosomes for other 7 days; proliferation was measured at day 9 and 16. ( F ) Cell proliferation of cMSCs or SW480 primary CRC (pCRC) cells incubated with pCRCexo or cMSCexo for 6 days at 1% FCS and pH 6.5 culture conditions. Results in D, E and F are expressed as optical density (mean ± SD, n = at least three independent sets of experiments (** p ≤ 0.005; (*** p ≤ 0.001;), compared to untreated cMSCs (CTR).
    Crc Press Balkema, supplied by Taylor & Francis, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Taylor & Francis edn crc press
    Colorectal cancer <t>exosomes</t> induce changes in colonic MSC morphology and growth rate ( A ) Transmission electron microscopy image of SW480 primary <t>CRC</t> derived exosomes (pCRCexo). Arrows indicate different size nanovesicles. Scale bar, 0.2 μM. ( B ) Western blot analysis of sucrose gradient fractions of pCRCexo blotted for the detection of carcinoembryonic antigen (CEA), tsg101 and CD81 (ubiquitous exosome markers) molecules. The density in which exosomes float corresponds to the tsg101- and CD81-positive fractions, and it is comprised between 0.90 and 1.22 g/ml. Total protein extracts of pCRC cells and their purified exosomes (pCRCexo) were loaded as control. M is the weight molecular protein marker; 1–12 correspond to the twelve fractions from sucrose density gradient. ( C ) Phase contrast microscopy (left panels) and scanning electron microscopy (SEM, right panels) images of colonic MSCs (cMSCs) treated for 6 days with pCRCexo. Arrows, asterisks and dotted circle indicate pseudopods, microvilli and vesicles respectively. 20X magnification in contrast microscopy; in SEM scale bar, 20 μM. Inserts represent a 2X magnification. Representative images of two independent experiments are reported. ( D ) Cell proliferation of cMSCs exposed to pCRCexo or cMSCs derived exosomes (cMSCexo) for 6 and 12 days; arrow indicates the exosomes re-feeding at day 9; proliferation was measured at day 6 and 12. ( E ) Cell proliferation of cMSCs incubated with pCRCexo or cMSCexo for 9 days and then replated in fresh medium without exosomes for other 7 days; proliferation was measured at day 9 and 16. ( F ) Cell proliferation of cMSCs or SW480 primary CRC (pCRC) cells incubated with pCRCexo or cMSCexo for 6 days at 1% FCS and pH 6.5 culture conditions. Results in D, E and F are expressed as optical density (mean ± SD, n = at least three independent sets of experiments (** p ≤ 0.005; (*** p ≤ 0.001;), compared to untreated cMSCs (CTR).
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    Colorectal cancer <t>exosomes</t> induce changes in colonic MSC morphology and growth rate ( A ) Transmission electron microscopy image of SW480 primary <t>CRC</t> derived exosomes (pCRCexo). Arrows indicate different size nanovesicles. Scale bar, 0.2 μM. ( B ) Western blot analysis of sucrose gradient fractions of pCRCexo blotted for the detection of carcinoembryonic antigen (CEA), tsg101 and CD81 (ubiquitous exosome markers) molecules. The density in which exosomes float corresponds to the tsg101- and CD81-positive fractions, and it is comprised between 0.90 and 1.22 g/ml. Total protein extracts of pCRC cells and their purified exosomes (pCRCexo) were loaded as control. M is the weight molecular protein marker; 1–12 correspond to the twelve fractions from sucrose density gradient. ( C ) Phase contrast microscopy (left panels) and scanning electron microscopy (SEM, right panels) images of colonic MSCs (cMSCs) treated for 6 days with pCRCexo. Arrows, asterisks and dotted circle indicate pseudopods, microvilli and vesicles respectively. 20X magnification in contrast microscopy; in SEM scale bar, 20 μM. Inserts represent a 2X magnification. Representative images of two independent experiments are reported. ( D ) Cell proliferation of cMSCs exposed to pCRCexo or cMSCs derived exosomes (cMSCexo) for 6 and 12 days; arrow indicates the exosomes re-feeding at day 9; proliferation was measured at day 6 and 12. ( E ) Cell proliferation of cMSCs incubated with pCRCexo or cMSCexo for 9 days and then replated in fresh medium without exosomes for other 7 days; proliferation was measured at day 9 and 16. ( F ) Cell proliferation of cMSCs or SW480 primary CRC (pCRC) cells incubated with pCRCexo or cMSCexo for 6 days at 1% FCS and pH 6.5 culture conditions. Results in D, E and F are expressed as optical density (mean ± SD, n = at least three independent sets of experiments (** p ≤ 0.005; (*** p ≤ 0.001;), compared to untreated cMSCs (CTR).
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    Colorectal cancer <t>exosomes</t> induce changes in colonic MSC morphology and growth rate ( A ) Transmission electron microscopy image of SW480 primary <t>CRC</t> derived exosomes (pCRCexo). Arrows indicate different size nanovesicles. Scale bar, 0.2 μM. ( B ) Western blot analysis of sucrose gradient fractions of pCRCexo blotted for the detection of carcinoembryonic antigen (CEA), tsg101 and CD81 (ubiquitous exosome markers) molecules. The density in which exosomes float corresponds to the tsg101- and CD81-positive fractions, and it is comprised between 0.90 and 1.22 g/ml. Total protein extracts of pCRC cells and their purified exosomes (pCRCexo) were loaded as control. M is the weight molecular protein marker; 1–12 correspond to the twelve fractions from sucrose density gradient. ( C ) Phase contrast microscopy (left panels) and scanning electron microscopy (SEM, right panels) images of colonic MSCs (cMSCs) treated for 6 days with pCRCexo. Arrows, asterisks and dotted circle indicate pseudopods, microvilli and vesicles respectively. 20X magnification in contrast microscopy; in SEM scale bar, 20 μM. Inserts represent a 2X magnification. Representative images of two independent experiments are reported. ( D ) Cell proliferation of cMSCs exposed to pCRCexo or cMSCs derived exosomes (cMSCexo) for 6 and 12 days; arrow indicates the exosomes re-feeding at day 9; proliferation was measured at day 6 and 12. ( E ) Cell proliferation of cMSCs incubated with pCRCexo or cMSCexo for 9 days and then replated in fresh medium without exosomes for other 7 days; proliferation was measured at day 9 and 16. ( F ) Cell proliferation of cMSCs or SW480 primary CRC (pCRC) cells incubated with pCRCexo or cMSCexo for 6 days at 1% FCS and pH 6.5 culture conditions. Results in D, E and F are expressed as optical density (mean ± SD, n = at least three independent sets of experiments (** p ≤ 0.005; (*** p ≤ 0.001;), compared to untreated cMSCs (CTR).
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    Colorectal cancer <t>exosomes</t> induce changes in colonic MSC morphology and growth rate ( A ) Transmission electron microscopy image of SW480 primary <t>CRC</t> derived exosomes (pCRCexo). Arrows indicate different size nanovesicles. Scale bar, 0.2 μM. ( B ) Western blot analysis of sucrose gradient fractions of pCRCexo blotted for the detection of carcinoembryonic antigen (CEA), tsg101 and CD81 (ubiquitous exosome markers) molecules. The density in which exosomes float corresponds to the tsg101- and CD81-positive fractions, and it is comprised between 0.90 and 1.22 g/ml. Total protein extracts of pCRC cells and their purified exosomes (pCRCexo) were loaded as control. M is the weight molecular protein marker; 1–12 correspond to the twelve fractions from sucrose density gradient. ( C ) Phase contrast microscopy (left panels) and scanning electron microscopy (SEM, right panels) images of colonic MSCs (cMSCs) treated for 6 days with pCRCexo. Arrows, asterisks and dotted circle indicate pseudopods, microvilli and vesicles respectively. 20X magnification in contrast microscopy; in SEM scale bar, 20 μM. Inserts represent a 2X magnification. Representative images of two independent experiments are reported. ( D ) Cell proliferation of cMSCs exposed to pCRCexo or cMSCs derived exosomes (cMSCexo) for 6 and 12 days; arrow indicates the exosomes re-feeding at day 9; proliferation was measured at day 6 and 12. ( E ) Cell proliferation of cMSCs incubated with pCRCexo or cMSCexo for 9 days and then replated in fresh medium without exosomes for other 7 days; proliferation was measured at day 9 and 16. ( F ) Cell proliferation of cMSCs or SW480 primary CRC (pCRC) cells incubated with pCRCexo or cMSCexo for 6 days at 1% FCS and pH 6.5 culture conditions. Results in D, E and F are expressed as optical density (mean ± SD, n = at least three independent sets of experiments (** p ≤ 0.005; (*** p ≤ 0.001;), compared to untreated cMSCs (CTR).
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    Colorectal cancer <t>exosomes</t> induce changes in colonic MSC morphology and growth rate ( A ) Transmission electron microscopy image of SW480 primary <t>CRC</t> derived exosomes (pCRCexo). Arrows indicate different size nanovesicles. Scale bar, 0.2 μM. ( B ) Western blot analysis of sucrose gradient fractions of pCRCexo blotted for the detection of carcinoembryonic antigen (CEA), tsg101 and CD81 (ubiquitous exosome markers) molecules. The density in which exosomes float corresponds to the tsg101- and CD81-positive fractions, and it is comprised between 0.90 and 1.22 g/ml. Total protein extracts of pCRC cells and their purified exosomes (pCRCexo) were loaded as control. M is the weight molecular protein marker; 1–12 correspond to the twelve fractions from sucrose density gradient. ( C ) Phase contrast microscopy (left panels) and scanning electron microscopy (SEM, right panels) images of colonic MSCs (cMSCs) treated for 6 days with pCRCexo. Arrows, asterisks and dotted circle indicate pseudopods, microvilli and vesicles respectively. 20X magnification in contrast microscopy; in SEM scale bar, 20 μM. Inserts represent a 2X magnification. Representative images of two independent experiments are reported. ( D ) Cell proliferation of cMSCs exposed to pCRCexo or cMSCs derived exosomes (cMSCexo) for 6 and 12 days; arrow indicates the exosomes re-feeding at day 9; proliferation was measured at day 6 and 12. ( E ) Cell proliferation of cMSCs incubated with pCRCexo or cMSCexo for 9 days and then replated in fresh medium without exosomes for other 7 days; proliferation was measured at day 9 and 16. ( F ) Cell proliferation of cMSCs or SW480 primary CRC (pCRC) cells incubated with pCRCexo or cMSCexo for 6 days at 1% FCS and pH 6.5 culture conditions. Results in D, E and F are expressed as optical density (mean ± SD, n = at least three independent sets of experiments (** p ≤ 0.005; (*** p ≤ 0.001;), compared to untreated cMSCs (CTR).
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    Image Search Results


    Clinical significance of FRA1 and FRA1 EMT genes in CRC. (A) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients according to expression of the FRA1 gene ( FOSL1 ). (B) Unsupervised clustering of stage B and stage C CRCs based on FRA1 EMT genes encompassing concordant probesets exhibiting significant expression differences between the two main groups. Clustering divides cancers into groups with mesenchymal and epithelial profiles. Samples are arranged along the X-axis and genes along the Y-axis. Genes are grouped into those downregulated (blue) or upregulated (orange) upon FRA1 knockdown in BE cells relative to the mean- and sample-centered scaled expression. (C) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients based on expression of both FOSL1 (low vs high) and mesenchymal (Mes, dark green) or epithelial (Epi, light green) subsets of FRA1 EMT genes. The log-rank test was used for comparisons.

    Journal: PLoS ONE

    Article Title: Widespread FRA1-Dependent Control of Mesenchymal Transdifferentiation Programs in Colorectal Cancer Cells

    doi: 10.1371/journal.pone.0088950

    Figure Lengend Snippet: Clinical significance of FRA1 and FRA1 EMT genes in CRC. (A) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients according to expression of the FRA1 gene ( FOSL1 ). (B) Unsupervised clustering of stage B and stage C CRCs based on FRA1 EMT genes encompassing concordant probesets exhibiting significant expression differences between the two main groups. Clustering divides cancers into groups with mesenchymal and epithelial profiles. Samples are arranged along the X-axis and genes along the Y-axis. Genes are grouped into those downregulated (blue) or upregulated (orange) upon FRA1 knockdown in BE cells relative to the mean- and sample-centered scaled expression. (C) Kaplan-Meier plots of recurrence-free survival in stage B and C CRC patients based on expression of both FOSL1 (low vs high) and mesenchymal (Mes, dark green) or epithelial (Epi, light green) subsets of FRA1 EMT genes. The log-rank test was used for comparisons.

    Article Snippet: More recently, several studies have identified EMT-related gene expression signatures as a common occurrence in primary CRCs, which are strongly associated with poor prognosis and resistance to targeted therapies – .

    Techniques: Expressing

    MLH1 and MSH2 protein domains annotated with somatic non-synonymous alterations observed in MSI-H CRCs from the COSMIC database A . MLH1 domains and variants. Three known domains are shown in the protein structure. The alterations including missense, nonsense and frameshift mutations are mapped with respect to known domains. Different numbers and colors of triangles in the same positions are representatives of frequency and diversity of mutations in the same spot, respectively. Red triangles represent the truncated mutations, while missense variants are shown in blue, brown and green. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle as well as red/orange rectangle. Red rectangles are representative of damaging mutations with high probability ( > 90%) and orange rectangles outline the mutations with possibility ( > 50%). B . MSH2 domains and variants.

    Journal: Oncotarget

    Article Title: BRCA2, EGFR, and NTRK mutations in mismatch repair-deficient colorectal cancers with MSH2 or MLH1 mutations

    doi: 10.18632/oncotarget.18098

    Figure Lengend Snippet: MLH1 and MSH2 protein domains annotated with somatic non-synonymous alterations observed in MSI-H CRCs from the COSMIC database A . MLH1 domains and variants. Three known domains are shown in the protein structure. The alterations including missense, nonsense and frameshift mutations are mapped with respect to known domains. Different numbers and colors of triangles in the same positions are representatives of frequency and diversity of mutations in the same spot, respectively. Red triangles represent the truncated mutations, while missense variants are shown in blue, brown and green. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle as well as red/orange rectangle. Red rectangles are representative of damaging mutations with high probability ( > 90%) and orange rectangles outline the mutations with possibility ( > 50%). B . MSH2 domains and variants.

    Article Snippet: Discovery cohort of CRC analyzed by genomic profiling identifies frequent BRCA2 mutations in MSI-H tumors We analyzed the mutation data for 26 MSI-H and 558 non-MSI-H CRCs that were profiled at Caris Life Sciences.

    Techniques:

    The BRCA2 gene is among the most highly mutated genes with a higher mean number of mutations per tumor in MSI-H CRCs A . Difference in number of mutated genes in CRC patients with MSI-H and non-MSI-H are plotted in box-plot (mutation counts are log10 scaled). B . Genes with different mutation frequencies among the MSI-H and non-MSI-H groups are shown with respect to matters of significance. C . The columns represent the mean of the number of mutations in the gene, across both MSI-H and non-MSI-H samples. The distribution of mutation counts between MSI-H and non-MSI-H samples were compared by Wilcoxon rank sum tests. Fisher exact test was applied to compare the categorical variables.

    Journal: Oncotarget

    Article Title: BRCA2, EGFR, and NTRK mutations in mismatch repair-deficient colorectal cancers with MSH2 or MLH1 mutations

    doi: 10.18632/oncotarget.18098

    Figure Lengend Snippet: The BRCA2 gene is among the most highly mutated genes with a higher mean number of mutations per tumor in MSI-H CRCs A . Difference in number of mutated genes in CRC patients with MSI-H and non-MSI-H are plotted in box-plot (mutation counts are log10 scaled). B . Genes with different mutation frequencies among the MSI-H and non-MSI-H groups are shown with respect to matters of significance. C . The columns represent the mean of the number of mutations in the gene, across both MSI-H and non-MSI-H samples. The distribution of mutation counts between MSI-H and non-MSI-H samples were compared by Wilcoxon rank sum tests. Fisher exact test was applied to compare the categorical variables.

    Article Snippet: Discovery cohort of CRC analyzed by genomic profiling identifies frequent BRCA2 mutations in MSI-H tumors We analyzed the mutation data for 26 MSI-H and 558 non-MSI-H CRCs that were profiled at Caris Life Sciences.

    Techniques: Mutagenesis

    BRCA2 protein domain structure annotated with somatic alterations in MSI-H vs non-MSI-H CRCs and coding microsatellites . A . BRCA2 mutations in MSI-H patient samples vs. non-MSI-H samples. Functional domains and interaction partner proteins are annotated in black and green, respectively. Truncating variants including nonsense and frameshift mutations are shown in red. Missense mutations are denoted in blue as well as brown in the same spot. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle as well as red/orange rectangle. Red rectangles are representative of damaging mutations with high probability ( > 90%) and orange rectangles outline the mutations with possibility ( > 50%). Synonymous variants are shown in white triangles. B . BRCA2 and mutations in coding repetitive sequences in both groups.

    Journal: Oncotarget

    Article Title: BRCA2, EGFR, and NTRK mutations in mismatch repair-deficient colorectal cancers with MSH2 or MLH1 mutations

    doi: 10.18632/oncotarget.18098

    Figure Lengend Snippet: BRCA2 protein domain structure annotated with somatic alterations in MSI-H vs non-MSI-H CRCs and coding microsatellites . A . BRCA2 mutations in MSI-H patient samples vs. non-MSI-H samples. Functional domains and interaction partner proteins are annotated in black and green, respectively. Truncating variants including nonsense and frameshift mutations are shown in red. Missense mutations are denoted in blue as well as brown in the same spot. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle as well as red/orange rectangle. Red rectangles are representative of damaging mutations with high probability ( > 90%) and orange rectangles outline the mutations with possibility ( > 50%). Synonymous variants are shown in white triangles. B . BRCA2 and mutations in coding repetitive sequences in both groups.

    Article Snippet: Discovery cohort of CRC analyzed by genomic profiling identifies frequent BRCA2 mutations in MSI-H tumors We analyzed the mutation data for 26 MSI-H and 558 non-MSI-H CRCs that were profiled at Caris Life Sciences.

    Techniques: Functional Assay

    EGFR mutations in kinase domain denoted on 2D and 3D model of EGFR protein structure A . EGFR protein domain structure are annotated with activating as well as potentially damaging somatic alterations in MSI-H vs. non-MSI-H CRCs. Functional domains are annotated in different colored-boxes. Truncating variants including nonsense and frameshift mutations are shown in red. Missense mutations are denoted in blue as well as brown in the same spot. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle. Orange rectangles outline the mutations with possibility ( > 50%). B . Model depicts mutations in tyrosine kinase domain of EGFR genes. The structure of EGFR kinase domain is showing the WT residues of mutations in orange spheres. The activation loop is colored in magenta and Phenylaniline residue of the DFG motif is shown in green sticks. The known responding mutations to TKI are denoted in red outlined. The figure is generated by PyMOL ( https://www.pymol.org/pymol ).

    Journal: Oncotarget

    Article Title: BRCA2, EGFR, and NTRK mutations in mismatch repair-deficient colorectal cancers with MSH2 or MLH1 mutations

    doi: 10.18632/oncotarget.18098

    Figure Lengend Snippet: EGFR mutations in kinase domain denoted on 2D and 3D model of EGFR protein structure A . EGFR protein domain structure are annotated with activating as well as potentially damaging somatic alterations in MSI-H vs. non-MSI-H CRCs. Functional domains are annotated in different colored-boxes. Truncating variants including nonsense and frameshift mutations are shown in red. Missense mutations are denoted in blue as well as brown in the same spot. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle. Orange rectangles outline the mutations with possibility ( > 50%). B . Model depicts mutations in tyrosine kinase domain of EGFR genes. The structure of EGFR kinase domain is showing the WT residues of mutations in orange spheres. The activation loop is colored in magenta and Phenylaniline residue of the DFG motif is shown in green sticks. The known responding mutations to TKI are denoted in red outlined. The figure is generated by PyMOL ( https://www.pymol.org/pymol ).

    Article Snippet: Discovery cohort of CRC analyzed by genomic profiling identifies frequent BRCA2 mutations in MSI-H tumors We analyzed the mutation data for 26 MSI-H and 558 non-MSI-H CRCs that were profiled at Caris Life Sciences.

    Techniques: Functional Assay, Activation Assay, Generated

    BRCA2 is highly mutated in MSI-H CRCs in a discovery cohort of CRCs profiled by Caris Life Sciences A . Selected genes including deregulated genes in CRC in MSI-H and non-MSI-H CRC subtypes is plotted with different mutation frequencies among the MSI-H and non-MSI-H groups are shown. The p -value

    Journal: Oncotarget

    Article Title: BRCA2, EGFR, and NTRK mutations in mismatch repair-deficient colorectal cancers with MSH2 or MLH1 mutations

    doi: 10.18632/oncotarget.18098

    Figure Lengend Snippet: BRCA2 is highly mutated in MSI-H CRCs in a discovery cohort of CRCs profiled by Caris Life Sciences A . Selected genes including deregulated genes in CRC in MSI-H and non-MSI-H CRC subtypes is plotted with different mutation frequencies among the MSI-H and non-MSI-H groups are shown. The p -value

    Article Snippet: Discovery cohort of CRC analyzed by genomic profiling identifies frequent BRCA2 mutations in MSI-H tumors We analyzed the mutation data for 26 MSI-H and 558 non-MSI-H CRCs that were profiled at Caris Life Sciences.

    Techniques: Mutagenesis

    MLH1 and MSH2 protein domains annotated with somatic non-synonymous alterations observed in MSI-H CRCs from the COSMIC database A . MLH1 domains and variants. Three known domains are shown in the protein structure. The alterations including missense, nonsense and frameshift mutations are mapped with respect to known domains. Different numbers and colors of triangles in the same positions are representatives of frequency and diversity of mutations in the same spot, respectively. Red triangles represent the truncated mutations, while missense variants are shown in blue, brown and green. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle as well as red/orange rectangle. Red rectangles are representative of damaging mutations with high probability ( > 90%) and orange rectangles outline the mutations with possibility ( > 50%). B . MSH2 domains and variants.

    Journal: Oncotarget

    Article Title: BRCA2, EGFR, and NTRK mutations in mismatch repair-deficient colorectal cancers with MSH2 or MLH1 mutations

    doi: 10.18632/oncotarget.18098

    Figure Lengend Snippet: MLH1 and MSH2 protein domains annotated with somatic non-synonymous alterations observed in MSI-H CRCs from the COSMIC database A . MLH1 domains and variants. Three known domains are shown in the protein structure. The alterations including missense, nonsense and frameshift mutations are mapped with respect to known domains. Different numbers and colors of triangles in the same positions are representatives of frequency and diversity of mutations in the same spot, respectively. Red triangles represent the truncated mutations, while missense variants are shown in blue, brown and green. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle as well as red/orange rectangle. Red rectangles are representative of damaging mutations with high probability ( > 90%) and orange rectangles outline the mutations with possibility ( > 50%). B . MSH2 domains and variants.

    Article Snippet: EGFR T725M detected in our discovery cohort MSI-H CRCs (Caris Life Sciences), is reported in cell-based assays to increase EGFR activity in the absence of EGFR ligand [ ].

    Techniques:

    The BRCA2 gene is among the most highly mutated genes with a higher mean number of mutations per tumor in MSI-H CRCs A . Difference in number of mutated genes in CRC patients with MSI-H and non-MSI-H are plotted in box-plot (mutation counts are log10 scaled). B . Genes with different mutation frequencies among the MSI-H and non-MSI-H groups are shown with respect to matters of significance. C . The columns represent the mean of the number of mutations in the gene, across both MSI-H and non-MSI-H samples. The distribution of mutation counts between MSI-H and non-MSI-H samples were compared by Wilcoxon rank sum tests. Fisher exact test was applied to compare the categorical variables.

    Journal: Oncotarget

    Article Title: BRCA2, EGFR, and NTRK mutations in mismatch repair-deficient colorectal cancers with MSH2 or MLH1 mutations

    doi: 10.18632/oncotarget.18098

    Figure Lengend Snippet: The BRCA2 gene is among the most highly mutated genes with a higher mean number of mutations per tumor in MSI-H CRCs A . Difference in number of mutated genes in CRC patients with MSI-H and non-MSI-H are plotted in box-plot (mutation counts are log10 scaled). B . Genes with different mutation frequencies among the MSI-H and non-MSI-H groups are shown with respect to matters of significance. C . The columns represent the mean of the number of mutations in the gene, across both MSI-H and non-MSI-H samples. The distribution of mutation counts between MSI-H and non-MSI-H samples were compared by Wilcoxon rank sum tests. Fisher exact test was applied to compare the categorical variables.

    Article Snippet: EGFR T725M detected in our discovery cohort MSI-H CRCs (Caris Life Sciences), is reported in cell-based assays to increase EGFR activity in the absence of EGFR ligand [ ].

    Techniques: Mutagenesis

    BRCA2 protein domain structure annotated with somatic alterations in MSI-H vs non-MSI-H CRCs and coding microsatellites . A . BRCA2 mutations in MSI-H patient samples vs. non-MSI-H samples. Functional domains and interaction partner proteins are annotated in black and green, respectively. Truncating variants including nonsense and frameshift mutations are shown in red. Missense mutations are denoted in blue as well as brown in the same spot. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle as well as red/orange rectangle. Red rectangles are representative of damaging mutations with high probability ( > 90%) and orange rectangles outline the mutations with possibility ( > 50%). Synonymous variants are shown in white triangles. B . BRCA2 and mutations in coding repetitive sequences in both groups.

    Journal: Oncotarget

    Article Title: BRCA2, EGFR, and NTRK mutations in mismatch repair-deficient colorectal cancers with MSH2 or MLH1 mutations

    doi: 10.18632/oncotarget.18098

    Figure Lengend Snippet: BRCA2 protein domain structure annotated with somatic alterations in MSI-H vs non-MSI-H CRCs and coding microsatellites . A . BRCA2 mutations in MSI-H patient samples vs. non-MSI-H samples. Functional domains and interaction partner proteins are annotated in black and green, respectively. Truncating variants including nonsense and frameshift mutations are shown in red. Missense mutations are denoted in blue as well as brown in the same spot. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle as well as red/orange rectangle. Red rectangles are representative of damaging mutations with high probability ( > 90%) and orange rectangles outline the mutations with possibility ( > 50%). Synonymous variants are shown in white triangles. B . BRCA2 and mutations in coding repetitive sequences in both groups.

    Article Snippet: EGFR T725M detected in our discovery cohort MSI-H CRCs (Caris Life Sciences), is reported in cell-based assays to increase EGFR activity in the absence of EGFR ligand [ ].

    Techniques: Functional Assay

    EGFR mutations in kinase domain denoted on 2D and 3D model of EGFR protein structure A . EGFR protein domain structure are annotated with activating as well as potentially damaging somatic alterations in MSI-H vs. non-MSI-H CRCs. Functional domains are annotated in different colored-boxes. Truncating variants including nonsense and frameshift mutations are shown in red. Missense mutations are denoted in blue as well as brown in the same spot. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle. Orange rectangles outline the mutations with possibility ( > 50%). B . Model depicts mutations in tyrosine kinase domain of EGFR genes. The structure of EGFR kinase domain is showing the WT residues of mutations in orange spheres. The activation loop is colored in magenta and Phenylaniline residue of the DFG motif is shown in green sticks. The known responding mutations to TKI are denoted in red outlined. The figure is generated by PyMOL ( https://www.pymol.org/pymol ).

    Journal: Oncotarget

    Article Title: BRCA2, EGFR, and NTRK mutations in mismatch repair-deficient colorectal cancers with MSH2 or MLH1 mutations

    doi: 10.18632/oncotarget.18098

    Figure Lengend Snippet: EGFR mutations in kinase domain denoted on 2D and 3D model of EGFR protein structure A . EGFR protein domain structure are annotated with activating as well as potentially damaging somatic alterations in MSI-H vs. non-MSI-H CRCs. Functional domains are annotated in different colored-boxes. Truncating variants including nonsense and frameshift mutations are shown in red. Missense mutations are denoted in blue as well as brown in the same spot. Variants predicted by PolyPhen-2 ( http://genetics.bwh.harvard.edu/pph2/ ) to be damaging are denoted in black-outlined triangle. Orange rectangles outline the mutations with possibility ( > 50%). B . Model depicts mutations in tyrosine kinase domain of EGFR genes. The structure of EGFR kinase domain is showing the WT residues of mutations in orange spheres. The activation loop is colored in magenta and Phenylaniline residue of the DFG motif is shown in green sticks. The known responding mutations to TKI are denoted in red outlined. The figure is generated by PyMOL ( https://www.pymol.org/pymol ).

    Article Snippet: EGFR T725M detected in our discovery cohort MSI-H CRCs (Caris Life Sciences), is reported in cell-based assays to increase EGFR activity in the absence of EGFR ligand [ ].

    Techniques: Functional Assay, Activation Assay, Generated

    BRCA2 is highly mutated in MSI-H CRCs in a discovery cohort of CRCs profiled by Caris Life Sciences A . Selected genes including deregulated genes in CRC in MSI-H and non-MSI-H CRC subtypes is plotted with different mutation frequencies among the MSI-H and non-MSI-H groups are shown. The p -value

    Journal: Oncotarget

    Article Title: BRCA2, EGFR, and NTRK mutations in mismatch repair-deficient colorectal cancers with MSH2 or MLH1 mutations

    doi: 10.18632/oncotarget.18098

    Figure Lengend Snippet: BRCA2 is highly mutated in MSI-H CRCs in a discovery cohort of CRCs profiled by Caris Life Sciences A . Selected genes including deregulated genes in CRC in MSI-H and non-MSI-H CRC subtypes is plotted with different mutation frequencies among the MSI-H and non-MSI-H groups are shown. The p -value

    Article Snippet: EGFR T725M detected in our discovery cohort MSI-H CRCs (Caris Life Sciences), is reported in cell-based assays to increase EGFR activity in the absence of EGFR ligand [ ].

    Techniques: Mutagenesis

    Plot of photon energy versus sensitivity for a Capintec CRC-15R dose calibrator. (Reprinted with permission of Capintec Inc. from the CRC-15R Owner's Manual).

    Journal: PLoS ONE

    Article Title: A Recommendation for Revised Dose Calibrator Measurement Procedures for 89Zr and 124I

    doi: 10.1371/journal.pone.0106868

    Figure Lengend Snippet: Plot of photon energy versus sensitivity for a Capintec CRC-15R dose calibrator. (Reprinted with permission of Capintec Inc. from the CRC-15R Owner's Manual).

    Article Snippet: In a conference proceedings in 2006 , Avila-Rodriguez et al. described using a calibration setting number of 465 for the Capintec CRC-15R.

    Techniques:

    Activity versus calibration setting number as measured on a Capintec CRC-15R dose calibrator for A) Zr-89 and B) I-124, measured in different geometries. Filled symbols identify the curves corresponding to the measurements with the copper filter; open symbols without the filter. Triangles correspond to the small volume in the 5 mL syringe, circles to the 3 mL volume in the 5 mL syringe and squares to the 10 mL volume in the liquid scintillation vial. Note that for I-124 the filled squares almost completely obscure the filled circles.

    Journal: PLoS ONE

    Article Title: A Recommendation for Revised Dose Calibrator Measurement Procedures for 89Zr and 124I

    doi: 10.1371/journal.pone.0106868

    Figure Lengend Snippet: Activity versus calibration setting number as measured on a Capintec CRC-15R dose calibrator for A) Zr-89 and B) I-124, measured in different geometries. Filled symbols identify the curves corresponding to the measurements with the copper filter; open symbols without the filter. Triangles correspond to the small volume in the 5 mL syringe, circles to the 3 mL volume in the 5 mL syringe and squares to the 10 mL volume in the liquid scintillation vial. Note that for I-124 the filled squares almost completely obscure the filled circles.

    Article Snippet: In a conference proceedings in 2006 , Avila-Rodriguez et al. described using a calibration setting number of 465 for the Capintec CRC-15R.

    Techniques: Activity Assay

    Triply heterozygous PCP mutant embryos have no more severe phenotypes than double heterozygotes. Embryos at E10.5 generated from intercross of a Celsr1 Crsh /+ female with a Vangl2 Lp /+ ; Scrib Crc /+ male. (A) Triple mutant Vangl2 Lp /+ ; Scrib Crc /+ ; Celsr1 Crsh /+ with craniorachischisis. (B) Triple mutant Vangl2 Lp /+ ; Scrib Crc /+ ; Celsr1 Crsh /+ with hindbrain exencephaly. (C) Double mutant Vangl2 Lp /+ ; Scrib + / + ; Celsr1 Crsh /+ with craniorachischisis. (D) Double mutant Vangl2 Lp /+ ; Scrib Crc /+ ; Celsr1 +/+ with a looped-tail phenotype. (E) Double mutant Vangl2 +/+ ; Scrib Crc /+ ; Celsr1 Crsh /+ with no overt phenotype. Arrows in A, B and C indicate the cranial and caudal ends of the open region, in each embryo. Scale bar: 1 mm.

    Journal: Disease Models & Mechanisms

    Article Title: Genetic interactions between planar cell polarity genes cause diverse neural tube defects in mice

    doi: 10.1242/dmm.016758

    Figure Lengend Snippet: Triply heterozygous PCP mutant embryos have no more severe phenotypes than double heterozygotes. Embryos at E10.5 generated from intercross of a Celsr1 Crsh /+ female with a Vangl2 Lp /+ ; Scrib Crc /+ male. (A) Triple mutant Vangl2 Lp /+ ; Scrib Crc /+ ; Celsr1 Crsh /+ with craniorachischisis. (B) Triple mutant Vangl2 Lp /+ ; Scrib Crc /+ ; Celsr1 Crsh /+ with hindbrain exencephaly. (C) Double mutant Vangl2 Lp /+ ; Scrib + / + ; Celsr1 Crsh /+ with craniorachischisis. (D) Double mutant Vangl2 Lp /+ ; Scrib Crc /+ ; Celsr1 +/+ with a looped-tail phenotype. (E) Double mutant Vangl2 +/+ ; Scrib Crc /+ ; Celsr1 Crsh /+ with no overt phenotype. Arrows in A, B and C indicate the cranial and caudal ends of the open region, in each embryo. Scale bar: 1 mm.

    Article Snippet: One Vangl2 Lp /+ ;Scrib Crc /+ fetus exhibited abdominal wall defect with a closed neural tube ( ).

    Techniques: Mutagenesis, Generated

    Delayed initiation of neural tube closure in Celsr1 Crsh /+ and Vangl2 Lp /+ but not in Scrib Crc /+ embryos. Proportion of E8.5 embryos that initiate neural tube closure in the four- to nine-somite stage interval is shown for wild type (solid line), heterozygous mutants (dashed line) and homozygous mutants (dotted line). (A) Vangl2 Lp mutant strain (congenic on C3H/HeH; n =22 +/+, 42 Lp /+, 16 Lp/Lp ); (B) Vangl2 Lp mutant strain (on LPT/Le × CBA background; n =55 +/+, 131 Lp /+, 49 Lp/Lp ); (C) Celsr1 Crsh mutant strain ( n =75 +/+, 175 Crsh /+, 61 Crsh/Crsh ); (D) Scrib Crc mutant strain (congenic on C3H/HeH; n =163 +/+, 371 Crc /+, 154 Crc/Crc ). Homozygotes all fail to initiate neural tube closure. Wild-type embryos undergo Closure 1 between the five- and eight-somite stages. Vangl2 Lp /+ and Celsr1 Crsh /+ heterozygotes are delayed in closure initiation compared with wild type ( Vangl2 Lp -C3H : P =0.03; Vangl2 Lp -LPT : P

    Journal: Disease Models & Mechanisms

    Article Title: Genetic interactions between planar cell polarity genes cause diverse neural tube defects in mice

    doi: 10.1242/dmm.016758

    Figure Lengend Snippet: Delayed initiation of neural tube closure in Celsr1 Crsh /+ and Vangl2 Lp /+ but not in Scrib Crc /+ embryos. Proportion of E8.5 embryos that initiate neural tube closure in the four- to nine-somite stage interval is shown for wild type (solid line), heterozygous mutants (dashed line) and homozygous mutants (dotted line). (A) Vangl2 Lp mutant strain (congenic on C3H/HeH; n =22 +/+, 42 Lp /+, 16 Lp/Lp ); (B) Vangl2 Lp mutant strain (on LPT/Le × CBA background; n =55 +/+, 131 Lp /+, 49 Lp/Lp ); (C) Celsr1 Crsh mutant strain ( n =75 +/+, 175 Crsh /+, 61 Crsh/Crsh ); (D) Scrib Crc mutant strain (congenic on C3H/HeH; n =163 +/+, 371 Crc /+, 154 Crc/Crc ). Homozygotes all fail to initiate neural tube closure. Wild-type embryos undergo Closure 1 between the five- and eight-somite stages. Vangl2 Lp /+ and Celsr1 Crsh /+ heterozygotes are delayed in closure initiation compared with wild type ( Vangl2 Lp -C3H : P =0.03; Vangl2 Lp -LPT : P

    Article Snippet: One Vangl2 Lp /+ ;Scrib Crc /+ fetus exhibited abdominal wall defect with a closed neural tube ( ).

    Techniques: Mutagenesis, Crocin Bleaching Assay

    Protein analysis suggests that Scrib Crc is a null mutant, whereas Vangl2 Lp and Celsr1 Crsh express mutant protein isoforms. Western blot analysis was performed on whole embryo lysates (unless otherwise stated) using antibodies specific for the individual PCP proteins. (A) Vangl2 protein expression in E8.5 wild-type, heterozygous and homozygous embryos for Scrib Crc , Vangl2 Lp and Celsr1 Crsh . Vangl2 has reduced abundance in Vangl2 Lp/Lp and to a lesser extent in Scrib Crc embryos. Fatty acid synthase (Fas) was used as loading control. (B) Vangl2 protein expression in membrane fractions from E10.5 wild-type and Vangl2 Lp/Lp embryos, following incubation with (+) or without (−) shrimp alkaline phosphatase (SAP). Vangl2 Lp/Lp mutants show reduced Vangl2 expression, and SAP treatment causes a shift in band sizes in wild type consistent with decreased phosphorylation in Vangl2 Lp/Lp mutants. (C) Vangl2 protein expression in wild-type E11.5 membrane and organelle fraction, treated with (+) or without (−) SAP, for times from 0 to 60 minutes as indicated above each lane. SAP incubation causes a shift in band distribution to a lower molecular weight, although three bands can still be seen (upper panel). This suggests that Vangl2 is phosphorylated endogenously, but that other modifications are also present, giving rise to the multiple bands observed. Extended exposure reveals bands at lower molecular weights (lower panel), indicating the existence of shorter isoforms (or cleavage products), that might correspond to alternative splice variants predicted on Ensembl. (D) Scrib protein expression in membrane fractions of E13.5 wild-type, Scrib Crc /+ and Scrib Crc/Crc fetuses. A duplicate blot was immunostained for β-tubulin. Scrib is detected as multiple isoforms from ~210 kDa (arrows). Scrib Crc/Crc mutants completely lack Scrib protein, with no evidence for stably expressed truncated product, even after extended exposures (right-hand panel). The monoclonal antibody detects a band at ~55 kDa, in both wild-type and Scrib Crc/Crc mutants; no known splice variants are predicted to generate a shorter isoform of this size, and this band seems likely the result of nonspecific antibody binding. (E) Scrib expression in E8.5 wild-type, heterozygous and homozygous embryos from Scrib Crc , Vangl2 Lp and Celsr1 Crsh litters. Scrib is absent from Scrib Crc/Crc embryos. The lower molecular weight bands varied in intensity between protein preparations and could be either degradation products of Scrib protein or alternatively spliced isoforms. (F,G) Celsr1 protein expression in membrane (Mem) and soluble (Sol) fractions of E10.5 embryos (F) and whole-cell lysates of E8.5 embryos (G) from Vangl2 Lp , Scrib Crc and Celsr1 Crsh litters. Celsr1 bands (arrows in F) are detected at ~350 kDa (F,G) and ~80 kDa (F), with no apparent change in any mutants. (H–J) Quantitation of Vangl2 (H), Scrib (I) and Celsr1 (J) protein expression in E8.5 Scrib Crc , Vangl2 Lp and Celsr1 Crsh embryos, normalized to β-tubulin (H) or Fas (I,J) levels. Data are the average of three experiments ± standard errors; expression levels that differ significantly from wild type are indicated with asterisks (* P

    Journal: Disease Models & Mechanisms

    Article Title: Genetic interactions between planar cell polarity genes cause diverse neural tube defects in mice

    doi: 10.1242/dmm.016758

    Figure Lengend Snippet: Protein analysis suggests that Scrib Crc is a null mutant, whereas Vangl2 Lp and Celsr1 Crsh express mutant protein isoforms. Western blot analysis was performed on whole embryo lysates (unless otherwise stated) using antibodies specific for the individual PCP proteins. (A) Vangl2 protein expression in E8.5 wild-type, heterozygous and homozygous embryos for Scrib Crc , Vangl2 Lp and Celsr1 Crsh . Vangl2 has reduced abundance in Vangl2 Lp/Lp and to a lesser extent in Scrib Crc embryos. Fatty acid synthase (Fas) was used as loading control. (B) Vangl2 protein expression in membrane fractions from E10.5 wild-type and Vangl2 Lp/Lp embryos, following incubation with (+) or without (−) shrimp alkaline phosphatase (SAP). Vangl2 Lp/Lp mutants show reduced Vangl2 expression, and SAP treatment causes a shift in band sizes in wild type consistent with decreased phosphorylation in Vangl2 Lp/Lp mutants. (C) Vangl2 protein expression in wild-type E11.5 membrane and organelle fraction, treated with (+) or without (−) SAP, for times from 0 to 60 minutes as indicated above each lane. SAP incubation causes a shift in band distribution to a lower molecular weight, although three bands can still be seen (upper panel). This suggests that Vangl2 is phosphorylated endogenously, but that other modifications are also present, giving rise to the multiple bands observed. Extended exposure reveals bands at lower molecular weights (lower panel), indicating the existence of shorter isoforms (or cleavage products), that might correspond to alternative splice variants predicted on Ensembl. (D) Scrib protein expression in membrane fractions of E13.5 wild-type, Scrib Crc /+ and Scrib Crc/Crc fetuses. A duplicate blot was immunostained for β-tubulin. Scrib is detected as multiple isoforms from ~210 kDa (arrows). Scrib Crc/Crc mutants completely lack Scrib protein, with no evidence for stably expressed truncated product, even after extended exposures (right-hand panel). The monoclonal antibody detects a band at ~55 kDa, in both wild-type and Scrib Crc/Crc mutants; no known splice variants are predicted to generate a shorter isoform of this size, and this band seems likely the result of nonspecific antibody binding. (E) Scrib expression in E8.5 wild-type, heterozygous and homozygous embryos from Scrib Crc , Vangl2 Lp and Celsr1 Crsh litters. Scrib is absent from Scrib Crc/Crc embryos. The lower molecular weight bands varied in intensity between protein preparations and could be either degradation products of Scrib protein or alternatively spliced isoforms. (F,G) Celsr1 protein expression in membrane (Mem) and soluble (Sol) fractions of E10.5 embryos (F) and whole-cell lysates of E8.5 embryos (G) from Vangl2 Lp , Scrib Crc and Celsr1 Crsh litters. Celsr1 bands (arrows in F) are detected at ~350 kDa (F,G) and ~80 kDa (F), with no apparent change in any mutants. (H–J) Quantitation of Vangl2 (H), Scrib (I) and Celsr1 (J) protein expression in E8.5 Scrib Crc , Vangl2 Lp and Celsr1 Crsh embryos, normalized to β-tubulin (H) or Fas (I,J) levels. Data are the average of three experiments ± standard errors; expression levels that differ significantly from wild type are indicated with asterisks (* P

    Article Snippet: One Vangl2 Lp /+ ;Scrib Crc /+ fetus exhibited abdominal wall defect with a closed neural tube ( ).

    Techniques: Mutagenesis, Western Blot, Expressing, Incubation, Molecular Weight, Stable Transfection, Binding Assay, Quantitation Assay

    PCP double heterozygotes exhibit a range of phenotypes. Lateral views of embryos at E14.5–E16.5, illustrating the range of phenotypes observed in each cross. (A–C) Vangl2 Lp /+ × Celsr1 Crsh /+ cross (E16.5). Wild-type embryo (A) shows complete neural tube closure, with closed eyelids. Double heterozygotes ( Vangl2 Lp /+ ; Celsr1 Crsh /+ ) have craniorachischisis without (B) or with (C) an abdominal wall defect, in which the liver and intestine protrude from the abdominal cavity (C). Both exhibit failed eyelid closure (B,C). (D–H) Scrib Crc /+ × Vangl2 Lp /+ cross, at E16.5 (D,E,G), E15.5 (F) or E14.5 (H). The Vangl2 Lp /+ ; Scrib Crc /+ double mutants exhibit isolated craniorachischisis (D), craniorachischisis and abdominal wall defect (E), exencephaly and a looped tail (F), closed neural tube but looped tail (G), or complete neural tube closure but abdominal wall defect with protruding liver (H). At E16.5, some double-mutant embryos exhibit failure of eyelid closure (D–F), whereas others have closed eyelids (G). (I–M) Embryos from Scrib Crc /+ × Celsr1 Crsh /+ cross, at E16.5 (I–K) or E15.5 (L,M). Scrib Crc /+ ; Celsr1 Crsh /+ double mutants exhibit isolated craniorachischisis (I), craniorachischisis and abdominal wall defect with protruding abdominal contents (J), lumbosacral spina bifida (K), isolated exencephaly (L), or appear morphologically normal (M). Both open (I,J) and closed (K) eyelids are observed. (N–P) Embryos from Celsr1 Scy /+ × Scrib Crc /+ cross at E16.5 (N,O) or E15.5 (P). Scrib Crc /+ ; Celsr1 Scy /+ double mutants exhibit isolated craniorachischisis (N), or craniorachischisis with abdominal wall defect (O), both with failure of eyelid closure. Other Scrib Crc /+ ; Celsr1 Scy /+ double mutants are overtly normal (P). (Q) Range and proportion of phenotypes observed in different doubly heterozygous mutants, on the C3H/HeH background. Phenotypes are craniorachischisis (black), craniorachischisis and abdominal wall defect (blue), abdominal wall defect without craniorachischisis (yellow), spina bifida (red), exencephaly (green) or no overt defect (orange). Data combined from the present study and from our previous work on Ptk7 chz mutant interactions ( Paudyal et al., 2010 ). Scale bar: 2 mm.

    Journal: Disease Models & Mechanisms

    Article Title: Genetic interactions between planar cell polarity genes cause diverse neural tube defects in mice

    doi: 10.1242/dmm.016758

    Figure Lengend Snippet: PCP double heterozygotes exhibit a range of phenotypes. Lateral views of embryos at E14.5–E16.5, illustrating the range of phenotypes observed in each cross. (A–C) Vangl2 Lp /+ × Celsr1 Crsh /+ cross (E16.5). Wild-type embryo (A) shows complete neural tube closure, with closed eyelids. Double heterozygotes ( Vangl2 Lp /+ ; Celsr1 Crsh /+ ) have craniorachischisis without (B) or with (C) an abdominal wall defect, in which the liver and intestine protrude from the abdominal cavity (C). Both exhibit failed eyelid closure (B,C). (D–H) Scrib Crc /+ × Vangl2 Lp /+ cross, at E16.5 (D,E,G), E15.5 (F) or E14.5 (H). The Vangl2 Lp /+ ; Scrib Crc /+ double mutants exhibit isolated craniorachischisis (D), craniorachischisis and abdominal wall defect (E), exencephaly and a looped tail (F), closed neural tube but looped tail (G), or complete neural tube closure but abdominal wall defect with protruding liver (H). At E16.5, some double-mutant embryos exhibit failure of eyelid closure (D–F), whereas others have closed eyelids (G). (I–M) Embryos from Scrib Crc /+ × Celsr1 Crsh /+ cross, at E16.5 (I–K) or E15.5 (L,M). Scrib Crc /+ ; Celsr1 Crsh /+ double mutants exhibit isolated craniorachischisis (I), craniorachischisis and abdominal wall defect with protruding abdominal contents (J), lumbosacral spina bifida (K), isolated exencephaly (L), or appear morphologically normal (M). Both open (I,J) and closed (K) eyelids are observed. (N–P) Embryos from Celsr1 Scy /+ × Scrib Crc /+ cross at E16.5 (N,O) or E15.5 (P). Scrib Crc /+ ; Celsr1 Scy /+ double mutants exhibit isolated craniorachischisis (N), or craniorachischisis with abdominal wall defect (O), both with failure of eyelid closure. Other Scrib Crc /+ ; Celsr1 Scy /+ double mutants are overtly normal (P). (Q) Range and proportion of phenotypes observed in different doubly heterozygous mutants, on the C3H/HeH background. Phenotypes are craniorachischisis (black), craniorachischisis and abdominal wall defect (blue), abdominal wall defect without craniorachischisis (yellow), spina bifida (red), exencephaly (green) or no overt defect (orange). Data combined from the present study and from our previous work on Ptk7 chz mutant interactions ( Paudyal et al., 2010 ). Scale bar: 2 mm.

    Article Snippet: One Vangl2 Lp /+ ;Scrib Crc /+ fetus exhibited abdominal wall defect with a closed neural tube ( ).

    Techniques: Isolation, Mutagenesis

    Vangl2 Lp , Scrib Crc and Celsr1 Crsh homozygous mutant embryos and doubly heterozygous mutants all exhibit craniorachischisis. Lateral views of whole embryos, showing similar defects in the different genotype combinations. Embryos are either single-mutant homozygotes: (A) Vangl2 Lp/Lp ; (B) Scrib Crc/Crc ; (C) Celsr1 Crsh/Crsh ; or double heterozygotes: (D) Vangl2 Lp /+ ; Celsr1 Crsh /+ ; (E) Scrib Crc /+ ; Celsr1 Crsh /+ ; (F) Vangl2 Lp /+ ; Scrib Crc /+ . In addition to craniorachischisis, defects of ventral body wall closure (B) and eyelid closure (A–E) are present.

    Journal: Disease Models & Mechanisms

    Article Title: Genetic interactions between planar cell polarity genes cause diverse neural tube defects in mice

    doi: 10.1242/dmm.016758

    Figure Lengend Snippet: Vangl2 Lp , Scrib Crc and Celsr1 Crsh homozygous mutant embryos and doubly heterozygous mutants all exhibit craniorachischisis. Lateral views of whole embryos, showing similar defects in the different genotype combinations. Embryos are either single-mutant homozygotes: (A) Vangl2 Lp/Lp ; (B) Scrib Crc/Crc ; (C) Celsr1 Crsh/Crsh ; or double heterozygotes: (D) Vangl2 Lp /+ ; Celsr1 Crsh /+ ; (E) Scrib Crc /+ ; Celsr1 Crsh /+ ; (F) Vangl2 Lp /+ ; Scrib Crc /+ . In addition to craniorachischisis, defects of ventral body wall closure (B) and eyelid closure (A–E) are present.

    Article Snippet: One Vangl2 Lp /+ ;Scrib Crc /+ fetus exhibited abdominal wall defect with a closed neural tube ( ).

    Techniques: Mutagenesis

    Chuzhoi mutants genetically interact with loop-tail and crash but not circletail . (A-C) Intercrosses of chuzhoi with Vangl2 Lp/+ , Scrib Crc/+ and Celsr1 Crsh /+ generated doubly heterozygous fetuses with either no overt phenotypic abnormality (A), craniorachischisis (B) or lumbosacral spina bifida (arrow, C). (D) Graphical representation of the proportion of doubly heterozygous embryos demonstrating each phenotype; the number of double mutants examined is given at the top of each column.

    Journal: BMC Developmental Biology

    Article Title: The novel mouse mutant, chuzhoi, has disruption of Ptk7 protein and exhibits defects in neural tube, heart and lung development and abnormal planar cell polarity in the ear

    doi: 10.1186/1471-213X-10-87

    Figure Lengend Snippet: Chuzhoi mutants genetically interact with loop-tail and crash but not circletail . (A-C) Intercrosses of chuzhoi with Vangl2 Lp/+ , Scrib Crc/+ and Celsr1 Crsh /+ generated doubly heterozygous fetuses with either no overt phenotypic abnormality (A), craniorachischisis (B) or lumbosacral spina bifida (arrow, C). (D) Graphical representation of the proportion of doubly heterozygous embryos demonstrating each phenotype; the number of double mutants examined is given at the top of each column.

    Article Snippet: All four mutants exhibit craniorachischisis and defects in eyelid closure, while a ventral closure defect is observed with high penetrance in Scrib Crc/Crc and lower penetrance in both Vangl2 Lp/Lp and Celsr1 Crsh/Crsh [ , , ].

    Techniques: Generated

    Examination of expression of Vangl2 and Celsr1 in chuzhoi mutants, and Ptk7 in Vangl2 and Celsr1 mutants . (A) Western blot analysis of Ptk7 expression in total cell lysates from E8.5 Scrib Crc/Crc , Vangl2 Lp/Lp , and Celsr1 Crsh / Crsh mutants, compared to heterozygous and wild-type littermates; fatty acid synthase (Fas) was used as a loading control. No obvious difference in Ptk7 expression levels was observed in any of the mutants. (B-D) Western blot analysis of Scrib (B), Vangl2 (C) and Celsr1 (D) expression in total cell lysates from E8.5 chuzhoi mutants, compared to heterozygous and wild-type littermates; fatty acid synthase (Fas) or β-tubulin were used as loading controls. Inclusion of protein extracts from circletail and loop-tail homozygotes were used to help validate anti-Scrib and anti-Vangl2 antibody specificity, respectively. No reproducible difference was observed between chuzhoi mutant and wild-type samples, for expression of either Scrib, Vangl2 or Celsr1. (E-K) Immunofluorescence on transverse sections of E8.0 embryos with antibodies for Ptk7 (E-G), Celsr1 (H, I) and Vangl2 (J, K) in wild-type (E, H, J), Celsr1 Crsh / Crsh (F), Vangl2 Lp/Lp (G) or chuzhoi mutant (I, K) embryos. Ptk7, Celsr1 and Vangl2 are detected around the membrane of neuroepithelial cells, and no clear expression difference was observed in the mutant embryos.

    Journal: BMC Developmental Biology

    Article Title: The novel mouse mutant, chuzhoi, has disruption of Ptk7 protein and exhibits defects in neural tube, heart and lung development and abnormal planar cell polarity in the ear

    doi: 10.1186/1471-213X-10-87

    Figure Lengend Snippet: Examination of expression of Vangl2 and Celsr1 in chuzhoi mutants, and Ptk7 in Vangl2 and Celsr1 mutants . (A) Western blot analysis of Ptk7 expression in total cell lysates from E8.5 Scrib Crc/Crc , Vangl2 Lp/Lp , and Celsr1 Crsh / Crsh mutants, compared to heterozygous and wild-type littermates; fatty acid synthase (Fas) was used as a loading control. No obvious difference in Ptk7 expression levels was observed in any of the mutants. (B-D) Western blot analysis of Scrib (B), Vangl2 (C) and Celsr1 (D) expression in total cell lysates from E8.5 chuzhoi mutants, compared to heterozygous and wild-type littermates; fatty acid synthase (Fas) or β-tubulin were used as loading controls. Inclusion of protein extracts from circletail and loop-tail homozygotes were used to help validate anti-Scrib and anti-Vangl2 antibody specificity, respectively. No reproducible difference was observed between chuzhoi mutant and wild-type samples, for expression of either Scrib, Vangl2 or Celsr1. (E-K) Immunofluorescence on transverse sections of E8.0 embryos with antibodies for Ptk7 (E-G), Celsr1 (H, I) and Vangl2 (J, K) in wild-type (E, H, J), Celsr1 Crsh / Crsh (F), Vangl2 Lp/Lp (G) or chuzhoi mutant (I, K) embryos. Ptk7, Celsr1 and Vangl2 are detected around the membrane of neuroepithelial cells, and no clear expression difference was observed in the mutant embryos.

    Article Snippet: All four mutants exhibit craniorachischisis and defects in eyelid closure, while a ventral closure defect is observed with high penetrance in Scrib Crc/Crc and lower penetrance in both Vangl2 Lp/Lp and Celsr1 Crsh/Crsh [ , , ].

    Techniques: Expressing, Western Blot, Mutagenesis, Immunofluorescence

    Plot of photon energy versus sensitivity for a Capintec CRC-15R dose calibrator. (Reprinted with permission of Capintec Inc. from the CRC-15R Owner's Manual).

    Journal: PLoS ONE

    Article Title: A Recommendation for Revised Dose Calibrator Measurement Procedures for 89Zr and 124I

    doi: 10.1371/journal.pone.0106868

    Figure Lengend Snippet: Plot of photon energy versus sensitivity for a Capintec CRC-15R dose calibrator. (Reprinted with permission of Capintec Inc. from the CRC-15R Owner's Manual).

    Article Snippet: Conclusion Based on this work, we propose a new calibration setting number, 517, to be used on a Capintec CRC-15R dose calibrator when measuring samples of 89 Zr.

    Techniques:

    Activity versus calibration setting number as measured on a Capintec CRC-15R dose calibrator for A) Zr-89 and B) I-124, measured in different geometries. Filled symbols identify the curves corresponding to the measurements with the copper filter; open symbols without the filter. Triangles correspond to the small volume in the 5 mL syringe, circles to the 3 mL volume in the 5 mL syringe and squares to the 10 mL volume in the liquid scintillation vial. Note that for I-124 the filled squares almost completely obscure the filled circles.

    Journal: PLoS ONE

    Article Title: A Recommendation for Revised Dose Calibrator Measurement Procedures for 89Zr and 124I

    doi: 10.1371/journal.pone.0106868

    Figure Lengend Snippet: Activity versus calibration setting number as measured on a Capintec CRC-15R dose calibrator for A) Zr-89 and B) I-124, measured in different geometries. Filled symbols identify the curves corresponding to the measurements with the copper filter; open symbols without the filter. Triangles correspond to the small volume in the 5 mL syringe, circles to the 3 mL volume in the 5 mL syringe and squares to the 10 mL volume in the liquid scintillation vial. Note that for I-124 the filled squares almost completely obscure the filled circles.

    Article Snippet: Conclusion Based on this work, we propose a new calibration setting number, 517, to be used on a Capintec CRC-15R dose calibrator when measuring samples of 89 Zr.

    Techniques: Activity Assay

    Colorectal cancer exosomes induce changes in colonic MSC morphology and growth rate ( A ) Transmission electron microscopy image of SW480 primary CRC derived exosomes (pCRCexo). Arrows indicate different size nanovesicles. Scale bar, 0.2 μM. ( B ) Western blot analysis of sucrose gradient fractions of pCRCexo blotted for the detection of carcinoembryonic antigen (CEA), tsg101 and CD81 (ubiquitous exosome markers) molecules. The density in which exosomes float corresponds to the tsg101- and CD81-positive fractions, and it is comprised between 0.90 and 1.22 g/ml. Total protein extracts of pCRC cells and their purified exosomes (pCRCexo) were loaded as control. M is the weight molecular protein marker; 1–12 correspond to the twelve fractions from sucrose density gradient. ( C ) Phase contrast microscopy (left panels) and scanning electron microscopy (SEM, right panels) images of colonic MSCs (cMSCs) treated for 6 days with pCRCexo. Arrows, asterisks and dotted circle indicate pseudopods, microvilli and vesicles respectively. 20X magnification in contrast microscopy; in SEM scale bar, 20 μM. Inserts represent a 2X magnification. Representative images of two independent experiments are reported. ( D ) Cell proliferation of cMSCs exposed to pCRCexo or cMSCs derived exosomes (cMSCexo) for 6 and 12 days; arrow indicates the exosomes re-feeding at day 9; proliferation was measured at day 6 and 12. ( E ) Cell proliferation of cMSCs incubated with pCRCexo or cMSCexo for 9 days and then replated in fresh medium without exosomes for other 7 days; proliferation was measured at day 9 and 16. ( F ) Cell proliferation of cMSCs or SW480 primary CRC (pCRC) cells incubated with pCRCexo or cMSCexo for 6 days at 1% FCS and pH 6.5 culture conditions. Results in D, E and F are expressed as optical density (mean ± SD, n = at least three independent sets of experiments (** p ≤ 0.005; (*** p ≤ 0.001;), compared to untreated cMSCs (CTR).

    Journal: Oncotarget

    Article Title: Exosomes from human colorectal cancer induce a tumor-like behavior in colonic mesenchymal stromal cells

    doi: 10.18632/oncotarget.10574

    Figure Lengend Snippet: Colorectal cancer exosomes induce changes in colonic MSC morphology and growth rate ( A ) Transmission electron microscopy image of SW480 primary CRC derived exosomes (pCRCexo). Arrows indicate different size nanovesicles. Scale bar, 0.2 μM. ( B ) Western blot analysis of sucrose gradient fractions of pCRCexo blotted for the detection of carcinoembryonic antigen (CEA), tsg101 and CD81 (ubiquitous exosome markers) molecules. The density in which exosomes float corresponds to the tsg101- and CD81-positive fractions, and it is comprised between 0.90 and 1.22 g/ml. Total protein extracts of pCRC cells and their purified exosomes (pCRCexo) were loaded as control. M is the weight molecular protein marker; 1–12 correspond to the twelve fractions from sucrose density gradient. ( C ) Phase contrast microscopy (left panels) and scanning electron microscopy (SEM, right panels) images of colonic MSCs (cMSCs) treated for 6 days with pCRCexo. Arrows, asterisks and dotted circle indicate pseudopods, microvilli and vesicles respectively. 20X magnification in contrast microscopy; in SEM scale bar, 20 μM. Inserts represent a 2X magnification. Representative images of two independent experiments are reported. ( D ) Cell proliferation of cMSCs exposed to pCRCexo or cMSCs derived exosomes (cMSCexo) for 6 and 12 days; arrow indicates the exosomes re-feeding at day 9; proliferation was measured at day 6 and 12. ( E ) Cell proliferation of cMSCs incubated with pCRCexo or cMSCexo for 9 days and then replated in fresh medium without exosomes for other 7 days; proliferation was measured at day 9 and 16. ( F ) Cell proliferation of cMSCs or SW480 primary CRC (pCRC) cells incubated with pCRCexo or cMSCexo for 6 days at 1% FCS and pH 6.5 culture conditions. Results in D, E and F are expressed as optical density (mean ± SD, n = at least three independent sets of experiments (** p ≤ 0.005; (*** p ≤ 0.001;), compared to untreated cMSCs (CTR).

    Article Snippet: Microscopy analyses cMSCs and ccMSCs cells were incubated with or without CRC-exosomes in 1:1000 (exosome μg/MSCs cell number) ratio for 48 or 72 hours.

    Techniques: Transmission Assay, Electron Microscopy, Derivative Assay, Western Blot, Purification, Marker, Microscopy, Incubation

    Colorectal cancer exosomes promote colonic MSC spheroids formation ( A ) Transmission electron microscopy image of SW620 metastatic CRC derived exosomes (mCRCexo). Arrows indicate different size nanovesicles. Scale bar, 0.2 μM. ( B ) Western blot analysis of sucrose gradient fractions of mCRCexo blotted with CEA, tsg101 and CD81 (ubiquitous exosome markers). The density in which CEA + exosomes float, correspond to the tsg101 + and to the CD81 + fractions, and it is comprised between 0.95 and 1.25 g/ml. Total protein extracts of mCRC and mCRCexo were loaded as control. 1–12 correspond to the twelve fractions from sucrose density gradient. ( C ) Measurements of the volume of colonic MSC spheroids (CTR), formed after the pCRCexo or mCRCexo treatments at 48 and 72 h. ( D ) pH measurements of colonic MSCs spheroids supernatants, derived from pCRCexo- or mCRCexo-treated spheroids (at 72 hours) compared to supernatants of untreated ones (CTR). Statistical analysis were performed by unpaired Student t -test (* p ≤ 0.05; ** p ≤ 0.005; *** p ≤ 0.001). ( E ) Confocal laser scanning microscopy of cMSCs spheroids incubated or not (CTR) with pCRCexo and mCRCexo and stained for V-ATPase proton pump molecule, followed by Alexa Fluor ® -488-conjugated secondary Ab (shown in white). Nuclei are reported in blue (DAPI). Scale bar, 40 μM.

    Journal: Oncotarget

    Article Title: Exosomes from human colorectal cancer induce a tumor-like behavior in colonic mesenchymal stromal cells

    doi: 10.18632/oncotarget.10574

    Figure Lengend Snippet: Colorectal cancer exosomes promote colonic MSC spheroids formation ( A ) Transmission electron microscopy image of SW620 metastatic CRC derived exosomes (mCRCexo). Arrows indicate different size nanovesicles. Scale bar, 0.2 μM. ( B ) Western blot analysis of sucrose gradient fractions of mCRCexo blotted with CEA, tsg101 and CD81 (ubiquitous exosome markers). The density in which CEA + exosomes float, correspond to the tsg101 + and to the CD81 + fractions, and it is comprised between 0.95 and 1.25 g/ml. Total protein extracts of mCRC and mCRCexo were loaded as control. 1–12 correspond to the twelve fractions from sucrose density gradient. ( C ) Measurements of the volume of colonic MSC spheroids (CTR), formed after the pCRCexo or mCRCexo treatments at 48 and 72 h. ( D ) pH measurements of colonic MSCs spheroids supernatants, derived from pCRCexo- or mCRCexo-treated spheroids (at 72 hours) compared to supernatants of untreated ones (CTR). Statistical analysis were performed by unpaired Student t -test (* p ≤ 0.05; ** p ≤ 0.005; *** p ≤ 0.001). ( E ) Confocal laser scanning microscopy of cMSCs spheroids incubated or not (CTR) with pCRCexo and mCRCexo and stained for V-ATPase proton pump molecule, followed by Alexa Fluor ® -488-conjugated secondary Ab (shown in white). Nuclei are reported in blue (DAPI). Scale bar, 40 μM.

    Article Snippet: Microscopy analyses cMSCs and ccMSCs cells were incubated with or without CRC-exosomes in 1:1000 (exosome μg/MSCs cell number) ratio for 48 or 72 hours.

    Techniques: Transmission Assay, Electron Microscopy, Derivative Assay, Western Blot, Confocal Laser Scanning Microscopy, Incubation, Staining

    Colorectal cancer exosomes increase the expression of vacuolar H+-ATPase (V-ATPase) and CEA in colonic (c) MSCs and colon cancer (cc) MSCs ( A ) Confocal laser scanning microscopy of 5 cMSC cells optical sections Z-projection taken from the bottom to the edge of cMSCs treated with primary CRC exosomes (pCRCexo) or with metastatic CRC exosomes (mCRCexo) for 72 hours and incubated with primary anti-V-ATPase antibody, followed by Alexa Fluor ® -488-conjugated secondary Ab (shown in white). Nuclei are reported in blue (DAPI). Scale bars, 40 μM. ( B ) Western blot analyses of V-ATPase, CEA and actin proteins, performed in total protein extracts of: pCRCexo or mCRCexo (50 μg), cMSC or ccMSC cells treated with pCRCexo or mCRCexo; Western blot analyses of V-ATPase and actin in Cytoskeletal/Membrane and Cytosol fractions; untreated cells (CTR). Results of densitometry analyses are reported as fold-increase in the expression of each molecule, related to actin loading.

    Journal: Oncotarget

    Article Title: Exosomes from human colorectal cancer induce a tumor-like behavior in colonic mesenchymal stromal cells

    doi: 10.18632/oncotarget.10574

    Figure Lengend Snippet: Colorectal cancer exosomes increase the expression of vacuolar H+-ATPase (V-ATPase) and CEA in colonic (c) MSCs and colon cancer (cc) MSCs ( A ) Confocal laser scanning microscopy of 5 cMSC cells optical sections Z-projection taken from the bottom to the edge of cMSCs treated with primary CRC exosomes (pCRCexo) or with metastatic CRC exosomes (mCRCexo) for 72 hours and incubated with primary anti-V-ATPase antibody, followed by Alexa Fluor ® -488-conjugated secondary Ab (shown in white). Nuclei are reported in blue (DAPI). Scale bars, 40 μM. ( B ) Western blot analyses of V-ATPase, CEA and actin proteins, performed in total protein extracts of: pCRCexo or mCRCexo (50 μg), cMSC or ccMSC cells treated with pCRCexo or mCRCexo; Western blot analyses of V-ATPase and actin in Cytoskeletal/Membrane and Cytosol fractions; untreated cells (CTR). Results of densitometry analyses are reported as fold-increase in the expression of each molecule, related to actin loading.

    Article Snippet: Microscopy analyses cMSCs and ccMSCs cells were incubated with or without CRC-exosomes in 1:1000 (exosome μg/MSCs cell number) ratio for 48 or 72 hours.

    Techniques: Expressing, Confocal Laser Scanning Microscopy, Incubation, Western Blot