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Increase in activity and level of pp60c-src in progressive stages of human colorectal cancer.
Open accessAbstract
Activation of the tyrosine kinase of the c-src gene product, pp60c-src, has been shown to occur in nearly every primary colorectal carcinoma, and is found as early as in polyps of high malignant potential. However, no studies have addressed potential pp60c-src changes which occur during progression. To examine this question, we have studied kinase activity and protein levels in 7 colonic polyps, 19 primary lesions, and 19 liver metastases relative to normal colonic mucosa. Significant increases in tyrosine kinase activity were seen as early as in colonic polyps of high malignant potential. Further increases were observed in activity and level in primary tumors. However, the greatest increases in activity and protein levels were observed in liver metastases. Additionally, six metastatic lesions were obtained in which synchronous primary tumor was resected. In each of these liver metastases, pp60c-src activity and level were significantly increased relative to the corresponding primary tumor, as well as to normal colonic mucosa. Our results demonstrate that progression of colon primary tumors to liver metastases correlates with increased pp60c-src kinase activity and protein level.
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“Moreover, the SRC activation signature score was significantly associated with metastasis and primary tumor stage I-IV progression (Fig. 2g,h), in agreement with previous studies in CRC [37–40].”
From An integrative gene expression signature analysis identifies CMS4 KRAS-mutated colorectal cancers sensitive to combined MEK and SRC targeted therapy (2022) · cites this paper as [40]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“Talamonti et al reported increased activity and expression of SFKs in progressive stages of human colorectal cancer, suggesting that colon cancer progression may be dependent on increased SFK protein level and subsequent activity (Talamonti et al., 1993).”
From Dasatinib sensitizes KRAS mutant colorectal tumors to cetuximab (2011) · cites this paper as Talamonti et al., 1993
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“Higher expression and activity of SRC has been documented in primary colon tumors compared with benign polyps or non-transformed colonic mucosa, and increased activity is observed in progressive stages of CRC [23–26].”
From Co-targeting SRC overcomes resistance to BRAF inhibitors in colorectal cancer (2025) · cites this paper as [25]
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“However, c-Src seems to experience a robust increase in expression and activity in CRC liver metastases compared with metastases derived from other tumors types [11, 12]”
From Dasatinib, a Src inhibitor, sensitizes liver metastatic colorectal carcinoma to oxaliplatin in tumors with high levels of phospho-Src (2016) · cites this paper as [12]
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“C-src, though, seems to have a robust increase regarding expression and activity in CRC liver metastases compared to those derived from other tumors types.3,11,13”
From The molecular rationale of Src inhibition in colorectal carcinomas (2014) · cites this paper as [11]
In the citing paper
“In CRC cell lines and primary tumors, both c-src kinase activity and protein expression levels have been found elevated compared either to normal colonic mucosal cells and fibroblasts or normal adjacent tissue, respectively.3,10,11”
From The molecular rationale of Src inhibition in colorectal carcinomas (2014) · cites this paper as [11]
In the citing paper
“Increased specific activity and expression levels have been detected in colonic polyps of high malignant potential and severe dysplasia.11,12”
From The molecular rationale of Src inhibition in colorectal carcinomas (2014) · cites this paper as [11]
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Mutation of the SRC Gene in Endometrial Carcinoma
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Metadata
- Authors
- Talamonti, M. S., Roh, M. S., Curley, S. A., & Gallick, G. E.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- ORCID
- Talamonti, M S
- Venue
- Journal of Clinical Investigation
- Published
- 1993-01-01
- Volume
- 91
- Issue
- 1
- Pages
- 53-60
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC329994
- OpenAlex
- W2030565228
- Cited by
- 399
- References
- 45
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 4 · 2023: 11 · 2022: 6 · 2021: 6 · 2020: 6 · 2019: 6 · 2018: 6 · 2017: 14 · 2016: 8 · 2015: 13 · 2014: 11 · 2013: 17 · 2012: 24
- FWCI
- 2.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ca053167-06)
- National Cancer Institute (CA09599, CA53167, T32CA009599)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Mechanisms and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
- Keywords
- Src kinase, tyrosine kinase activity, colorectal cancer, tumor progression, colonic polyps, liver metastasis, synchronous primary tumors, oncogene activation
- MeSH terms
- Adenocarcinoma, Adenoma, Antigen-Antibody Complex, Colonic Neoplasms, Colonic Polyps, Humans, Intestinal Mucosa, Liver Neoplasms, Neoplasm Metastasis, Neoplasm Staging, Phosphopyruvate Hydratase, Phosphorylation, Protein Kinases, Protein-Tyrosine Kinases, Rectal Neoplasms, Reference Values, Immunoblotting, Proto-Oncogene Proteins pp60(c-src)
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