Activation of Src kinase in primary colorectal carcinoma: An indicator of poor clinical prognosis

Allgayer, Heike; Boyd, Douglas D.; Heiss, Markus M.; Abdalla, Eddie K.; Curley, Steven A.; Gallick, Gary E.

doi:10.1002/cncr.10221

Cited by 254Cancer Mechanisms and TherapyProtein Kinase Regulation and GTPase SignalingColorectal Cancer Treatments and Studies

Activation of Src kinase in primary colorectal carcinoma: An indicator of poor clinical prognosis

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Allgayer, Heike, Boyd, Douglas D., Heiss, Markus M., Abdalla, Eddie K., Curley, Steven A., Gallick, Gary E.·2002·Cancer

DOI 10.1002/cncr.10221

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Abstract

BACKGROUND: The specific activity of the non‐receptor protein tyrosine kinase, Src, is increased in the majority of colon and rectal adenocarcinomas compared to normal mucosa. However, the prognostic significance of this difference is unknown. The objective of the current study was to determine if Src activity is a marker for poor clinical prognosis in colon carcinoma patients. As Src activation leads to expression of urokinase/plasminogen activator receptor (u‐PAR), expression of Src and u‐PAR were correlated with patient survival. METHODS: Tumors and adjacent normal colonic mucosae from 45 patients with colorectal carcinoma were screened for Src activity by the immune complex kinase assay. Expression of u‐PAR was determined by enzyme linked immunoabsorbent assay. The primary tumor‐to‐normal mucosa ratios of activity were compared following classification and regression tree (CART) analysis to determine the prognostic significance of elevated specific Src activity. Expression of u‐PAR was correlated with Src activity. RESULTS: By CART analysis, Src activity in tumors elevated more than twofold over normal mucosa was significant. Increased Src activity significantly correlated with Dukes stage, pT and pN classification, and increased u‐PAR levels (P < 0.001). Kaplan Meier analysis showed a significant association between elevated Src activity and shorter overall survival of all patients (P = 0.0004) and of Dukes Stage A‐C patients (P = 0.0037). In patients who underwent curative resection, a significant correlation with a decreased disease‐free survival rate was found (P < 0.0001). Multivariate analysis revealed that elevated Src activity was a prognostic parameter independent of M classification (P = 0.0125, relative risk 3.54, 95% confidence interval 1.31 – 9.76). CONCLUSIONS: Src activity is an independent indicator of poor clinical prognosis in all stages of human colon carcinoma. These data suggest that Src‐specific inhibitors may have a therapeutic role in inhibiting tumor progression and metastasis, and that measurement of Src activity may aid in selection of early stage patients for adjuvant therapy. Cancer 2002;94:344–51. © 2002 American Cancer Society.

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Src family kinase activity has been reported as a marker of poor clinical prognosis.
“In addition to SFK activity and CRC progression, SFK activity has been reported as a marker of poor clinical prognosis (Aligayer et al., 2002).”
From Dasatinib sensitizes KRAS mutant colorectal tumors to cetuximab (2011) · cites this paper as Aligayer et al., 2002
Aberrant SRC activation is associated with a more aggressive phenotype and worse prognosis in colorectal cancer patients.
“Moreover, aberrant SRC activation has been associated with a more aggressive phenotype and a worse prognosis in CRC patients [27, 28].”
From Co-targeting SRC overcomes resistance to BRAF inhibitors in colorectal cancer (2025) · cites this paper as [28]
Aberrant SRC activation has been associated with a more aggressive phenotype and a worse prognosis in CRC patients.
“Aberrant SRC activation has been associated with a more aggressive phenotype and a worse prognosis in CRC patients [27, 28, 39].”
From Co-targeting SRC overcomes resistance to BRAF inhibitors in colorectal cancer (2025) · cites this paper as [28]
Increased c-Src levels correlate with worse patient survival.
“and increased c-Src levels correlate with worse patient survival [13].”
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 [13]
High c-src activity correlates with dismal survival and is an independent aggravating prognostic factor in CRC.
“c-src high activity was proved to be correlated with dismal survival, emerging as an independent aggravating prognostic factor.14”
From The molecular rationale of Src inhibition in colorectal carcinomas (2014) · cites this paper as [14]

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The Role of Src in Colon Cancer and Its Therapeutic Implications
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Identification of potential biomarkers for measuring inhibition of Src kinase activity in colon cancer cells following treatment with dasatinib
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Progress towards the development of SH2 domain inhibitors
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Novel Mechanistic Insights into Ectodomain Shedding of EGFR Ligands Amphiregulin and TGF-α: Impact on Gastrointestinal Cancers Driven by Secondary Bile Acids
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Src Family Kinases: Potential Targets for the Treatment of Human Cancer and Leukemia
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The role of Src in solid and hematologic malignancies
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Targeted Inhibition of Src Kinase Signaling Attenuates Pancreatic Tumorigenesis
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Chemopreventive Activity of Plant Flavonoid Isorhamnetin in Colorectal Cancer Is Mediated by Oncogenic Src and β-Catenin
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Src family kinase activity is required for signal tranducer and activator of transcription 3 and focal adhesion kinase phosphorylation and vascular endothelial growth factor signaling in vivo and for anchorage-dependent and -independent growth of human tumor cells.
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A phase II trial of the Src-kinase inhibitor AZD0530 in patients with advanced castration-resistant prostate cancer: a California Cancer Consortium study
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Antiangiogenic and Antitumor Effects of Src Inhibition in Ovarian Carcinoma
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Overcoming resistance to molecularly targeted anticancer therapies: Rational drug combinations based on EGFR and MAPK inhibition for solid tumours and haematologic malignancies
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Simultaneous inhibition of focal adhesion kinase and SRC enhances detachment and apoptosis in colon cancer cell lines.
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Regulation of Src Family Kinases during Colorectal Cancer Development and Its Clinical Implications
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Drosophila C-Terminal Src Kinase Negatively Regulates Organ Growth and Cell Proliferation through Inhibition of the Src, Jun N-Terminal Kinase, and STAT Pathways
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The sensors and regulators of cell–matrix surveillance in anoikis resistance of tumors
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Update on Targets and Novel Treatment Options for High-Grade Osteosarcoma and Chondrosarcoma
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Targeting Signal Transduction Pathways in Colorectal Cancer—More Than Skin Deep
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AP23846, a novel and highly potent Src family kinase inhibitor, reduces vascular endothelial growth factor and interleukin-8 expression in human solid tumor cell lines and abrogates downstream angiogenic processes
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Bosutinib: A review of preclinical studies in chronic myelogenous leukaemia
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Src/FAK-mediated regulation of E-cadherin as a mechanism for controlling collective cell movement
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Src as the link between inflammation and cancer
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Phosphorylation of BCKDK of BCAA catabolism at Y246 by Src promotes metastasis of colorectal cancer
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Dual Inhibition of EGFR and c-Src by Cetuximab and Dasatinib Combined with FOLFOX Chemotherapy in Patients with Metastatic Colorectal Cancer
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Design strategies, structure activity relationship and mechanistic insights for purines as kinase inhibitors
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Recurrent Genomic Alterations With Impact on Survival in Colorectal Cancer Identified by Genome-Wide Array Comparative Genomic Hybridization
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Src activation in melanoma and Src inhibitors as therapeutic agents in melanoma
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Src kinases in chondrosarcoma chemoresistance and migration: dasatinib sensitises to doxorubicin in TP53 mutant cells
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The E3 ubiquitin ligase TRIM7 suppressed hepatocellular carcinoma progression by directly targeting Src protein
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Exosomal miR-940 maintains SRC-mediated oncogenic activity in cancer cells: a possible role for exosomal disposal of tumor suppressor miRNAs
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The relationship between tumour site, clinicopathological characteristics and cancer‐specific survival in patients undergoing surgery for colorectal cancer
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HMGCS2 enhances invasion and metastasis via direct interaction with PPARα to activate Src signaling in colorectal cancer and oral cancer
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Targeting Src signaling in metastatic bone disease
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Src as a therapeutic target in anti-hormone/anti-growth factor-resistant breast cancer
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The guanine nucleotide exchange factor Arhgef5 plays crucial roles in Src-induced podosome formation
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A Conformation Selective Mode of Inhibiting SRC Improves Drug Efficacy and Tolerability
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Src, chemoresistance and epithelial to mesenchymal transition: are they related?
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Cell growth, global phosphotyrosine elevation, and c-Met phosphorylation through Src family kinases in colorectal cancer cells
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Srcasm Inhibits Fyn-Induced Cutaneous Carcinogenesis with Modulation of Notch1 and p53
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miR-205 is frequently downregulated in prostate cancer and acts as a tumor suppressor by inhibiting tumor growth
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Phase II study of saracatinib (AZD0530) in patients with previously treated metastatic colorectal cancer
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Dasatinib in previously treated metastatic colorectal cancer: a phase II trial of the University of Chicago Phase II Consortium
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Receptor-type protein tyrosine phosphatase κ directly dephosphorylates CD133 and regulates downstream AKT activation
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Activation of Abl Family Kinases in Solid Tumors
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Analysis of Specific Transcriptional Regulators as Early Predictors of Independent Prognostic Relevance in Resected Colorectal Cancer
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Diacylglycerol kinase α promotes 3D cancer cell growth and limits drug sensitivity through functional interaction with Src
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Degradation of Epidermal Growth Factor Receptor Mediates Dasatinib-Induced Apoptosis in Head and Neck Squamous Cell Carcinoma Cells
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HBx protein induces EMT through c-Src activation in SMMC-7721 hepatoma cell line
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The molecular rationale of Src inhibition in colorectal carcinomas
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Dynamic Change of Polarity in Primary Cultured Spheroids of Human Colorectal Adenocarcinoma and Its Role in Metastasis
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Natural compound Oblongifolin C confers gemcitabine resistance in pancreatic cancer by downregulating Src/MAPK/ERK pathways
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Suppression of lung cancer progression by isoliquiritigenin through its metabolite 2, 4, 2’, 4’-Tetrahydroxychalcone
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Quantification of β-Catenin Signaling Components in Colon Cancer Cell Lines, Tissue Sections, and Microdissected Tumor Cells using Reaction Monitoring Mass Spectrometry
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Reversion-induced LIM interaction with Src reveals a novel Src inactivation cycle
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Potential Molecular Mechanism for c-Src Kinase-mediated Regulation of Intestinal Cell Migration
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Cigarette Smoke Activates the Proto-Oncogene c-Src to Promote Airway Inflammation and Lung Tissue Destruction
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CD24 Induces Expression of the Oncomir miR-21 via Src, and CD24 and Src Are Both Post-Transcriptionally Downregulated by the Tumor Suppressor miR-34a
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Docking, 3D-QSAR studies and in silico ADME prediction on c-Src tyrosine kinase inhibitors
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Basis and Importance of SRC as a Target in Cancer
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Divergent Roles of c-Src in Controlling Platelet-derived Growth Factor-dependent Signaling in Fibroblasts
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Phosphorylated c-Src in the nucleus is associated with improved patient outcome in ER-positive breast cancer
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ICAM-1 promotes cancer progression by regulating SRC activity as an adapter protein in colorectal cancer
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Cooperative expression of junctional adhesion molecule‐C and ‐B supports growth and invasion of glioma
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c-Src activation promotes nasopharyngeal carcinoma metastasis by inducing the epithelial-mesenchymal transition via PI3K/Akt signaling pathway: a new and promising target for NPC
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Src Induces Urokinase Receptor Gene Expression and Invasion/Intravasation via Activator Protein-1/p-c-Jun in Colorectal Cancer
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Combination of an Src Kinase Inhibitor with a Novel Pharmacological Antagonist of the Urokinase Receptor Diminishes in Vitro Colon Cancer Invasiveness
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Phosphorylation of TOPK at Y74, Y272 by Src increases the stability of TOPK and promotes tumorigenesis of colon
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Kinome Array Profiling of Patient-Derived Pancreatic Ductal Adenocarcinoma Identifies Differentially Active Protein Tyrosine Kinases
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Mechanisms of resistance to EGFR inhibitors
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Prognostic relevance of Src activation in stage II-III colon cancer
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Activación de Src quinasa: implicaciones predictivas y pronósticas en pacientes con cáncer de colon.
Martínez Pérez, J. E. (2018) · idUS (Universidad de Sevilla)
Expression of hypoxia-inducible factor-1α in oligodendrogliomas
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Contribution of plasminogen activators and their inhibitors to the survival prognosis of patients with Dukes' stage B and C colorectal cancer
Ganesh, S., Sier, C. F. M., HEERDING, M., van Krieken, J., Griffioen, G. G., Welvaart, K., van de Velde, C., Verheijen, J. H., Lamers, C. B. H. W., & Verspaget, H. W. (1997) · British Journal of Cancer · doi:10.1038/bjc.1997.306 · Cited by 40 · see citing works

Authors: Allgayer, H., Boyd, D. D., Heiss, M. M., Abdalla, E. K., Curley, S. A., & Gallick, G. E.
Affiliations: Ludwig-Maximilians-Universität München (DE)
The University of Texas MD Anderson Cancer Center (US)
Corresponding author: Gallick, Gary E.
ORCID: Allgayer, Heike
Boyd, Douglas D.
Heiss, Markus M.
Curley, Steven A.
Venue: Cancer
Publisher: Wiley
Published: 2002-01-15
Volume: 94
Issue: 2
Pages: 344-351
ISSN: 0008-543X (ISSN-L)
1097-0142
DOI: 10.1002/cncr.10221
OpenAlex: W1532635242
Cited by: 251
References: 51
Citations by year: 2025: 3 · 2024: 3 · 2023: 1 · 2022: 4 · 2021: 7 · 2020: 9 · 2019: 11 · 2018: 7 · 2017: 9 · 2016: 11 · 2015: 14 · 2014: 16 · 2013: 16 · 2012: 13
FWCI: 5.73
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 3 d)
Locations: Cancer (publishedVersion)
PubMed (publishedVersion)
Funders: Gillson Longenbaugh Foundation
Deutsche Krebshilfe
National Institutes of Health (5r01ca065527-07)
National Cancer Institute (CA65527, CA69926, CA53617, CA 58311)
National Institute of Dental and Craniofacial Research (DE10845, R01DE010845)
Topics: Health Sciences › Medicine › Pathology and Forensic Medicine › Cancer Mechanisms and Therapy
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
Keywords: Src kinase, colorectal cancer, prognostic factors, urokinase-type plasminogen activator receptor, non-receptor tyrosine kinase, overall survival, disease-free survival, Dukes stage, adjuvant therapy selection, Src kinase inhibitor, metastasis
MeSH terms: CSK Tyrosine-Protein Kinase, Adenocarcinoma, Adult, Aged, Aged, 80 and over, Enzyme Activation, Female, Humans, Male, Middle Aged, Mucous Membrane, Protein-Tyrosine Kinases, Receptors, Cell Surface, Colorectal Neoplasms, Survival Rate, src Homology Domains, src-Family Kinases, Receptors, Urokinase Plasminogen Activator

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Activation of Src kinase in primary colorectal carcinoma: An indicator of poor clinical prognosis

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