Imatinib in the Treatment of Colorectal Cancer—Molecular Targets, Preclinical Evidence and Clinical Limitations
- 1Doctoral School of Exact and Natural Sciences, University of Lodz, 90-237 Lodz, Poland
- 2Department of Molecular Biotechnology and Genetics, Faculty of Biology and Environmental Protection, University of Lodz, 90-237 Lodz, Poland
Abstract
Colorectal cancer (CRC) remains a major therapeutic challenge, despite substantial advances in molecular characterization and targeted treatment. The heterogeneity of CRC and the development of treatment resistance highlight the need for novel therapeutic strategies and rational drug repurposing approaches. Imatinib, a well-established tyrosine kinase inhibitor, exerts pharmacological activity beyond ABL1/ABL2, targeting KIT, PDGFR, DDR1, and potentially LCK, which may contribute to distinct mechanisms of CRC progression. This review examines the emerging evidence on the potential role of imatinib in CRC, including its effects on tumor-cell proliferation and survival, invasion and metastasis, extracellular-matrix remodeling, tumor–stroma interactions, treatment resistance, and immune regulation. Preclinical studies indicate promising antitumor activity in selected molecular and biological contexts, particularly in KIT-positive tumors, PDGFR-rich stroma, mesenchymal/CMS4 tumors, and models characterized by aberrant DDR1 signaling. However, clinical evidence remains limited and does not currently support imatinib as a standard treatment for unselected CRC. Biomarker-guided patient selection, rational combination strategies, and tumor microenvironment-directed approaches may enhance its therapeutic potential. Further well-designed clinical studies are required to determine whether these biological effects can translate into meaningful clinical benefit.
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BibTeX
@article{wanke2026imatinib,
title = {{Imatinib in the Treatment of Colorectal Cancer—Molecular Targets, Preclinical Evidence and Clinical Limitations}},
author = {Katarzyna Wanke and Mateusz Kciuk and Beata Marciniak and Renata Kontek},
journal = {Molecules},
year = {2026},
month = nov,
doi = {10.3390/molecules31213933},
url = {https://www.mdpi.com/1420-3049/31/21/3933},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Imatinib in the Treatment of Colorectal Cancer—Molecular Targets, Preclinical Evidence and Clinical Limitations
AU - Katarzyna Wanke
AU - Mateusz Kciuk
AU - Beata Marciniak
AU - Renata Kontek
PY - 2026
DA - 2026/11/01
JO - Molecules
DO - 10.3390/molecules31213933
UR - https://www.mdpi.com/1420-3049/31/21/3933
AB - Colorectal cancer (CRC) remains a major therapeutic challenge, despite substantial advances in molecular characterization and targeted treatment. The heterogeneity of CRC and the development of treatment resistance highlight the need for novel therapeutic strategies and rational drug repurposing approaches. Imatinib, a well-established tyrosine kinase inhibitor, exerts pharmacological activity beyond ABL1/ABL2, targeting KIT, PDGFR, DDR1, and potentially LCK, which may contribute to distinct mechanisms of CRC progression. This review examines the emerging evidence on the potential role of imatinib in CRC, including its effects on tumor-cell proliferation and survival, invasion and metastasis, extracellular-matrix remodeling, tumor–stroma interactions, treatment resistance, and immune regulation. Preclinical studies indicate promising antitumor activity in selected molecular and biological contexts, particularly in KIT-positive tumors, PDGFR-rich stroma, mesenchymal/CMS4 tumors, and models characterized by aberrant DDR1 signaling. However, clinical evidence remains limited and does not currently support imatinib as a standard treatment for unselected CRC. Biomarker-guided patient selection, rational combination strategies, and tumor microenvironment-directed approaches may enhance its therapeutic potential. Further well-designed clinical studies are required to determine whether these biological effects can translate into meaningful clinical benefit.
SN - 1420-3049
ER -