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Updated: Aug 8, 2026

Heterotypic Three-dimensional In Vitro Modeling of Stromal-Epithelial Interactions During Ovarian Cancer Initiation and Progression
Published on: August 28, 2012
Expression of c-ABL, c-KIT, and platelet-derived growth factor receptor-beta in ovarian serous carcinoma and normal
Rosemarie E Schmandt1, Russell Broaddus, Karen H Lu
1Department of Gynecologic Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA. rschand@mdanderson.org
Background:
Tyrosine kinases, such as c-KIT, c-ABL, and platelet-derived growth factor-beta (PDGFR-beta), are important regulators of cell growth. Highly potent and selective inhibitors of tyrosine kinases are being investigated as alternatives to standard chemotherapy. One such inhibitor, imatinib mesylate, is being used to treat gastrointestinal stromal tumors and chronic myelogenous leukemia. Ovarian carcinomas frequently develop resistance to conventional chemotherapeutic agents. Immunohistochemical expression of c-ABL, PDGFR-beta, and c-KIT was evaluated in ovarian carcinomas to determine whether treatment with imatinib mesylate might be feasible.
Methods:
The expression of c-ABL, c-KIT, and PDGFR-beta in tumors was evaluated by immunohistochemical analysis of 52 ovarian serous carcinomas, including 21 low-grade (well differentiated) and 31 high-grade (poorly differentiated) tumors. Fourteen normal ovaries were also evaluated.
Results:
In normal ovarian surface epithelium, c-ABL was expressed universally. PDGFR-beta was expressed in the majority (93%) of samples of normal ovarian epithelium, whereas the c-KIT protein was undetectable in normal ovarian surface epithelium. Overall, c-ABL was expressed in 71% of serous carcinomas. c-ABL was expressed more frequently in the low-grade serous carcinomas (81%) compared with the high-grade serous carcinomas (65%). PDGFR-beta expression was observed in 81% of serous carcinomas overall and was observed more frequently in higher-grade tumors. c-KIT immunohistochemical staining was absent in low-grade tumors but was present in 26% of high-grade serous carcinomas.
Conclusions:
The majority of ovarian serous carcinomas express one or more of the kinases targeted by the tyrosine kinase inhibitor, imatinib mesylate, suggesting the potential usefulness of this drug in the treatment of ovarian carcinoma.
Insights
Ovarian carcinomas often resist chemotherapy. This study found most ovarian cancers express targets of imatinib mesylate, a tyrosine kinase inhibitor, suggesting its potential as a novel ovarian cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Drug Discovery
Background:
- Tyrosine kinases (c-KIT, c-ABL, PDGFR-beta) regulate cell growth and are targets for novel cancer therapies.
- Imatinib mesylate, a tyrosine kinase inhibitor, is effective against certain cancers but its utility in ovarian cancer is unexplored.
- Ovarian carcinomas frequently exhibit resistance to conventional chemotherapy.
Purpose of the Study:
- To evaluate the expression of c-ABL, c-KIT, and PDGFR-beta in ovarian carcinomas.
- To determine the feasibility of using imatinib mesylate for ovarian cancer treatment based on target kinase expression.
Main Methods:
- Immunohistochemical analysis was performed on 52 ovarian serous carcinomas (21 low-grade, 31 high-grade) and 14 normal ovaries.
- Expression levels of c-ABL, c-KIT, and PDGFR-beta were quantified in tumor and normal tissues.
Main Results:
- c-ABL was expressed in 71% of serous carcinomas, more frequently in low-grade tumors.
- PDGFR-beta was expressed in 81% of serous carcinomas, with higher expression in high-grade tumors.
- c-KIT was present in 26% of high-grade serous carcinomas but absent in low-grade tumors.
Conclusions:
- The majority of ovarian serous carcinomas express at least one kinase targeted by imatinib mesylate.
- These findings suggest imatinib mesylate holds potential as a therapeutic agent for ovarian carcinoma.
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