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Increased c-kit (CD117) expression in malignant mammary phyllodes tumors
Gary M K Tse1, Thomas C Putti, Philip C W Lui
1Department of Anatomical and Cellular Pathology, Prince of Wales Hospital, Chinese University of Hong Kong, Hong Kong. garytse@cuhk.edu.hk
Summary
Mammary phyllodes tumors show increasing c-kit (CD117) expression with higher malignancy. This suggests c-kit involvement in phyllodes tumor development and potential use of targeted therapies like STI571 (Gleevec).
Area of Science:
- Oncology
- Pathology
- Molecular Biology
Background:
- Mammary phyllodes tumors are rare stromal neoplasms with varying recurrence and metastasis potential based on malignancy grade.
- c-kit (CD117) is a proto-oncogene encoding a tyrosine kinase receptor, crucial in gastrointestinal stromal tumors (GIST) management.
Purpose of the Study:
- To investigate c-kit expression in mammary phyllodes tumors.
- To correlate c-kit expression with tumor malignancy and histological features.
- To explore potential therapeutic implications of c-kit targeting.
Main Methods:
- Immunohistochemistry was used to assess c-kit expression in 179 mammary phyllodes tumors (101 benign, 50 borderline, 28 malignant).
- Staining results were compared against histological criteria including malignancy grade, stromal cellularity, mitotic activity, nuclear pleomorphism, and stromal overgrowth.
Main Results:
- Overall c-kit expression was observed in 29% of tumors.
- Positive c-kit staining rates were 17% in benign, 24% in borderline, and 46% in malignant phyllodes tumors.
- A significant increase in c-kit expression correlated with increasing tumor malignancy (chi2=13.844, P=0.001).
Conclusions:
- c-kit receptor tyrosine kinase is implicated in the pathogenesis of mammary phyllodes tumors.
- The escalating expression of c-kit with malignancy suggests its role in tumor progression.
- Targeted therapies like STI571 (Gleevec) may offer a potential treatment avenue for malignant phyllodes tumors.