Related Experiment Video
Updated: Jul 14, 2026
Transgenic Rodent Assay for Quantifying Male Germ Cell Mutant Frequency
Published on: August 6, 2014
Kit expression in male germ cell tumors
M Nikolaou1, C Valavanis, G Aravantinos
1Second Department of Internal Medicine-Propaedeutic, Attikon Hospital, Athens University Medical School, Greece. m_nikolaou@panafonet.gr
Objective:
KIT functions as the receptor for stem cell factor (SCF) and this interaction is essential for regulation of proliferation and survival, particularly for germ cells since it regulates oogenesis, folliculogenesis and spermatogenesis. Up-regulation of KIT signalling has been associated with oncogenic transformation in cells expressing the molecule. Our objective was to investigate the expression of KIT in germ cell tumor patients and correlate it with the patients' clinical characteristics.
Patients And Methods:
One hundred and seventy-three archival blocks of formalin fixed, paraffin-embedded tumor samples from histologically confirmed germ cell tumor (GCT) patients were included in the study. Immunohistochemical staining for KIT was performed and the percentage of positive cells was calculated by an independent pathologist. KIT expression was considered as positive if > 10% of tumor cells displayed membranous or cytoplasmic staining.
Results:
Sixty-one patients with seminomatous (49 pure, 11 anaplastic, 1 spermocytic) and 112 with non-seminomatous GCTs (36 malignant teratoma undifferentiated (MTU), 15 malignant teratoma trophoblastic (MTT), 20 malignant teratoma intermediate (MTI), 35 malignant teratoma combined (MTC) and six others) were identified. Among pure seminoma patients, 38 (77.5%) revealed a positive staining for KIT, while only two out of eleven (18.2%) anaplastic seminoma patients were identified as positive. This difference was statistically significant (p < 0.001). Among 35 patients with an MTC, 48.6% had a positive KIT staining while only two of the remaining patients with a non-seminomatous GCT had a positive staining. Although KIT was strongly correlated with seminomatous histology (p < 0.001), it failed to correlate with stage (p = 0.19) or treatment response (p = 0.11) in these patients. Overall, four (one seminoma, three MTC) out of 22 chemoresistant patients showed a positive staining for KIT.
Conclusion:
KIT is expressed in the majority of seminomas and in seminomatous components of the combined tumors, but only in a minority of anaplastic seminomas and rarely in non-seminomatous GCTs. The recent development of tyrosine kinase inhibitors may offer a possibility of cure in chemoresistant patients overexpressing KIT.
Insights
KIT receptor tyrosine kinase is highly expressed in most seminomas and combined tumors, but rarely in non-seminomatous germ cell tumors. This finding suggests potential therapeutic strategies for chemoresistant germ cell tumors overexpressing KIT.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- KIT receptor tyrosine kinase (RTK) signaling is crucial for germ cell development and survival.
- Aberrant KIT signaling is implicated in oncogenesis, particularly in cells expressing the receptor.
- Understanding KIT expression in germ cell tumors (GCTs) is vital for potential targeted therapies.
Purpose of the Study:
- To investigate KIT expression in patients with germ cell tumors (GCTs).
- To correlate KIT expression with clinical characteristics of GCT patients.
- To explore the potential of KIT as a therapeutic target in GCTs.
Main Methods:
- Analysis of 173 formalin-fixed, paraffin-embedded GCT samples using immunohistochemistry for KIT.
- Quantification of KIT-positive cells by an independent pathologist, with positivity defined as >10% membranous or cytoplasmic staining.
- Correlation of KIT expression with GCT histology, stage, and treatment response.
Main Results:
- KIT expression was detected in 77.5% of pure seminomas and 48.6% of malignant teratoma combined (MTC) GCTs.
- KIT positivity was significantly higher in seminomas compared to anaplastic seminomas (p < 0.001).
- KIT expression strongly correlated with seminomatous histology but not with tumor stage or treatment response.
Conclusions:
- KIT is predominantly expressed in seminomas and seminomatous components of mixed GCTs.
- KIT expression is limited in anaplastic seminomas and rare in non-seminomatous GCTs.
- Targeting KIT with tyrosine kinase inhibitors may offer a therapeutic avenue for chemoresistant GCTs with KIT overexpression.
