Arch Gynecol Obstet (2012) 286:197–200 DOI 10.1007/s00404-012-2276-8 123 GYNECOLOGIC ONCOLOGY c-Kit proto-oncogene expression in endometrial hyperplasia and endometrial cancer Ercan Yilmaz · Onder Celik · Yavuz Simsek · Ilgin Turkcuoglu · Ebru Celik · Mehmet Gül · Seyma Hascalik · Engin Aydin Received: 27 September 2011 / Accepted: 23 February 2012 / Published online: 6 March 2012  Springer-Verlag 2012 Abstract Purpose To evaluate the expression of c-kit (CD117) in endometrial hyperplasia and endometrial cancer. Methods Expression of c-kit in 10 normal endometrium, 18 simple endometrial hyperplasia, 16 complex endome- trial hyperplasia (10 cases with atypia and 6 cases without atypia), and 6 endometrial cancer were investigated by immunohistochemistry. Results c-Kit expression decreased as the lesion pro- gressed to endometrial cancer. Immunostaining was mostly focal and weak in the normal endometrium and was mostly diVuse and strong in the simple and complex endometrial hyperplasia. Conclusions Simple and complex hyperplastic endome- trial tissues express diVuse cytoplasmic staining for c-kit and the expression decreases with the progression of the lesion. Keywords Endometrial hyperplasia · Endometrium · c-Kit · CD117 · Endometrial cancer Introduction Endometrial hyperplasia is related to prolonged estrogen stimulation in association with a diminished to absent pro- gestational activity. The World Health Organization, based on previous studies by Kurman et al., has accepted a classi- Wcation that includes four diagnostic categories: simple hyperplasia, complex hyperplasia, simple atypical hyper- plasia, and complex atypical hyperplasia [1]. Hyperplastic glands may retain some of their architectural abnormalities, but the glandular cells show attenuation [2]. The proto- oncogene c-kit is the cellular homologue of the oncogene v-Kit of HZ4 feline sarcoma virus. It is located on chromo- some 4 (4q11–12) in the human genome [3]. c-Kit encodes a 145-kDa transmembrane tyrosine kinase receptor (CD117), the ligand of which is stem cell factor (SCF) [4, 5]. c-Kit receptor-ligand system has been shown to have an important role in the embryonic development of migratory cell lineages, including primordial germ cells [4]. It has been suggested that c-kit, together with its ligand SCF, may also contribute to tumor development via stimulation of growth in an autocrine and/or paracrine fashion [5]. Such interactions between c-kit and SCF have been shown to have a mitogenic eVect in various tumors including ovary, breast carcinomas, and small cell carcinomas of the lung [6, 7]. Expression of the KIT receptor has also been reported in normal tissues of the human female genital tract, including the uterus [5] and the ovaries [8]. Several gynecological malignancies, such as endometrial [5] and ovarian cancer appear to produce the KIT receptor. Because of its role in regulating cell diVerentiation and tissue morphogenesis, the loss of c-kit expression may be a required step in malignant transformation and tumor progression in endometrial hyperplasia. With this study, we sought to evaluate c-kit E. Yilmaz (&) · O. Celik · Y. Simsek · I. Turkcuoglu · E. Celik Department of Obstetrics and Gynecology, Inonu University School of Medicine, 44100 Malatya, Turkey e-mail: ercanyilmazgyn@yahoo.com M. Gül Department of Histology and Embryology, Inonu University School of Medicine, Malatya, Turkey S. Hascalik Division of Obstetrics and Gynecology, Park Hospital, Malatya, Turkey E. Aydin Department of Pathology, Inonu University School of Medicine, Malatya, Turkey