dysgerminoma/tyrosine

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c-KIT codon 816 mutation in a recurrent and metastatic dysgerminoma of a 14-year-old girl: case study.

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Dysgerminomas are rare female germ-cell tumors that correspond histologically and immunohistochemically to seminomas. Analogous to seminomas, most dysgerminomas respond very well to cisplatin- or carboplatin-based chemotherapy and to radiotherapy. KIT tyrosine kinase is crucial for normal germ-cell

Gonadoblastoma: evidence for a stepwise progression to dysgerminoma in a dysgenetic ovary.

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Gonadoblastomas are neoplasms of dysgenetic gonads which may undergo regression or become overgrown by malignant germ cell tumors (mGCTs). Since little is known about their relationship to normal gonadal development and mGCTs, we studied the phenotype and antigenic profile of gonadoblastomas in

Expression of CD117 (c-kit) receptor in dysgerminoma of the ovary: diagnostic and therapeutic implications.

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The proto-oncogene c-kit encodes a tyrosine kinase receptor, c-kit (CD117), which has been implicated in the development of a number of human malignancies. While the preferential expression of this protein has been well documented in testicular seminomas, there is little data concerning its

Coexpression of the c-kit receptor and the stem cell factor in gynecological tumors.

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The protooncogene c-kit encodes a transmembrane receptor-type tyrosine kinase which belongs to the beta-PDGER/CSF-1 receptor tyrosine kinase family. The interaction between c-kit receptor and its corresponding ligand, stem cell factor (SCF), has been suggested to be involved in embryogenesis as well

Current controversies in the management of germ cell ovarian tumours.

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OBJECTIVE Fewer than 70 new cases of malignant ovarian germ cell tumours (MOGCTs) are seen each year in the UK. Because of their rarity, no randomized trials have been reported and many of the advances in management have arisen from adopting practices developed for managing male germ cell tumours

KIT mutations are common in testicular seminomas.

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Expression of KIT tyrosine kinase is critical for normal germ cell development and is observed in the majority of seminomas. Activating mutations in KIT are common in gastrointestinal stromal tumors and mastocytosis. In this study we examined the frequency and spectrum of KIT mutations in 54

Expression and mutation of c-Kit in intracranial germ cell tumors: A single-centre retrospective study of 30 cases in China.

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Although primary central nervous system (CNS) germ cell tumors (GCTs) are one of the most treatable types of malignant brain tumor, a subset of patients remain resistant to standard chemotherapy. Gain-of-function mutations of the c-Kit gene, and KIT protein expression, have been observed in a number

The proto-oncogene c-kit is expressed in leiomyosarcomas of the uterus.

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OBJECTIVE The proto-oncogene c-kit encodes for a 145-kDa transmembrane tyrosine kinase receptor. Interaction with its ligand, stem cell factor, is essential in the development of hematopoietic stem cells, mast cells, gametocytes, melanocytes, and interstitial cells of Cajal. C-kit expression has

A variant c-KIT mutation, D816H, fundamental to the sequential development of an ovarian mixed germ cell tumor and systemic mastocytosis with chronic myelomonocytic leukemia.

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An activating point mutation of the c-KIT tyrosine kinase receptor gene, D816H, has been described in germ cell tumors (GCTs). We report an adolescent diagnosed with an ovarian mixed GCT and systemic mastocytosis with chronic myelomonocytic leukemia (SM-CMML). The teratoma and dysgerminoma differed

Activating c-kit gene mutations in human germ cell tumors.

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The c-kit gene encodes a tyrosine kinase receptor (KIT) that is required in normal spermatogenesis and is expressed in seminomas and dysgerminomas, a subset of human germ cell tumors (GCTs). To determine whether activating mutations of the c-kit gene occur in GCTs, primary tissue samples of 33

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