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[Familial occurrence of thyroid tumors]
K Kameyama1, H Takami, Y Hosoda
1Department of Pathology, Keio University School of Medicine.
Nihon Rinsho. Japanese Journal of Clinical Medicine
|November 1, 1995
Summary
Familial medullary thyroid carcinoma (FMTC) and multiple endocrine neoplasia (MEN) are linked to RET proto-oncogene mutations. Understanding RET
Area of Science:
- Oncology
- Genetics
- Endocrinology
Background:
- Familial medullary thyroid carcinoma (FMTC) was clinically recognized in 1986 as distinct from multiple endocrine neoplasia (MEN).
- The RET proto-oncogene was identified in 1985 and mapped to chromosome 10, showing high expression in medullary thyroid carcinoma (MTC).
- RET mutations were identified in MEN2A and FMTC patients in 1993, with numerous mutations clarified since.
Purpose of the Study:
- To investigate the normal function of the RET proto-oncogene.
- To elucidate the mechanisms by which RET mutations contribute to tumor formation in MEN and FMTC.
Main Methods:
- Review of historical clinical and genetic studies.
- Analysis of RET proto-oncogene identification and mapping.
- Examination of mutation identification in MEN2A and FMTC.
Main Results:
- The RET proto-oncogene is implicated in the development of MTC, MEN2A, and FMTC.
- Numerous RET mutations have been identified in patients with these conditions.
- Ongoing research focuses on RET's normal function and its role in tumorigenesis.
Conclusions:
- RET mutations are a key factor in the pathogenesis of FMTC and MEN syndromes.
- Further research is crucial to fully understand RET's function and its link to thyroid cancer.