Open AccessInactivation of the p53 Gene Is not Required for Tumorigenesis of Medullary Thyroid Carcinoma or Pheochromocytoma
Author(s) -
Yana Ikuo,
Nakamura Tsutomu,
Shin Eisei,
Karakawa Katsu,
Kurahashi Hiroki,
Kurita Yoshihiro,
Kobayashi Tetsuro,
Mori Takesada,
Nishisho Isamu,
Takai Shinichiro
Publication year - 1992
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1992.tb02730.x
Subject(s) - pheochromocytoma , carcinogenesis , thyroid carcinoma , transversion , biology , gene , polymerase chain reaction , medullary carcinoma , multiple endocrine neoplasia type 2 , cancer research , microbiology and biotechnology , pathology , thyroid , genetics , medicine , endocrinology , mutation , germline mutation
A polymerase chain reaction (PCR)‐mediated RNase protection analysis was performed to detect subtle genetic alterations of p53 in medullary thyroid carcinoma (MTC) and pheochromocytoma. None of the 30 pheochromocytomas showed abnormal RNase protection patterns. Only one of 32 MTCs showed an abnormal pattern, and subsequent DNA sequencing of the PCR product revealed that it had a G to C transversion in codon 49 that resulted in a change from aspartic acid to histidine. However, this was a sporadic MTC with no specific clinicopathological characteristics. On the basis of a previous report that genes on chromosome 17p were not deleted in MTCs and were relatively infrequently deleted in pheochromocytomas, our results suggest that the p53 gene is not involved in tumorigenesis of MTC or pheochromocytoma.