Ito T, Seyama T, Hayashi Y, Dohi K, Akiyama M
Dept. of Radiobiology, Hiroshima City Asa Hospital.
Nihon Rinsho. 1994 Apr;52(4):1069-74.
In thyroid there is a wide variety of tumors varying from slowly growing differentiated adenocarcinomas to rapidly proliferating undifferentiated carcinomas. There has been some histopathological evidence that the undifferentiated thyroid carcinomas are derived from differentiated carcinomas. Moreover, it is suspected that some genetic events might be associated with such changes. To identify these genetic events that must be involved in thyroid tumor progression, we initially investigated p53 gene alterations in 10 papillary adenocarcinomas, 4 follicular adenocarcinomas, and 8 undifferentiated carcinomas. Base substitutional mutations in exons 5 to 8 and loss of heterozygosity (LOH) of the p53 gene were not detected in papillary or follicular adenocarcinomas. However, 7 of 8 undifferentiated carcinomasa were carrying base substitutional mutations, and LOH was detected in 3 of 5 informative cases. These results strongly suggest that the mutated p53 gene plays a crucial role in de-differentiation during the progression of thyroid tumors.
甲状腺中存在各种各样的肿瘤，从生长缓慢的分化型腺癌到迅速增殖的未分化癌。有一些组织病理学证据表明，未分化甲状腺癌源自分化型癌。此外，有人怀疑某些基因事件可能与这种变化有关。为了确定这些必然参与甲状腺肿瘤进展的基因事件，我们首先研究了10例乳头状腺癌、4例滤泡状腺癌和8例未分化癌中的p53基因改变。在乳头状或滤泡状腺癌中未检测到第5至8外显子的碱基替换突变以及p53基因的杂合性缺失（LOH）。然而，8例未分化癌中有7例携带碱基替换突变，并且在5例信息充分的病例中有3例检测到了LOH。这些结果有力地表明，突变的p53基因在甲状腺肿瘤进展过程中的去分化过程中起着关键作用。
