作者: Takehisa Hashimoto , Yoshio Tokuchi , Moriaki Hayashi , Yasuhito Kobayashi , Kazunori Nishida
DOI: 10.1016/S0002-9440(10)64851-1
关键词: Carcinoma 、 Tobacco smoke 、 Carcinogen 、 Mutation frequency 、 Mutation 、 Biology 、 Adenocarcinoma 、 CpG site 、 Cell type 、 Cancer research 、 Pathology
摘要: Human lung adenocarcinomas are only relatively weakly associated with tobacco smoke, and other etiological factors need to be clarified. These may also vary the histopathology. Because p53 mutation status (frequency spectrum) of a carcinoma can provide clues causative agents, we subclassified 113 into five cell types: hobnail, columnar/cuboidal, mixed, polygonal, goblet (54, 23, 18, 13, 5, respectively) investigated relationships mutations smoking history. In hobnail type, low mutational frequency (37%) high proportion transitions (65%), especially G:C A:T at CpG dinucleotides (45%) spontaneous mutations, were found weak relation smoke. contrast, (70%) higher transversions (50%), T:A (44%) on nontranscribed DNA strand, caused by exogenous carcinogenic agents like observed for columnar as squamous carcinomas. results indicate that two major subtypes adenocarcinoma exist, one probably possibly due mutations. For prevention adenocarcinomas, in addition stopping smoking, elucidation endogenous mechanisms is important.