Genetics of cancer predisposition.
Genetics of cancer predisposition.
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癌症易感性的遗传学。
作者：
M. Hansen;W. Cavenee
对癌症的正式遗传学分析产生了几种矛盾的情况：（a）尽管家族性病例已被很好地描述，但大多数疾病都是零星的孤立病例;（B）即使在那些遗传后出现的病例中，肿瘤本质上也是局灶性的，而不是影响特定组织的所有细胞;（c）在这些家族中，表现出高度恶性倾向的个体似乎处于广泛但特定的癌症亚群的风险中。在这里，我们有来自家庭，流行病学的证据，细胞遗传学和分子遗传学研究，支持癌症是一种根深蒂固的遗传疾病的概念，并有助于解释上述看似矛盾的现象。我们回顾了分子生物学技术解决这些问题的方法和结果，并推测了遗传病变的性质对癌症的易感性。
Formal genetic analysis of cancer engenders several paradox ical situations: (a) although familial instances are well de scribed, most disease occurs as sporadic isolated cases; (b) even in those cases arising subsequent to inheritance, tumors are focal in nature rather than affecting all cells of a particular tissue; (c) individuals in those families who exhibit high pro pensities to malignancy appear to be at risk for broad, but specific, subsets of cancer. Here we have consolidated evidence from familial, epidemiológica!, cytogenetic, and molecular ge netic studies which support the notion that cancer is a pro foundly genetic disease and which help explain the aforemen tioned seeming paradoxes. We review approaches and results addressing these questions afforded by molecular biological technologies and speculate on the nature of genetic lesions responsible for predisposition to cancer.
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影响因子：
11.2
作者：
E. Srivatsan;W. Benedict;E. Stanbridge
通讯作者：
E. Srivatsan;W. Benedict;E. Stanbridge
DOI：
10.1073/pnas.82.18.6216
发表时间：
1985-01-01
影响因子：
11.1
作者：
HANSEN, MF;KOUFOS, A;CAVENEE, WK
通讯作者：
CAVENEE, WK
影响因子：
158.5
作者：
CAVENEE, WK;MURPHREE, AL;NORDENSKJOLD, M
通讯作者：
NORDENSKJOLD, M
影响因子：
56.9
作者：
YUNIS, JJ
通讯作者：
YUNIS, JJ
影响因子：
56.9
作者：
SPARKES, RS;MURPHREE, AL;BENEDICT, WF
通讯作者：
BENEDICT, WF