Cancer surveys最新文献_第10页

Oncogenic role of heterotrimeric G proteins. 异源三聚体G蛋白的致癌作用。

Cancer surveys Pub Date : 1996-01-01

L Vallar

引用次数: 0

CDKN2 mutations in melanoma. 黑色素瘤中的CDKN2突变。

Cancer surveys Pub Date : 1996-01-01

N C Dracopoli, J W Fountain

引用次数: 0

Neoplastic transformation: the contrasting stability of human and mouse cells. 肿瘤转化:人和小鼠细胞的稳定性对比。

Cancer surveys Pub Date : 1996-01-01

R Holliday

{"title":"Neoplastic transformation: the contrasting stability of human and mouse cells.","authors":"R Holliday","doi":"","DOIUrl":"","url":null,"abstract":"The probability of a mouse cell becoming fully transformed in vivo or in vitro is enormously greater than that of a human cell. The number of events in tumour progression is similar in rodent and human cells, and it is unlikely that the difference in neoplastic transformation frequency can be explained on the basis of gene mutation in oncogenes and tumour suppressor genes. Instead, it is proposed that mouse cells may be (a) more subject to destabilization of the karyotype, (b) have less efficient check point cell cycle controls after DNA is damaged and/or (c) have less stringent epigenetic controls of gene activity, based on DNA methylation. Much evidence exists that mouse or rat cells are less efficient in DNA repair, maintenance of DNA methylation and other aspects of DNA metabolism. These relate to the difference in longevity in these and other mammalian species. Ageing is likely to be due to the failure of cell and tissue maintenance. Long lived species invest more in various somatic maintenance mechanisms than do short lived ones, and this includes protection against neoplastic transformation. The future study of the basis of the difference between human and mouse or rat cells in resistance to transformation is likely to yield important insights into the sequential events in tumour progression.","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"28 ","pages":"103-15"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19938609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mutation in resting cells: the role of endogenous DNA damage. 静息细胞中的突变:内源性DNA损伤的作用。

Cancer surveys Pub Date : 1996-01-01

B A Bridges

{"title":"Mutation in resting cells: the role of endogenous DNA damage.","authors":"B A Bridges","doi":"","DOIUrl":"","url":null,"abstract":"In E coli, new spontaneous mutations can arise in bacteria that are non-dividing and in which there is little or no DNA synthesis. These mutations are almost invariably those that enable the cell to resume growth, a phenomenon that has been termed directed or adaptive mutation. Evidence is accumulating from studies with DNA repair deficient strains that damage produced by endogenous mutagens may be an important source of such mutations. A DNA lesion that can miscode can explain the apparent adaptive behaviour since if a \"mutant\" RNA transcript confers sufficient advantage that the cell is triggered into a cycling state, the ensuing round of DNA replication will be likely to fix the mutation by means of a DNA miscoding event. The most important lesion in this respect appears to be 8-oxoG, which can pair equally well with adenine or cytosine and so give rise to G to T transversions. It is responsible for almost half the G to T transversions arising in non-growing repair proficient bacteria. Alkylations contribute to the production of both transitions and transversions but only those at A:T base pairs are important in repair proficient bacteria. There is also a report of a lesion susceptible to UvrA,B,C dependent excision repair, but whether it is important in bacteria possessing excision repair has not been addressed. Data on mammalian cells are almost non-existent, but there is evidence that point mutations can occur in vivo in postmitotic neurons. The underlying assumption that there is little or no DNA synthesis in non-dividing bacteria has been challenged by recent data suggesting that there may be extensive cryptic DNA turnover.","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"28 ","pages":"155-67"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19938612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Regulation of genomic instability in preneoplastic cells. 肿瘤前细胞基因组不稳定性的调控。

Cancer surveys Pub Date : 1996-01-01

T D Tlsty

引用次数: 0

Animal models of melanoma. 黑色素瘤的动物模型。

Cancer surveys Pub Date : 1996-01-01

D F Kusewitt, R D Ley

引用次数: 0

Relevance of in vitro melanocytic cell studies to the understanding of melanoma. 体外黑色素细胞研究与黑色素瘤认识的相关性。

Cancer surveys Pub Date : 1996-01-01

C Linge