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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
{"title":"Relevance of in vitro melanocytic cell studies to the understanding of melanoma.","authors":"C Linge","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"26 ","pages":"71-87"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19756114","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
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
{"title":"CDKN2 mutations in melanoma.","authors":"N C Dracopoli, J W Fountain","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"26 ","pages":"115-32"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19756116","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
The role of atypical mole syndrome and cutaneous naevi in the development of melanoma. 非典型痣综合征和皮肤痣在黑色素瘤发展中的作用。
Cancer surveys Pub Date : 1996-01-01
D Easton
{"title":"The role of atypical mole syndrome and cutaneous naevi in the development of melanoma.","authors":"D Easton","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"26 ","pages":"237-49"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19756123","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
The development of therapeutic vaccines of the management of malignant melanoma. 恶性黑色素瘤治疗性疫苗的开发。
Cancer surveys Pub Date : 1996-01-01
A G Dalgleish, B E Souberbielle
{"title":"The development of therapeutic vaccines of the management of malignant melanoma.","authors":"A G Dalgleish, B E Souberbielle","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"26 ","pages":"289-319"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19756126","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
Treatment of melanoma in-transit metastases confined to the limb. 转移到肢体的黑色素瘤的治疗。
Cancer surveys Pub Date : 1996-01-01
A M Eggermont
{"title":"Treatment of melanoma in-transit metastases confined to the limb.","authors":"A M Eggermont","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"26 ","pages":"335-49"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19756128","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
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":"<p><p>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.</p>","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":"<p><p>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.</p>","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
{"title":"Regulation of genomic instability in preneoplastic cells.","authors":"T D Tlsty","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Recent insights into the action of TP53 have uncovered signal transduction pathways that maintain genomic integrity. TP53 was the first gene demonstrated to be involved in these pathways, but mutation of several other genes can have a similar terminal effect. The characterization of these signal transduction pathways should provide further targets for the improvement of neoplastic diagnosis as well as therapeutic efficacy.</p>","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"28 ","pages":"217-24"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19938615","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
The role of papillomaviruses in human non-melanoma skin cancer. 乳头瘤病毒在人类非黑色素瘤皮肤癌中的作用。
Cancer surveys Pub Date : 1996-01-01
J M McGregor, C M Proby
{"title":"The role of papillomaviruses in human non-melanoma skin cancer.","authors":"J M McGregor,&nbsp;C M Proby","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"26 ","pages":"219-36"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19756122","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
Serine/threonine kinase receptors: mediators of transforming growth factor beta family signals. 丝氨酸/苏氨酸激酶受体:转化生长因子β家族信号的介质。
Cancer surveys Pub Date : 1996-01-01
J Massagué, F Weis-Garcia
{"title":"Serine/threonine kinase receptors: mediators of transforming growth factor beta family signals.","authors":"J Massagué,&nbsp;F Weis-Garcia","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>TGF beta represents the largest and most versatile cytokine family known in metazoans. The recent identification of transmembrane serine/threonine kinases as TGF beta family receptors represents a major milestone towards understanding how these factors elicit their varied responses. Genetic and biochemical evidence suggests a general model for the mechanism of activation of these receptors. In this model, the ligand acts as an adaptor, bringing a primary receptor kinase in contact with a second kinase, which becomes phosphorylated and thereby competent to propagate the signal to downstream components. Such a kinase cascade on the membrane defines a new variation in signal transduction. Although many details of this mechanism remain to be clarified, its combinatorial capacity may explain the multifunctional nature of its ligands. Several key genes have been identified whose regulation by these signals mediates cellular responses such as cell cycle arrest. This field is advancing at a fast pace, and the identity of components that carry the receptor signals to these genes should soon be unveiled. It is expected that these advances, as they unfold, will in turn clarify the role of miscreant TGF beta signalling in human diseases, cancer included.</p>","PeriodicalId":77062,"journal":{"name":"Cancer surveys","volume":"27 ","pages":"41-64"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19873573","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
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