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Genetic alterations in human gastric cancer. 人类胃癌的基因改变。
Cancer cells (Cold Spring Harbor, N.Y. : 1989) Pub Date : 1991-02-01
S Hirohashi, T Sugimura
{"title":"Genetic alterations in human gastric cancer.","authors":"S Hirohashi,&nbsp;T Sugimura","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Most types of human tumors display a consistent set of genetic alterations that are thought to play a role in tumor development and progression. In the case of gastric carcinomas, consistent genetic changes have been difficult to identify because (1) the tumor DNA samples are often heavily contaminated with DNA from normal stromal cells and (2) the tumors are heterogeneous in origin. However, with the recent application of more refined molecular genetic techniques, it has become clear that gastric carcinomas display some of the same genetic alterations observed in other common carcinomas. These changes include point mutation of the ras oncogene and the p53 tumor suppressor gene, gene amplification, and chromosomal loss of heterozygosity.</p>","PeriodicalId":77504,"journal":{"name":"Cancer cells (Cold Spring Harbor, N.Y. : 1989)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13186132","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
Targets for trans-activation by myb. myb反式激活的目标。
Cancer cells (Cold Spring Harbor, N.Y. : 1989) Pub Date : 1991-01-01
T J Gonda
{"title":"Targets for trans-activation by myb.","authors":"T J Gonda","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77504,"journal":{"name":"Cancer cells (Cold Spring Harbor, N.Y. : 1989)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13182238","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
Chemical carcinogenesis--reflections on the development of a field. 化学致癌——一个领域发展的思考。
Cancer cells (Cold Spring Harbor, N.Y. : 1989) Pub Date : 1991-01-01
P F Swann
{"title":"Chemical carcinogenesis--reflections on the development of a field.","authors":"P F Swann","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77504,"journal":{"name":"Cancer cells (Cold Spring Harbor, N.Y. : 1989)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13182239","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
Is there a common pathway mediating growth inhibition by TGF-beta and the retinoblastoma gene product? 是否有一个共同的途径介导tgf - β和视网膜母细胞瘤基因产物的生长抑制?
Cancer cells (Cold Spring Harbor, N.Y. : 1989) Pub Date : 1991-01-01
A B Roberts, S J Kim, M B Sporn
{"title":"Is there a common pathway mediating growth inhibition by TGF-beta and the retinoblastoma gene product?","authors":"A B Roberts,&nbsp;S J Kim,&nbsp;M B Sporn","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77504,"journal":{"name":"Cancer cells (Cold Spring Harbor, N.Y. : 1989)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13182237","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
Longwave ultraviolet radiation and promotion of skin cancer. 长波紫外线辐射与促进皮肤癌。
Cancer cells (Cold Spring Harbor, N.Y. : 1989) Pub Date : 1991-01-01
M S Matsui, V A DeLeo
{"title":"Longwave ultraviolet radiation and promotion of skin cancer.","authors":"M S Matsui,&nbsp;V A DeLeo","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Exposure to solar ultraviolet (UV) radiation is recognized as an important cause of skin cancer. The carcinogenic effects of UV radiation have been attributed almost entirely to wavelengths in the mid-range (UVB, 290-320 nm). However, the development of potent UVB sunscreens has allowed individuals to increase the length of time that they spend sunbathing and, as a consequence, they may be exposed to massive doses of longwave UV radiation (UVA, 320-400 nm). There is now much evidence to suggest that UVA acts to promote tumors that have been initiated by UVB. This review considers possible mechanisms by which UVA promotes tumorigenesis. Evidence is presented which suggests that UVA acts through modulation of protein kinase C.</p>","PeriodicalId":77504,"journal":{"name":"Cancer cells (Cold Spring Harbor, N.Y. : 1989)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13182240","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
Inflammation and oxidative stress in carcinogenesis. 癌变中的炎症和氧化应激。
Cancer cells (Cold Spring Harbor, N.Y. : 1989) Pub Date : 1991-01-01
P A Cerutti, B F Trump
{"title":"Inflammation and oxidative stress in carcinogenesis.","authors":"P A Cerutti,&nbsp;B F Trump","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Oxidants, which are generated by multiple pathways in mammalian organisms, may be natural carcinogens and contribute to several stages of malignant transformation. Active oxygen released by inflammatory phagocytes and more stable \"clastogenic factors\" can induce mutations and chromosomal aberrations in neighboring target cells. These oxidant-induced DNA sequence changes, though rare, may affect the activities of proto-oncogenes and suppressor genes. In addition, oxidants can promote cell growth. Like polypeptide growth factors they activate kinases. Because they break DNA, they also induce the poly ADP-ribosylation of chromosomal proteins. Both phosphorylation and poly ADP-ribosylation appear to participate in the transcriptional induction of the growth-related proto-oncogene c-fos. Growth stimulation by oxidants is modulated by the cellular antioxidant defenses. Maximal growth promotion is observed when cells are protected from excessive toxicity but still maintain a sufficient oxidant signal for the induction of growth-competence genes.</p>","PeriodicalId":77504,"journal":{"name":"Cancer cells (Cold Spring Harbor, N.Y. : 1989)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13182236","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
DNA topoisomerases in chemotherapy. 化疗中的DNA拓扑异构酶。
Cancer cells (Cold Spring Harbor, N.Y. : 1989) Pub Date : 1991-01-01
S Kaufmann
{"title":"DNA topoisomerases in chemotherapy.","authors":"S Kaufmann","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77504,"journal":{"name":"Cancer cells (Cold Spring Harbor, N.Y. : 1989)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13011621","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 influence of immunosenescence on tumor growth and spread: lessons from animal models. 免疫衰老对肿瘤生长和扩散的影响:来自动物模型的启示。
Cancer cells (Cold Spring Harbor, N.Y. : 1989) Pub Date : 1991-01-01
M J Volk, W B Ershler
{"title":"The influence of immunosenescence on tumor growth and spread: lessons from animal models.","authors":"M J Volk,&nbsp;W B Ershler","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>There has been a long-standing clinical impression that tumor grow more slowly in elderly patients, but, because of confounding variables, this impression has been difficult to substantiate by epidemiologic data. Animal models offer a way to explore the relationship between host age and tumor growth under more controlled conditions. Our studies with murine B16 melanoma xenografts, discussed here, show that tumor growth and spread is in fact reduced in older animals and suggest that age-associated changes in immune function may be partially responsible.</p>","PeriodicalId":77504,"journal":{"name":"Cancer cells (Cold Spring Harbor, N.Y. : 1989)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12989300","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
Transforming growth factor-alpha: an oncodevelopmental growth factor. 转化生长因子:一种肿瘤发育生长因子。
Cancer cells (Cold Spring Harbor, N.Y. : 1989) Pub Date : 1990-12-01
D S Salomon, N Kim, T Saeki, F Ciardiello
{"title":"Transforming growth factor-alpha: an oncodevelopmental growth factor.","authors":"D S Salomon,&nbsp;N Kim,&nbsp;T Saeki,&nbsp;F Ciardiello","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Transforming growth factor-alpha (TGF-alpha) is a 50-amino-acid mitogenic peptide that is structurally and, in some cases, functionally related to members of the epidermal growth factor (EGF) family of peptides. TGF-alpha is initially synthesized as a high-molecular-weight, glycosylated, membrane-associated precursor of approximately 160 amino acids. The low-molecular-weight TGF-alpha peptide as well as the precursor are biologically active in a number of systems and can function as transforming proteins when overexpressed. TGF-alpha binds to and activates the EGF receptor, and TGF-alpha and the EGF receptor are coexpressed in a number of human and rodent tumors and tumor cell lines--which suggests that TGF-alpha can function as an autocrine or paracrine growth factor. TGF-alpha is transiently expressed in some fetal and adjacent maternal tissues during development and is also expressed in a number of adult tissues; this pattern of expression suggests that the growth factor is involved in several distinct physiological functions.</p>","PeriodicalId":77504,"journal":{"name":"Cancer cells (Cold Spring Harbor, N.Y. : 1989)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1990-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13243804","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 Raf-1 kinase as a transducer of mitogenic signals. 作为有丝分裂信号转换器的Raf-1激酶。
Cancer cells (Cold Spring Harbor, N.Y. : 1989) Pub Date : 1990-12-01
D K Morrison
{"title":"The Raf-1 kinase as a transducer of mitogenic signals.","authors":"D K Morrison","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cells respond to proliferative signals generated by growth factors and oncogenes with a complex array of biochemical and physiological events, culminating in DNA synthesis and cell division. One of the molecules thought to be critical for the transmission and amplification of mitogenic signals from the cell surface to the nucleus is the proto-oncogene product Raf-1. Raf-1 is a serine-threonine kinase that is itself phosphorylated in response to mitogenic stimulation. The phosphorylation state of Raf-1 appears to modulate its kinase activity. Experiments linking Raf-1 to other characterized components of the signal transduction machinery are reviewed here.</p>","PeriodicalId":77504,"journal":{"name":"Cancer cells (Cold Spring Harbor, N.Y. : 1989)","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1990-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13305444","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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