{"title":"肿瘤抑制因子对恶性黑色素瘤生长的控制。","authors":"A Coleman, G Robertson, T G Lugo","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The development of malignant melanoma is accompanied by an accumulation of genetic damage that is evident within tumor cells at both cytogenetic and molecular levels, and mutations at several gene loci are thought to contribute to malignant progression. Some of these loci are known oncogenes and tumor suppressor genes; others remain to be identified, although their chromosomal locations have been determined. Gene mapping studies indicate the presence of melanoma tumor suppressor genes on chromosomes 1, 6, and 9. The presence of a tumor suppressor gene on a particular chromosome can be demonstrated by transfer of an intact, normal copy of the chromosome into tumor cells. We have used this approach to investigate the mechanisms by which chromosome 6 suppresses the growth and tumorigenicity of human malignant melanoma cells.</p>","PeriodicalId":21112,"journal":{"name":"Receptor","volume":"5 1","pages":"9-19"},"PeriodicalIF":0.0000,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Growth control by tumor suppressors in malignant melanoma.\",\"authors\":\"A Coleman, G Robertson, T G Lugo\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The development of malignant melanoma is accompanied by an accumulation of genetic damage that is evident within tumor cells at both cytogenetic and molecular levels, and mutations at several gene loci are thought to contribute to malignant progression. Some of these loci are known oncogenes and tumor suppressor genes; others remain to be identified, although their chromosomal locations have been determined. Gene mapping studies indicate the presence of melanoma tumor suppressor genes on chromosomes 1, 6, and 9. The presence of a tumor suppressor gene on a particular chromosome can be demonstrated by transfer of an intact, normal copy of the chromosome into tumor cells. We have used this approach to investigate the mechanisms by which chromosome 6 suppresses the growth and tumorigenicity of human malignant melanoma cells.</p>\",\"PeriodicalId\":21112,\"journal\":{\"name\":\"Receptor\",\"volume\":\"5 1\",\"pages\":\"9-19\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1995-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Receptor\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Receptor","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Growth control by tumor suppressors in malignant melanoma.
The development of malignant melanoma is accompanied by an accumulation of genetic damage that is evident within tumor cells at both cytogenetic and molecular levels, and mutations at several gene loci are thought to contribute to malignant progression. Some of these loci are known oncogenes and tumor suppressor genes; others remain to be identified, although their chromosomal locations have been determined. Gene mapping studies indicate the presence of melanoma tumor suppressor genes on chromosomes 1, 6, and 9. The presence of a tumor suppressor gene on a particular chromosome can be demonstrated by transfer of an intact, normal copy of the chromosome into tumor cells. We have used this approach to investigate the mechanisms by which chromosome 6 suppresses the growth and tumorigenicity of human malignant melanoma cells.