摘要:

Cancer develops when one or more cells begin to grow uncontrollably, presumably as a result of alterations in the highly regulated processes of normal cell division. These changes may result from germline or somatic mutations in genes that control normal cell proliferation, resulting in oncogenes. Oncogenes-originally defined as viral genes that transformed mammalian host cells-code for proteins with diverse functions. Antioncogenes, or tumor-suppressor genes, code for proteins acting as brakes in the cell cycle. Mutations in or deletions of these genes release the brakes. An overview of cellular signaling pathways, how they may be altered in cancers, and recently reported clinical implications of abnormal expression of some oncogenes and tumor-suppressor genes will be presented here.

ISSN:1040-8746    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

Angiogenesis is a key step in tumor growth and metastasis. Many angiogenic factors have been described, including vascular endothelial growth factor, basic fibroblast growth factor, and thymidine phosphorylase. More recently, a number of naturally occurring inhibitors of angiogenesis, including throm-bospondin and angiostatin, have also been identified. The control of angiogenesis by inhibitors regulated by suppressor oncogenes or produced by tumors has emerged as an important mechanism. The development of quantitative assessment of vascular density in primary human tumors has produced a new independent marker of prognosis and could be helpful in selecting patients for antiangiogenic therapy. A large number of antiangiogenic agents are in development, however, new ways to assess their antitumor effects will be necessary for the treatment of advanced cancer. Stabilization of disease may occur by inhibiting new vessel growth, and thus, evidence for a decrease in blood supply should be sought by positron emission tomography scanning, magnetic resonance imaging, or other methods. Markers of angiogenesis in urine or blood will prove to be helpful in the monitoring of treatments.

ISSN:1040-8746    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

The chromosome ends are specialized nucleoprotein structures called telomeres, which are essential for stable chromosome maintenance. In tumor-derived cell lines telomeres are maintained by the ribonucleoprotein enzyme telomerase. Telomerase activity is repressed in almost all normal human somatic cells. Due to the end replication problem, progressive telomere shortening occurs in normal somatic cells, leading to a limited replicative capacity and eventually resulting in cellular senescence. In the presence of viral oncogenes or some somatic mutations that block cellular senescence, cells continue to divide and telomere erosion continues. This continuing telomere erosion ultimately leads to the activation of telomerase, a necessary event for the sustained growth of most human tumors.

ISSN:1040-8746    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

The context of this review highlights current strategies being employed in gene therapy for neoplastic diseases. Three main approaches, mutation compensation, molecular chemotherapy, and genetic immunopotentiation, have been undertaken. Mutation compensation relies on strategies to ablate activated oncogenes or augment tumor-suppressor gene expression. Molecular chemotherapy uses delivery of a toxin gene to tumor cells for eradication. Genetic immunopotentiation augments the host immune response against tumor-associated antigens via delivery of immune stimulatory molecules or delivery of foreign genes. Rapid implementation of a variety of gene therapy strategies have been undertaken for human clinical trials.

ISSN:1040-8746    

出版商:OVID    

年代:1996

数据来源: OVID