Journal Article

Tumor progression and metastasis

Jun Yokota

in Carcinogenesis

Volume 21, issue 3, pages 497-503
Published in print March 2000 | ISSN: 0143-3334
Published online March 2000 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/21.3.497
Tumor progression and metastasis

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It is now widely accepted that cancer is attributed to the accumulation of genetic alterations in cells. Thus, to understand the molecular mechanisms of cancer metastasis, it is indispensable to identify the genes whose alterations accumulate during cancer progression as well as the genes whose expression is responsible for the acquisition of metastatic potential in cancer cells. Molecular analyses of cancer cells in various stages of progression have revealed that alterations in tumor suppressor genes and oncogenes accumulate during tumor progression and correlate with the clinical aggressiveness of cancer. Comparative analyses of gene expression profiles between metastatic and non-metastatic cells have revealed that various genes are differentially expressed in association with the metastatic potential of cancer cells. A number of genes have been also identified as having functions in inducing or suppressing metastasis in experimental models. However, the association between causative genetic alterations and resulting phenotypic alterations with respect to the metastatic potential of cancer cells is not fully understood. Therefore, elucidation of genotype–phenotype correlation will be required to further understand a complex process of metastasis. Here, I review the progress on molecular studies of tumor progression and metastasis of the past 20 years and discuss the future direction in this field of science.

Keywords: HNPCC, hereditary non-polyposis colorectal cancer; LOH, loss of heterozygosity; MMP, microsatellite mutator phenotype; RFLP, restriction fragment length polymorphism; SCLC, small-cell lung carcinoma.

Journal Article.  6038 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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