[Oncogenes and tumor suppressor genes involved in the development of malignant lymphomas].
In comparison with the molecular mechanism of myeloid malignancies, the characteristic point in that of lymphoid tumors is that they develop from errors in the recombination of either immunoglobulin genes or T cell receptor genes. In myeloid malignancies, chimeric fusion genes are frequently detected as a results of chromosomal translocation, whereas unregulated expression of oncogenes or loss of expression of tumor suppressor genes are often found in lymphoid tumors. Recent advances in understanding the molecular development of lymphomas have provided a new insight into the roles of the cell cycle machinery in human lymphomagenesis. In this review, representative mechanisms are discussed to understand a conceptual framework for the growing literatures.
Hirai
H
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Department of Cell Therapy and Transplantation Medicine, University of Tokyo.
D002453:Cell Cycle; D002872:Chromosome Deletion; D016147:Genes, Tumor Suppressor; D019942:Genes, p16; D016158:Genes, p53; D006801:Humans; D007136:Immunoglobulins / Q000235:genetics; D008223:Lymphoma / Q000235:genetics*; D009857:Oncogenes; D011948:Receptors, Antigen, T-Cell / Q000235:genetics; D014178:Translocation, Genetic
D007136:Immunoglobulins; D011948:Receptors, Antigen, T-Cell