occur as a very early event in tumors with these translocations. Studies on other kinds of tumors show that both copies of the retinoblastoma (RB) gene at 13q14 must be inactivated to eliminate its tumor suppressor function. However, biallelic deletion, inactivating mutations and lack of RB expression appear to occur only rarely, even in advanced myeloma tumors and cell lines. Notably, loss of 13q14 sequences is frequent in chronic lymphocytic leukemia, but is not associated with a poor prognosis. So, there might be a tumor suppressor gene on 13q that is unique to MM. In addition, there is evidence that a number of well-known tumor suppressor genes are sometimes involved in myeloma.
on K- and N-ras). Tumors that overexpress FGFR3 as a result of a t(4;14) translocation can have activating mutations of Ras or FGFR3 but not both, consistent with constitutive activation of the mitogen-activated protein kinase (MAPK) pathway in each case. Transfection studies of an IL-6-depen-dent HMCL show that activating mutations of either N- or K-Ras, or FGFR3, enhance growth and decrease the amount of IL-6 that is required for survival and growth. K-Ras mutation is associated with shortened survival, whereas patients whose myeloma tumors have N-Ras mutations have a similar prognosis to those who do not have Ras mutations.
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