作者: Y Hatta , Y Yamada , M Tomonaga , HP Koeffler
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摘要: The retinoblastoma susceptibility gene (Rb) plays a key role in regulating the cell cycle association with cyclins and cyclin-dependent kinases (CDKs). Alteration of Rb as well CDK inhibitors (CDKIs) leads to deregulated cellular growth which promotes cancer formation. We examined genomic configuration entire 40 primary adult T leukemias/lymphomas (ATL) two ATL lines by Southern blotting also polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analyses. Homozygous loss exon 1 was identified one 21 acute ATL, 15 chronic none four lymphomatous samples. No point mutations were identified. Previously, we found that 10 these same samples had alterations either p16(INK4A) (homozygous deletion) or p27(kip1) deletion mutation). Although numbers are very low, an aberrant altered CDKI vice versa, suggesting both genes probably operate common pathway alteration can provide cells advantage.