The design of a multiple drug combination for treating stage 1 bladder cancer depends on a strategy of inhibiting the highly expressed genes ADRM1, COPS5, PSMD8, SUMO2, CALR, PDIA3, DNAJB11, HSPA5, RPN1, CUL1, HSP90B1, KPNA2, PSMD12, ECT2, TK1, TUBA1C, HN1, and ENO1; activating the suppressed genes UBC, JUN, RARRES3, and FOS; and suppressing the drug's effect on the nondifferentially expressed genes BAG6, HUWE1, PAAF1, PSMD10, FAF2, PCYT1A, and PSMD10.
The design of a multiple drug combination for treating stage 4 bladder cancer depends on a strategy of inhibiting the highly expressed genes ADRM1, COPS5, PSMD8, SUMO2, RNF126, CALR, PDIA3, DNAJB11, HSPA5, RPN1, HSP90AA1, HSPA1B, METTL23, RARRES3, KPNA2, PSMD12, ECT2, JUN, TK1, TUBA1C, HN1, and ENO1; activating the suppressed genes BCL3, FOS, UBC, and GTF2A1; and suppressing the drug's effect on the nondifferentially expressed genes, which are the same as those in stage 1 bladder cancer.
A comprehensive analysis led scientists to two specific genes, Chaf1a and Sumo2, that are the key factors linked to proviral silencing.
Further studies on the roles of Chaf1a and Sumo2 in stem cell proviral silencing can shed new light on stem cells and virus biology that could translate into valuable therapeutic and diagnostic applications.