“…Examples include a translocation breakpoint in RARa at the genetic lesion of acute promyelocytic leukemia ( The data from panel a were quanti®ed by densitometry and expressed relative to S26 mRNA levels which serve as control of RNA loading. This experiment was performed twice dominant negative RARa mutants in retinoid-resistant embryonic carcinoma lines (Pratt et al, 1990;Kruyt et al, 1992), in RA-resistant HL-60 cells (Collins et al, 1990;Robertson et al, 1992), expression of dominant negative RXRb mutant in P19 embryonal carcinoma cells (Minucci et al, 1994), absence of RXRa expression in RA-resistant myogenic C2 cells (Froeschle et al, 1996) and F9 embryonal carcinoma cells bearing single and compound RAR and RXR mutations (Boylan et al, 1993(Boylan et al, , 1995Cli ord et al, 1996;Chiba et al, 1997). Interestingly, in all these cases, proliferation characteristics and/or retinoidinduced di erentiation are altered.…”