To determine whether genetic alterations of p16 and p27 genes play an important role in MDS pathogenesis, we examined DNA from 51 patients classified as 17 refractory anemias (RA), four refractory anemias with ringed sideroblasts (RARS), 19 refractory anemias with an excess of blasts (RAEB), 5 refractory anemias with excess of blasts in transformation (RAEB-t) and 6 chronic myelomonocytic leukemias (CMML).
We previously showed that the expression of p16(ink4a) (p16), in conjunction with retinoic acid (RA) treatment in the p16-deficient astrocytoma cell line, U343 MG-A, induced a potent cell cycle arrest in G(1) associated with changes in morphology.
Low levels of wild-type (wt)COUP-TFI transgene expression did not inhibit neural cell fate and primarily enhanced neuron outgrowth from RA-treated P19 aggregates.