These genetic alterations may be of a hereditary origin, forming the basis for familial cancers, or may be of somatic origin. We have also found that human relapse T-ALL cells that possess specific mutant alleles of the p53 gene behave aggressively in vivo , as shown by their propensity to spread throughout the body of SCID mice. Some of our work focuses on strategies designed to correct the genetic defects of cancer cells in an attempt to inhibit their malignant phenotype through the use of autologous bone marrow transplantation models.
Cancer cells are immortal.
Similar gene transduction into normal diploid cells does, however, not result in the induction of senescence. T-ALL cells and glioma cells have been shown to lose their tumor phenotype by reactivation of the p16INK4a gene, or by transduction of the p16 or p21 genes. Independent induction of senescence by p16 INK4a and p21 CIP1 in spontaneously immortalized human fibroblasts. The effect of different chemotherapeutic agents on the enrichment of DNA mismatch repair-deficient tumor cells. A fluorescent p53GFP fusion protein facilitates its detection in mammalian cells while retaining the properties of wild-type p53.