Genomic Alterations Involving the C-Myc Proto-Oncogene Locus During the Evolution of a Case of Chronic Granulocytic Leukaemia

Mutator phenotype of BCR – ABL transfected Ba/F3 cell lines and its association with enhanced expression of DNA polymerase β

“…Strong evidence supported that this phenotypic evolution is associated with the induction of genetic instability at the chromosomal level, including both numerical and structural chromosomal abnormalities in p210bcr/abl transformed cells, but these events are relatively rare occurrences in culture cells unless defects in DNA metabolism like repair, recombination, or replication, suggesting that genetic alteration at the nucleotide level may be involved (Laneuville et al, 1992). Furthermore, the secondary activation of N-ras (Ahuja et al, 1991;Collins et al, 1989;LeMaistre et al, 1989) and c-myc (McCarthy et al, 1984) genes and the functional inactivation of the anti-oncogene p53 observed frequently in patients developing blast crisis support the hypothesis of an early alteration of a genè guardian' of the genome confering a mutator phenotype at the nucleotide level (Loeb, 1991). Finally, genomic instability of microsatellite repeats associated with a late genetic event during the evolution of CML has been demonstrated (Wada et al, 1994).…”

Oncogenes, cancer and analytical cytology

“…In one patient with chronic myelocytic leukaemia, the c-myc gene was amplified 16-fold and rearranged within the genome during episodes of transformation (72). Amplification of the c-myc gene has also been reported in cell lines derived from a very poor prognosis group of patients with small cell lung cancer (69).…”

“…Apart from oncogene amplification which has been documented in a number of human tumours (32, 66,69,72,108), there seems to be little doubt that oncogenes are significantly involved in human malignancy at the level of transcription. The c-myc oncogene is expressed in tumour material from patients with haemopoetic neoplasia (99) and genes of the ras family appear to be over-expressed in a number of tumours.…”

Oncogenes and human leukemias

“…In the HL-60 myeloid cell line and in fresh leukemia cells from patients, c-myc was reportedly amplified [21,22]; it was also amplified in one case of CML during progression from chronic to acute phase [23] and in [24]. Several authors have reported amplification of c-abl in K562, an erythroleukemia cell line containing the t(9;22) translocation typical of CML [25].…”