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Specific chromosomal mutagenesis observed in stimulated lymphocytes from patients with S‐ANLL
Author(s) -
Mamuris Zissis,
Dumont Jeanine,
Dutrillaux Bernard,
Aurias Alain
Publication year - 1990
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910460402
Subject(s) - biology , leukemia , mutagenesis , cancer research , chromosomal translocation , lymphoma , gene , chromatid , carcinogenesis , genetics , mutation , chromosome , immunology
An analysis of R‐banded PHA‐stimulated lymphocytes from 13 patients with secondary acute non‐lymphocytic leukemia (S‐ANLL) following breast cancer or lymphoma, and treatment by alkylating agents and/or radiotherapy, is reported. We found that chromosomes 5, 7, 11 and 17 are over‐involved in structural rearrangements. These anomalies are similar to those observed in the same categories of patients without S‐ANLL, and after in vitro treatment of normal lymphocytes by the alkylating agent melphalan. These anomalies are thus likely to be induced by treatment, independently of S‐ANLL. However, the same chromosomes (5, 7, 11 and 17) are recurrently deficient in leukemic S‐ANLL clones. In spite of these similarities, it remains unlikely that the deficiencies observed in leukemic clones were directly induced at the time of treatment. Probably, treatment of primary cancers induces nonrandom mutations of recessive genes located on these chromosomes as also indicated by chromosomal lesions. Various rearrangements including deletions of the homologous normal counterparts may then occur, unmasking mutated recessive genes. The latter stage would be concomitant with the leukemogenic process.