Mamuris Z, Dumont J, Dutrillaux B, Aurias A
C.N.R.S. URA 620 Structure et Mutagenèse Chromosomiques, Institut Curie, Paris, France.
Int J Cancer. 1990 Oct 15;46(4):563-8. doi: 10.1002/ijc.2910460402.
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.
本文报道了对13例乳腺癌或淋巴瘤继发急性非淋巴细胞白血病(S-ANLL)患者经烷化剂和/或放疗治疗后,R带PHA刺激淋巴细胞的分析。我们发现5号、7号、11号和17号染色体过度参与结构重排。这些异常与未患S-ANLL的同类患者以及正常淋巴细胞经烷化剂美法仑体外处理后观察到的异常相似。因此,这些异常可能是由治疗引起的,与S-ANLL无关。然而,相同的染色体(5号、7号、11号和17号)在白血病S-ANLL克隆中反复出现缺失。尽管有这些相似之处,但白血病克隆中观察到的缺失在治疗时直接诱发的可能性仍然不大。原发性癌症的治疗可能诱导了位于这些染色体上的隐性基因发生非随机突变,染色体损伤也表明了这一点。随后可能会发生各种重排,包括同源正常对应物的缺失,从而暴露突变的隐性基因。后一阶段将与白血病发生过程同时出现。