Premium
Chromosomes and causation of human cancer and leukemia. XVII. Banding studies in acute myeloblastic leukemia (AML)
Author(s) -
Oshimura Mitsuo,
Hayata Isamu,
Kakati Surabhi,
Sandberg Avery A.
Publication year - 1976
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(197608)38:2<748::aid-cncr2820380218>3.0.co;2-u
Subject(s) - karyotype , acute myeloblastic leukemia , chromosomal translocation , trisomy , leukemia , g banding , pathology , biology , chromosome , giemsa stain , genetics , medicine , gene
Chromosomes were studied in the bone marrow and/or blood cells from 38 patients with acute myeloblastic leukemia (AML). The initial analysis with conventional Giemsa staining revealed that 16 of the 38 patients with AML studied had chromosomal abnormalities. The cells of these 38 patients (16 with abnormal karyotypes and 22 with normal karyotypes) were re‐examined with Q‐ and G‐banding techniques. Twenty‐two patients with conventionally stained normal karyotypes did not show any abnormalities, even with banding techniques. Three cases had a common translocation between the long arm of #8 and #21, i.e., [t(8;21)(q22;q22)], the so‐called prototypic karyotype. Two cases had a 45, XX, ‐21 karyotype; and three cases had trisomy of the long arm of chromosome #1. The banding patterns revealed that in two of the three latter cases, the presence of the trisomy of the long arm of #1 apparently occurred late in the disease. Therefore, it is possible that the trisomy of the long arm of #1 might bear a relationship to selective growth advantage of the leukemic cells in some cases with AML. The presence of extra #8 and #9 chromosomes and deletion of the long arm of #7, frequently reported in several leukemic disorders, were also found in the present cases, but with other chromosomal abnormalities. Chromosomes #6,#15,#19,#20, and X were not involved in any structural and/or numerical changes. The present data suggest that some chromosomal changes are nonrandom in AML and that further chromosomal studies may lead to a division of AML patients into subgroups on the basis of their karyotypes.