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Cytogenetic, spectral karyotyping, fluorescence in situ hybridization, and comparative genomic hybridization characterization of two new secondary leukemia cell lines with 5q deletions, and MYC and MLL amplification
Author(s) -
Knutsen Turid,
Pack Svetlana,
Petropavlovskaja Maria,
PadillaNash Hesed,
Knight Clement,
Mickley Lyn A.,
Ried Thomas,
Elwood Patrick C.,
Roberts Susan J.
Publication year - 2003
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.10200
Subject(s) - fluorescence in situ hybridization , chromosomal translocation , biology , karyotype , comparative genomic hybridization , cytogenetics , myeloid leukemia , leukemia , genetics , cancer research , microbiology and biotechnology , chromosome , gene
Abstract Cytogenetic studies of patients with therapy‐induced acute myeloid leukemia (t‐AML) have demonstrated whole chromosome loss or q‐arm deletion of chromosomes 5 and/or 7 in a majority of cases. We have established two cell lines, SAML‐1 and SAML‐2, from two patients who developed t‐AML after radiation and chemotherapy for Hodgkin disease. In both cases, the leukemia cells contained 5q deletions. SAML‐1 has 58 chromosomes and numerous abnormalities, including der(1)(1qter→1p22::5q31→5qter), der(5)(5pter→5q22::1p22→1pter), +8, der(13)i(13)(q10)del(13)(q11q14.1), and t(10;11). Fluorescence in situ hybridization (FISH) with unique sequence probes for the 5q31 region showed loss of IL4 , IL5 , IRF1 , and IL3 , and translocation of IL9 , DS5S89 , EGR1 , and CSFIR to 1p. SAML‐2 has 45 chromosomes, del(5)(q11.2q31) with a t(12;13)ins(12;5), leading to the proximity of IRF1 and RB1 , and complex translocations of chromosomes 8 and 11, resulting in amplification of MYC and MLL . Comparative genomic hybridization and spectral karyotyping were consistent with the G‐banding karyotype and FISH analyses. Because a potential tumor suppressor(s) in the 5q31 region has yet to be identified, these cell lines should prove useful in the study of the mechanisms leading to the development of t‐AML. © 2003 Wiley‐Liss, Inc.