Nonrandom chromosomal rearrangements of 14q32.3 and 19p13.3 and preferential deletion of 1p in 21 patients with multiple myeloma and plasma cell leukemia

Nishida, Kazuhiro; Takashima, T; Nakagawa, Hiromi; Fujii, Hidetaka; Tamaki, Toshiharu; Shimazaki, Chihiro; Horiike, Shigeo; Misawa, Shinichi; Abe, T

doi:10.1182/blood.v84.7.2283.bloodjournal8472283

Cited by 17 publications

(23 citation statements)

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“…Specimens analyzed in our study include primary plasma cell leukemias that represent advanced-stage disease. Limited cytogenetic data available for PCL indicate that the majority of cases are pseudodiploid Taniwaki et al, 1994;Perez et al, 1994;Heim and Mitelman, 1995). In less advanced stages, pseudodiploid tumors occur in only 10% of patients (Dimopoulos et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…It is recognized that approximately 30-50% of MM patients carry cytogenetically abnormal clones (Kowalczyk et al, 1991;Durie, 1992;Jelinek et al, 1993;Lee et al, 1993;Ankathil et al, 1995;Sawyer et al, 1995). Nonrandom rearrangements involving chromosomes 1 and 14 (particularly 14q32), preferential gains of chromosomes 3, 5, 7, 9, 11, 15, and 19, and total or partial monosomies of chromosomes 6 and 13 (Dewald et al, 1985;Gould et al, 1988;van den Berghe, 1990;Weh et al, 1990;Taniwaki et al, 1994;Lai et al, 1995;Sawyer et al, 1995) have been reported. Structural rearrangements and gain or loss of sequences on chromosomes 1, 6, 13 and 14 occur in PCL Taniwaki et al, 1994;Perez et al, 1994;Dimopoulos et al, 1994;Heim and Mitelman, 1995).…”

Section: Introductionmentioning

confidence: 99%

“…Nonrandom rearrangements involving chromosomes 1 and 14 (particularly 14q32), preferential gains of chromosomes 3, 5, 7, 9, 11, 15, and 19, and total or partial monosomies of chromosomes 6 and 13 (Dewald et al, 1985;Gould et al, 1988;van den Berghe, 1990;Weh et al, 1990;Taniwaki et al, 1994;Lai et al, 1995;Sawyer et al, 1995) have been reported. Structural rearrangements and gain or loss of sequences on chromosomes 1, 6, 13 and 14 occur in PCL Taniwaki et al, 1994;Perez et al, 1994;Dimopoulos et al, 1994;Heim and Mitelman, 1995). However, identification of cytogenetic aberrations in MM has been complicated by a low proliferative index that limits generation of sufficient numbers of high quality metaphase cells for in-depth banding analyses.…”

Section: Introductionmentioning

confidence: 99%

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Molecular cytogenetic abnormalities in multiple myeloma and plasma cell leukemia measured using comparative genomic hybridization

Avet‐Loiseau

Andree-Ashley

Moore

et al. 1997

Genes Chromosom. Cancer

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Comparative genomic hybridization (CGH) was used to identify recurrent regions of DNA sequence loss and gain in 21 multiple myeloma (MM) and plasma cell leukemia (PCL) primary tumor specimens and cell lines. Multiple regions of non‐random sequence loss and gain were observed in 8/8 primary advanced stage tumors and 13/13 cell lines. Identification of sequence copy number changes was facilitated by statistical analyses that reduce subjectivity associated with identification of copy number changes and by requiring that sequence changes are visible using both red‐ and green‐labeled tumor DNA. Loss of sequence on 13q and 14q and gain of sequence on 1q and chromosome 7 occurred in 50–60% of the population. In general, cell lines carry more and larger regions of sequence gain and loss than primary tumors. Regions of sequence copy number change that recur among MM cell lines and primary tumors include, in order of prevalence, enh(1q12qter), dim(13), enh(7), enh(3q22q29), enh(11q13.3qter), dim(14q11.2q31), enh(8q21qter), enh(3p25pter), dim(17p11.2p13), and dim(6q22.1q23). Population distributions of genome‐wide changes in primary tumors reveal “hot‐spots” of sequence loss from 13q12.1‐q21, 13q32‐q34, 14q11.2‐q13, and 14q23‐q31. Genomic changes detected using CGH are consistent with those identified using banding analyses, although recurrent involvement of additional regions of the genome are also evident. A higher prevalence of genomic changes is visible using CGH compared to banding. Identification of recurrent regions of sequence gain and loss provides opportunities to identify regions of the genome that may be involved in the malignant phenotype and/or disease progression. Genes Chromosom. Cancer 19:124–133, 1997. © 1997 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Molecular cytogenetic abnormalities in multiple myeloma and plasma cell leukemia measured using comparative genomic hybridization

Avet‐Loiseau

Andree-Ashley

Moore

et al. 1997

Genes Chromosom. Cancer

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“…Chromosome changes in multiple myeloma are far from well characterized, mainly due to the low mitotic index which results in a small number of metaphases suitable for analysis. Still, more than 1000 cases of MM and related disorders with detailed cytogenetics have been reported (Dewald et al, 1985;Weh et al, 1993;Cigudosa et al, 1994;Taniwaki et al, 1994;Smadja et al, 1995;Laï et al, 1995;Sawyer et al, 1995;Calasanz et al, 1997) and some chromosome features can be summarized. (a) The proportion of abnormal karyotypes is about 40%, but varies between 20% and 60% depending on the series.…”

Section: Introductionmentioning

confidence: 99%

Hypodiploidy and 22q11 rearrangements at diagnosis are associated with poor prognosis in patients with multiple myeloma

et al. 1997

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Summary.Our aim was to evaluate the clinical use of cytogenetic analysis as a prognostic factor in the outcome of newly diagnosed multiple myeloma (MM) patients. The present series includes 111 newly diagnosed MM patients treated with one of three standard-dose regimens or autologous transplantation over an 8-year time interval. As expected, the presence of an abnormal karyotype (39% of patients) correlated with poor prognosis (progression rate 63% v 47%, P ¼ 0 . 042), shorter event-free (EFS, P ¼ 0 . 014) and overall (OS, P ¼ 0 . 005) survival. Two distinct cytogenetic abnormalities were the most significant variables that influenced EFS and OS in the univariate analysis. The presence of hypodiploid karyotypes or rearrangements of band 22q11 were associated with higher progression rate (P ¼ 0 . 001) and shorter EFS (P < 0 . 024) and OS (P < 0 . 004). The median EFS and OS for patients with hypodiploidy was 4 and 7 months respectively. Multivariate analysis showed that absence of hypodiploidy was the most favourable prognostic variable for OS (P ¼ 0 . 022) followed by stage рIIA, serum calcium р2875 mmol/l, and absence of abnormalities 22q. The data suggest that the presence of hypodiploid karyotypes and rearrangements on 22q11 band show a higher progression rate and shorter survival in MM patients.

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“…Cytogenetic analysis. The karyotypes of the bone marrow cells and the OHN-GM cells were analysed by G-banding (Taniwaki et al, 1994). Chromosome identification and karyotype designation were performed according to the recommendations of the International System for Human Cytogenetic Nomenclature (ISCN, 1991).…”

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confidence: 99%

Alterations of p53 and Rb genes in a novel human GM‐CSF‐dependent myeloid cell line (OHN‐GM) established from therapy‐related leukaemia

et al. 1997

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Summary.A novel GM-CSF-dependent myeloid cell line, OHN-GM, was established from a patient who developed acute myelogenous leukaemia (AML) as a consequence of myelodysplastic syndrome (MDS). As the patient had previously received cytotoxic chemotherapy for Hodgkin's disease, the MDS and AML were probably related to such therapy. Sequential karyotypic analysis established a del(5q) as the initial cytogenetic abnormality. Additional alterations, including t(10;13)(q24;q14), had developed subsequently during disease progression. Southern blot analysis of OHN-GM cells suggested deletion of one allele of the IRF-1 gene, although no aberrant transcripts were detected. Fluorescence in situ hybridization analysis revealed the deletion of the Rb gene due to the t(10;13)(q24;q14) translocation, and Western blot analysis demonstrated the absence of Rb protein in OHN-GM cells. Finally, the OHN-GM cells exhibited two missense point mutations in highly conserved regions of the p53 gene. These observations suggest that a multistep process, involving alterations of Rb and p53 genes, may have contributed to the patient's disease development and progression. To our knowledge, OHN-GM is the first cell line derived from a therapy-related AML. These cells may aid the investigation of leukaemogenesis as well as the biology of secondary leukaemia.

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Nonrandom chromosomal rearrangements of 14q32.3 and 19p13.3 and preferential deletion of 1p in 21 patients with multiple myeloma and plasma cell leukemia

Cited by 17 publications

References 0 publications

Molecular cytogenetic abnormalities in multiple myeloma and plasma cell leukemia measured using comparative genomic hybridization

Molecular cytogenetic abnormalities in multiple myeloma and plasma cell leukemia measured using comparative genomic hybridization

Hypodiploidy and 22q11 rearrangements at diagnosis are associated with poor prognosis in patients with multiple myeloma

Alterations of p53 and Rb genes in a novel human GM‐CSF‐dependent myeloid cell line (OHN‐GM) established from therapy‐related leukaemia

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