Cytogenetic studies in patients with multiple myeloma

Kowalczyk, Jerzy; Dmoszyńska, Anna; Chobotow, Malgorzata; Sokołowska, Bożena

doi:10.1016/0165-4608(91)90075-6

Cited by 10 publications

(9 citation statements)

References 9 publications

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“…In plasma cell leukemia (PCL), morphologically distinct myeloma cells are present in the circulation. 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.…”

Section: Introductionmentioning

confidence: 99%

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: Introductionmentioning

confidence: 99%

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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“…Philip et al (1980) investigated 25 MM patients, of which 16 (64%) were karyotypically abnormal. The corresponding success rates were 50% and 30% in the studies reported by Ferti et al (1984) and Kowalczyk et al (1991) respectively. In the present series, 59% of the cytogenetically successfully analysed 32 patients and 34 samples were shown to harbour chromosomal aberrations, using G‐banding, with the frequency being higher in the MM patients (63%) than among the MGUS/SMM patients (50%) (Tables III and IV respectively).…”

Section: Discussionmentioning

confidence: 81%

“…Multiple myelomas are definitely characterized by the latter growth pattern, considering that short‐term culturing, with or without various cytokines, yield abnormal karyotypes in only approximately 50% of MM (Nilsson et al , 2002), despite the fact that interphase FISH analyses reveal aberrations in close to 100% (Flactif et al , 1995). We know of only a few series where DCP have been used for cytogenetic analyses of MM and related PC dyscrasias (Philip et al , 1980; Ferti et al , 1984; Ranni et al , 1987; Clark et al , 1989; Kowalczyk et al , 1991; Carbone et al , 1992; Ankathil et al , 1995; Sawyer et al , 1995; Tricot et al , 1997). These investigations have rarely provided detailed karyotypic information based on DCP alone; most studies have combined the cytogenetic results obtained by DCP and short‐term culturing, thus excluding proper evaluation of DCP alone.…”

Section: Discussionmentioning

confidence: 99%

High frequencies of chromosomal aberrations in multiple myeloma and monoclonal gammopathy of undetermined significance in direct chromosome preparation

Nilsson¹,

Lenhoff²,

Rylander³

et al. 2004

Br J Haematol

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SummaryAlthough many cases of multiple myeloma (MM) and monoclonal gammopathy of undetermined significance (MGUS) are cytogenetically normal, interphase fluorescence in situ hybridization (FISH) analyses reveal aberrations in the majority of the cases. Most likely, non-neoplastic cells are more prone to divide in culture than neoplastic cells. Direct chromosome preparations (DCP) would be one way to circumvent this methodological problem. We have investigated 47 bone marrow samples from 39 patients by DCP. A median of 58 metaphases (range 9-158) was analysed per sample. Interphase FISH analyses using probes to detect IGH rearrangements, -13/13q-, +3, +7, and +11 were also performed. Abnormal karyotypes were detected in 15 (63%) of 24 MM and in 4 (50%) of eight MGUS/smouldering MM (SMM) cases that could be successfully cytogenetically analysed. Age, sex, or degree of bone marrow plasma cell (PC) infiltration did not influence the karyotypic patterns (P > 0AE05). However, the frequencies of aberrant karyotypes varied in relation to the Colcemide concentrations used -7% (30 ng/ml) versus 69% and 67% (100 and 200 ng/ml, respectively) (P ¼ 0AE01). Combining the G-banding and FISH results, abnormalities were detected in 29 of 31 (94%) MM and in six of eight (75%) MGUS/SMM patients. Thus, cytogenetic and FISH analyses after DCP using 100-200 ng Colcemide/ml identified aberrations in most MM/MGUS/SMM, irrespective of PC percentages.

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“…Second, CDH9 and CDH12 (5p14), CDH6 (5p15. [1][2][3][4][5][6][7][8][9][10][11][12][13][14] and CDH18 (5p15.2-15.1) are also located in the vicinity of 5p15.3, which is identified as the SRO among the PEorigin cell lines (Fig. 2C).…”

Section: Discussionmentioning

confidence: 99%

“…Low proliferative activity of myeloma cells makes it difficult to get analyzable metaphase cells, resulting in detection of clonal chromosomal abnormalities in only 30-50% of MM cases (2)(3)(4)(5), whereas DNA content measurement using flow cytometry or computerized image microscopy detected aneuploidy in 80-90% of the cases (6,7). In chromosomal analysis, duplication of chromosome 1q and deletion of 6q and 13q have been frequently noted (4,5), and clustering of rearranged breakpoints at bands 14q32, 16q11 and 22q11 have been shown (8,9).…”

Section: Introductionmentioning

confidence: 99%

Comparative Genomic Hybridization Detected Nonrandom Chromosomal Gains and Losses in Three Pairs of Sister Myeloma Cell Lines Established from bone Marrow- and Pleural Effusion-cells from the Same Patient

et al. 2004

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Cytogenetic studies in patients with multiple myeloma

Cited by 10 publications

References 9 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

High frequencies of chromosomal aberrations in multiple myeloma and monoclonal gammopathy of undetermined significance in direct chromosome preparation

Comparative Genomic Hybridization Detected Nonrandom Chromosomal Gains and Losses in Three Pairs of Sister Myeloma Cell Lines Established from bone Marrow- and Pleural Effusion-cells from the Same Patient

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