Chromosomes and survival in multiple myeloma. A banding study of 25 cases

Philip, Preben; Drivsholm, Aage; Hansen, Niels Ebbe; Jensen, Mogens Krogh; Killmann, Sven‐Aage

doi:10.1016/0165-4608(80)90031-x

Cited by 53 publications

(23 citation statements)

References 19 publications

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“…Karyotyping and CGH analyses have identified total or partial 1q gain (consistently involving 1q21) in 40 -60% of MM as well as in plasma cell leukemia and plasmacytoma (Philip et al, 1980;Smadja et al, 1998;Aalto et al, 1999). Aberrations affecting 1q are not restricted to lymphoid tumors; chromosomal translocations affecting 1q12-23 are common in acute leukemia of both myeloid and lymphoid origin Busson-Le Coniat et al, 1999).…”

Section: Introductionmentioning

confidence: 92%

Novel evidence of a role for chromosome 1 pericentric heterochromatin in the pathogenesis of B‐cell lymphoma and multiple myeloma

Baccon

Leroux

Dascalescu

et al. 2001

Genes Chromosomes & Cancer

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1q rearrangement is a remarkably frequent secondary chromosomal change in both non-Hodgkin's lymphoma (NHL) and multiple myeloma (MM), where it is associated with tumor progression. To gain insight into 1q rearrangement-associated disease mechanisms, we used fluorescence in situ hybridization (FISH) to search for recurring 1q breaks in 35 lymphoma samples (31 NHL patients and 4 lymphoma-derived cell lines) as well as 22 MM patients with cytogenetically determined 1q abnormalities. Strikingly, dual-color FISH analysis with chromosome 1 centromere and 1q12-specific probes identified constitutive heterochromatin band 1q12 as the single most frequent breakpoint site in both NHL and MM (39% and 89% of 1q breaks, respectively). These rearrangements consistently generated aberrant heterochromatin/euchromatin junctions and gain of 1q12 material. A further 30% of NHL 1q breaks specifically involved two other novel, closely spaced sites (clusters I and II) within a 2.5 Mb region of proximal 1q21 (D1S3620 to D1S3623). A possible association between these sites and NHL subtype was evident; the cluster I rearrangement was frequent in follicular and diffuse large cell lymphoma, whereas the cluster II rearrangement was more frequently observed in diffuse small-cell lymphoma (2/2 marginal zone lymphomas, 1/2 atypical chronic lymphocytic leukemias, and 1 lymphoplasmacytic lymphoma in this series). Candidate oncogenes bordering this interval (BCL9 and AF1Q) were not rearranged in any patient except one (AF1Q). This study provides the first evidence of involvement of 1q12 constitutive heterochromatin in the pathogenesis of NHL and MM and indicates proximal 1q21 to be of specific pathological significance in NHL.

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Section: Introductionmentioning

confidence: 92%

Novel evidence of a role for chromosome 1 pericentric heterochromatin in the pathogenesis of B‐cell lymphoma and multiple myeloma

Baccon

Leroux

Dascalescu

et al. 2001

Genes Chromosomes & Cancer

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“…Cytogenetic studies in multiple myeloma patients (prior to treatment) have revealed that the most commonly affected chromosomes have been Chr 1 and Chr 14 (59). Common abnormalities include chromosomal breakpoints (59)(60)(61)(62)(63) and deletions or duplications (59,64,65) of the chromosome ranging from lpll-35 and lq22-43. In addition, tumor samples from 10 Burkitt lymphoma patients had partial trisomy for Chr lq (62), bone marrow cells from a single patient with a plasma cell leukemia were carrying a translocation involving Chr 1 and Chr 6 (66), and 28 DLLC samples had chromosomal breaks at either 1p32-36 or 1p22 (67).…”

Section: Methodsmentioning

confidence: 99%

Genetic mapping of tumor susceptibility genes involved in mouse plasmacytomagenesis.

Mock

Krall

Dosik

1993

Proc. Natl. Acad. Sci. U.S.A.

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Plasmacytomas (PCTs) were induced in 47%of BALB/cAnPt mice by the intraperitoneal injection of pristane, in 2% of (BALB/c x DBA/2N)F1, and in 11% of 773 BALB/cAnPt x (BALB/cAnPt x DBA/2N)F1 N2 backcross mice. This result indicates a multigenic mode of inheritance for PCT susceptibility. To locate genes controlling this complex genetic trait, tumor susceptibility in backcross progeny generated from BALB/c and DBA/2N (resistant) mice was correlated with alleles of 83 marker loci. -5). Most other inbred strains of mice are resistant to PCT induction by these agents. The incidence of induced PCTs in backcross and recombinant inbred mice derived from resistant (R) and susceptible (S) progenitors has indicated that PCT susceptibility is under multigenic control (6-10).To localize genes involved in plasmacytomagenesis, associations of tumor susceptibility with alleles of genetic markers distributed across the mouse genome were examined in backcross progeny from a cross of S (BALB/c) and R (DBA/2) strains of mice. Our approach was similar to that used in the dissection of complex genetic traits associated with other disease processes (11)(12)(13)(14). The genotypes of the mice that developed PCTs were examined for homozygosity (C/C) at specific loci or sequence tagged sites (STSs). In this study, regions of mouse chromosome (Chr) 4 and Chr 1 have been implicated in the genetic control of plasmacytomagenesis. MATERIALS AND METHODSTumor Induction. A panel of 821 backcross progeny was generated from a cross between 24 BALB/cAnPt (PCTsusceptible) females and 8 (BALB/cAnPt x DBA/2N)F1 (PCT-resistant) males; these mice were bred and maintained in our closed conventional mouse colony. Six-to 10-week-old mice [100 BALB/cAnPt, 100 (C x D)F1, and 773 first generation backcross progeny] were inoculated i.p. with three 0.5-ml injections of pristane (2,6,10,14-tetramethylpentadecane) on days 0, 60, and 120.The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.Diagnosis. Starting at day 134, Giemsa-stained slides of ascites smears from peritoneal exudate cells were examined on a biweekly basis for the presence of atypical plasma cells. Mice were diagnosed as PCT-positive when accumulations of 10 or more atypical plasma cells were seen in the ascites smears. At this time, ascites samples from individual tumorbearing mice were transferred i.p. to pristane-pretreated CDF1 hybrids for purposes of generating tumor tissue for viable freezing and immortalization. Host (spleen, kidney, and liver) and tumor (mesenteric oil granuloma) tissues were removed and frozen in liquid nitrogen.Marker Typing and Molecular Analyses of Tumors. DNA isolation (tumor and kidney), restriction enzyme digestion, agarose gel electrophoresis, Southern blotting, and restriction fragment length polymorphism (RFLP) analyses were performed as described (15). D4Rck clones were amplified and labeled by PCR a...

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“…Wilms' tumor-WAGR complex^I de la Chapelle and Berger (HGM7); Narahara et al (1984); Kondo et al (1984); Douglass et al (1985); Slater et al (1985) t ( 11 ; 14) Fukuhara et al (1983); Van den Berghe et al (1984); Ferti et al (1984) t(ll;14)(ql3.3;q32.3) ML I Fleischman and Prigogina (1977); Bloomfield et al (1983); 1lql3-q 14 Deletions, translocations ANLL-M4 and M5 II de la Chapelle and Berger (HGM7); IWCL IV (1984) t(10;11)(P14;ql3-ql4) II see chromosome 10 1 lq 14 del(11)(q 14) MDS I Swansbury and Lawler (1980); Swolin et al(1981); Mitelman et al (1981); Kardon et al (1982); Mufti et al (1982) Reported most commonly as a constitutional abnormality but homozygosity for del(11) and loss of normal 11 observed 2 in several tumors (Koufos et al 1984, Orkin et al 1984, Fearon et al 1984 Wilms' tumor, aniridia, genital anomalies, mental retardation Chromosome 11 continues on next page Tilly et al (1984); Becroft et al (1984); Prieto et al (1985); Workman et al (1985) Trisomy 11 Multiple myeloma Liang et al (1979); Philip et al (1980); Lewis and Mackenzie (1984) The same translocation has been observed in two cases of neuroepithelioma (Whang-Peng et al 1984b) (1983); Gibas et al (1984c); Delozier-Blanchet et al (1985) 12ql3-q22 dup(12)(ql3q22) ML II de la Chapelle and Berger (HGM7); Bloomfield et al (1983) Trisomy 12 B-CLL de la Chapelle and Berger (HGM7); Han et al (1984); Pittman and Catovsky (1984) ML Bloomfield et al (1983); …”

Section: Sporadic Recurrent Translocationsmentioning

confidence: 99%

Report of the committee on chromosome rearrangements in neoplasia and on fragile sites

Berger¹,

Cd²,

Sutherland³

1985

Cytogenet Genome Res

251

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Chromosomes and survival in multiple myeloma. A banding study of 25 cases

Cited by 53 publications

References 19 publications

Novel evidence of a role for chromosome 1 pericentric heterochromatin in the pathogenesis of B‐cell lymphoma and multiple myeloma

Novel evidence of a role for chromosome 1 pericentric heterochromatin in the pathogenesis of B‐cell lymphoma and multiple myeloma

Genetic mapping of tumor susceptibility genes involved in mouse plasmacytomagenesis.

Report of the committee on chromosome rearrangements in neoplasia and on fragile sites

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