Translocations between the Long Arms of Chromosomes 1 and 5 in Hematologic Malignancies Are Strongly Associated with Neoplasms of the Myeloid Lineages

Johansson, Bertil; Brøndum‐Nielsen, Karen; Billström, Rolf; Schiødt, Ida; Mitelman, Felix

doi:10.1016/s0165-4608(97)00198-2

Cited by 16 publications

(14 citation statements)

References 18 publications

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“…According to our mapping studies, the ADAM-TS12 gene is located at the telomeric region of the long arm of chromosome 5. It is of interest that this region (5q35) has been found to be a recurrent site of translocations in hematological malignancies (31,32). In addition, a putative tumor suppressor gene involved in the development of hepatocellular carcinomas without liver cirrhosis has been mapped to 5q35-qter (33).…”

Section: Discussionmentioning

confidence: 99%

Identification, Characterization, and Intracellular Processing of ADAM-TS12, a Novel Human Disintegrin with a Complex Structural Organization Involving Multiple Thrombospondin-1 Repeats

Cal

Argüelles

Fernández

et al. 2001

Journal of Biological Chemistry

101

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We have identified and cloned a human fetal lung cDNA encoding a new protein of the ADAM-TS family (a disintegrin and metalloproteinase domain, with thrombospondin type-1 modules) that has been called ADAM-TS12. This protein exhibits a domain organization similar to the remaining family members including a propeptide and metalloproteinase-like, disintegrin-like, and cysteine-rich domains. However, the number and organization of the TS repeats is unique with respect to other human ADAM-TSs. A total of eight TS-1 repeats arranged in three groups are present in this novel ADAM-TS. Analysis of intracellular processing of ADAM-TS12 revealed that it is synthesized as a precursor molecule that is first activated by cleavage of the prodomain in a furin-mediated process and subsequently processed into two fragments of different size: a 120-kDa N-terminal proteolytically active fragment containing the metalloproteinase and disintegrin domains, and a 83-kDa C-terminal fragment containing most of the TS-1 repeats. Somatic cell hybrid and radiation hybrid mapping experiments showed that the human ADAM-TS12 gene maps to 5q35, a location that differs from all ADAM genes mapped to date. Northern blot analysis of RNAs from human adult and fetal tissues demonstrated that ADAM-TS12 transcripts are only detected at significant levels in fetal lung but not in any other analyzed tissues. In addition, ADAM-TS12 transcripts were detected in gastric carcinomas and in tumor cell lines from diverse sources, being induced by transforming growth factor-␤ in KMST human fibroblasts. These data suggest that ADAM-TS12 may play roles in pulmonary cells during fetal development or in tumor processes through its proteolytic activity or as a molecule potentially involved in regulation of cell adhesion.

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Section: Discussionmentioning

confidence: 99%

Identification, Characterization, and Intracellular Processing of ADAM-TS12, a Novel Human Disintegrin with a Complex Structural Organization Involving Multiple Thrombospondin-1 Repeats

Cal

Argüelles

Fernández

et al. 2001

Journal of Biological Chemistry

101

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“…Breakpoints in 1q21 are observed in 39% of marginal zone B-cell lymphoma (15), and, in Burkitts lymphoma, the t(8;14) is frequently associated with dup(1)(q21q32) (20%) (12). It should be noted that aberrations affecting 1q21-23 are not restricted to B-cell NHL, as evidenced by frequent implication of this region in primary chromosomal translocations in hematological malignancies of myeloid origin (16).…”

mentioning

confidence: 99%

The IgG Fc receptor, FcγRIIB, is a target for deregulation by chromosomal translocation in malignant lymphoma

Callanan

Baccon

Mossuz

et al. 2000

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

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Rearrangement of chromosomal bands 1q21–23 is one of the most frequent chromosomal aberrations observed in hematological malignancy. The genes affected by these rearrangements remain poorly characterized. Typically, 1q21–23 rearrangements arise during tumor evolution and accompany disease-specific chromosomal rearrangements such as t(14;18) ( BCL2 ) and t(8;14) ( MYC ), where they are thus thought to play an important role in tumor progression. The pathogenetic basis of this 1q21–23-associated disease progression is currently unknown. In this setting, we surveyed our series of follicular lymphoma for evidence of recurring 1q21–23 breaks and identified three cases in which a t(14;18)(q32;q21) was accompanied by a novel balanced t(1;22)(q22;q11). Molecular cloning of the t(1;22) in a cell line (B593) derived from one of these cases and detailed fluorescent in situ hybridization mapping in the two remaining cases identified the FCGR2B gene, which encodes the immunoreceptor tyrosine-based inhibition motif-bearing IgG Fc receptor, FcγRIIB, as the target gene of the t(1;22)(q22;q11). We demonstrate deregulation of FCGR2B leading to hyperexpression of FcγRIIb2 as the principal consequence of the t(1;22). This is evidence that IgG Fc receptors can be targets for deregulation through chromosomal translocation in lymphoma. It suggests that dysregulation of FCGR2B may play a role in tumor progression in follicular lymphoma.

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“…20 Also, LOH has been reported at 1q23-32 in breast cancer. 25 Translocation between 1q and 5q, 26 trisomy 1q, 27 and either rearrangement or duplication of chromosome 1q 28 have been observed in MDS. However, deletion of chromosome 1q in MDS has rarely been reported.…”

Section: Discussionmentioning

confidence: 99%

“…Besides the loss of tumor suppressor genes, chromosome translocations, rearrangements or duplications of chromosome have been observed in MDS. 26,28 In addition, mismatch repair genes such as MSH2 can be altered leading to microsatellite instability as well as generalize genetic instability. 38 Furthermore, mitotic checkpoint genes can be abnormal leading to aueuploidy.…”

Section: Discussionmentioning

confidence: 99%

Allelotype analysis of the myelodysplastic syndrome

et al. 2000

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Myelodysplastic syndromes (MDS) are a group of clonal hematologic disorders found predominantly in the elderly. The molecular mechanisms underlying the development of MDS remain obscure. In order to begin to identify tumor suppressor genes involved in these disorders, we performed a detailed microsatellite allelotype of chromosomal deletions associated with MDS. DNAs from both bone marrow and peripheral blood of 32 MDS patients were studied using 84 highly informative microsatellite markers on all autosomal arms, excluding the short arms of the acrocentric chromosomes. A high percentage of loss of heterozygosity (LOH) was identified on chromosome 5q (40% of informative cases), 7q (45%), 17p (23%) and 20q (20%), which corresponds to the most common cytogenetic abnormalities reported in MDS. In addition, a high incidence of LOH (у20%) was observed on chromosomal arms which had not been previously reported including 1p (36%), 1q (35%), and 18q (23%). This extensive allelotype analysis focuses attention on several novel genomic regions that probably contain novel tumor suppressor genes whose loss of function contributes to the development of MDS. Leukemia (2000) 14, 805-810.

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Translocations between the Long Arms of Chromosomes 1 and 5 in Hematologic Malignancies Are Strongly Associated with Neoplasms of the Myeloid Lineages

Cited by 16 publications

References 18 publications

Identification, Characterization, and Intracellular Processing of ADAM-TS12, a Novel Human Disintegrin with a Complex Structural Organization Involving Multiple Thrombospondin-1 Repeats

Identification, Characterization, and Intracellular Processing of ADAM-TS12, a Novel Human Disintegrin with a Complex Structural Organization Involving Multiple Thrombospondin-1 Repeats

The IgG Fc receptor, FcγRIIB, is a target for deregulation by chromosomal translocation in malignant lymphoma

Allelotype analysis of the myelodysplastic syndrome

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