Molecular anatomy of chromosome 7q deletions in myeloid neoplasms

Evidence for multiple critical loci

Hong Liang, Jeff Fairman, David Claxton, Peter C. Nowell, Eric D. Green, Lalitha Nagarajan

Research output: Contribution to journalArticle

127 Citations (Scopus)

Abstract

Complete or partial deletions of the long arm of chromosome 7 (7q- and - 7) are nonrandom abnormalities seen in primary and therapy-induced myelodysplasia (MDS) and acute myelogenous leukemia (AML). Monosomy 7, occurring as the sole cytogenetic anomaly in a small but significant number of cases, may denote a dominant mechanism involving critical tumor suppressor gene(s). We have determined the extent of allele loss in cytogenetically prescreened MDS and AML patients for microsatellite markers from chromosome 7q22 and 7q31. Whereas >80% of these cases revealed allele loss for the entire region, a rare case of the 7q- chromosome showed allele loss for only the proximal 7q31.1 loci flanked by the markers D7S486 and D7S2456, and a case of monosomy 7 revealed allele loss for loci at both 7q31 and 7q22 with retention of sequences between these sets of loci. Furthermore, a case of AML with no cytogenetic anomaly of chromosome 7 revealed a submicroscopic allelic imbalance for a third distal locus, D7S677. These findings suggest the presence of three distinct critical loci that may contribute alone or in combination to the evolution of MDS and AML. The data also provide molecular evidence for unbalanced translocation with noncontiguous deletions, as an alternate mechanism underlying monosomy 7.

Original languageEnglish (US)
Pages (from-to)3781-3785
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume95
Issue number7
DOIs
StatePublished - Mar 31 1998

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Chromosome Deletion
Acute Myeloid Leukemia
Anatomy
Alleles
Chromosomes, Human, Pair 7
Cytogenetics
Neoplasms
Chromosomes
Allelic Imbalance
Tumor Suppressor Genes
Microsatellite Repeats
Monosomy Chromosome 7
Therapeutics

All Science Journal Classification (ASJC) codes

  • General

Cite this

Liang, Hong ; Fairman, Jeff ; Claxton, David ; Nowell, Peter C. ; Green, Eric D. ; Nagarajan, Lalitha. / Molecular anatomy of chromosome 7q deletions in myeloid neoplasms : Evidence for multiple critical loci. In: Proceedings of the National Academy of Sciences of the United States of America. 1998 ; Vol. 95, No. 7. pp. 3781-3785.
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abstract = "Complete or partial deletions of the long arm of chromosome 7 (7q- and - 7) are nonrandom abnormalities seen in primary and therapy-induced myelodysplasia (MDS) and acute myelogenous leukemia (AML). Monosomy 7, occurring as the sole cytogenetic anomaly in a small but significant number of cases, may denote a dominant mechanism involving critical tumor suppressor gene(s). We have determined the extent of allele loss in cytogenetically prescreened MDS and AML patients for microsatellite markers from chromosome 7q22 and 7q31. Whereas >80{\%} of these cases revealed allele loss for the entire region, a rare case of the 7q- chromosome showed allele loss for only the proximal 7q31.1 loci flanked by the markers D7S486 and D7S2456, and a case of monosomy 7 revealed allele loss for loci at both 7q31 and 7q22 with retention of sequences between these sets of loci. Furthermore, a case of AML with no cytogenetic anomaly of chromosome 7 revealed a submicroscopic allelic imbalance for a third distal locus, D7S677. These findings suggest the presence of three distinct critical loci that may contribute alone or in combination to the evolution of MDS and AML. The data also provide molecular evidence for unbalanced translocation with noncontiguous deletions, as an alternate mechanism underlying monosomy 7.",
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Molecular anatomy of chromosome 7q deletions in myeloid neoplasms : Evidence for multiple critical loci. / Liang, Hong; Fairman, Jeff; Claxton, David; Nowell, Peter C.; Green, Eric D.; Nagarajan, Lalitha.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 95, No. 7, 31.03.1998, p. 3781-3785.

Research output: Contribution to journalArticle

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