Retained heterodisomy is associated with high gene expression in hyperhaploid inflammatory leiomyosarcoma.

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Hansén Nord, KarolinLund University,Lunds universitet,Avdelningen för klinisk genetik,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Clinical Genetics,Department of Laboratory Medicine,Faculty of Medicine (author)

Retained heterodisomy is associated with high gene expression in hyperhaploid inflammatory leiomyosarcoma.

Article/chapterEnglish2012

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Elsevier BV,2012

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LIBRIS-ID:oai:lup.lub.lu.se:87892d99-132d-48eb-8a96-d388da4d309c
https://lup.lub.lu.se/record/3123527URI
http://kipublications.ki.se/Default.aspx?queryparsed=id:125958811URI
https://doi.org/10.1593/neo.12930DOI

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Language:English
Summary in:English

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Inflammatory leiomyosarcoma (ILMS) is a soft tissue tumor that morphologically resembles conventional leiomyosarcoma (LMS) admixed with a prominent inflammatory infiltrate. Genetic data on ILMS are still limited but have suggested that this entity is characterized by hyperhaploidy (24-34 chromosomes). This low chromosome number is otherwise uncommon in neoplasia and has been found only in 0.2% to 0.3% of cytogenetically investigated tumors. Here, three ILMS were investigated using cytogenetic, single-nucleotide polymorphism (SNP) array, and global gene expression analyses. All cases displayed a hyperhaploid origin. Combined with previously reported cases, hyperhaploidy has been found in six of seven cytogenetically investigated ILMS. The copy number distribution of individual chromosomes is clearly nonrandom; the hyperhaploid clones of all six cases displayed disomy for chromosomes 5 and 20, and two copies of chromosomes 18, 21, and 22 were also common. All chromosomes identified as disomic showed a biparental origin by SNP array analysis; whether this is of pathogenetic importance is not known. Compared with conventional LMS, ILMS had a distinct gene expression signature. Furthermore, the number of chromosome copies correlated well with gene expression levels; disomic chromosomes showed higher gene expression levels than monosomic chromosomes, a finding that has not previously been reported for hyperhaploid tumors. Taken together, our findings suggest that disomy for some chromosomes, notably 5 and 20, as well as distorted gene expression achieved through massive loss of other chromosomes are essential features of ILMS.

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Paulsson, KajsaLund University,Lunds universitet,Avdelningen för klinisk genetik,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Clinical Genetics,Department of Laboratory Medicine,Faculty of Medicine(Swepub:lu)kgen-kpa (author)
Veerla, SrinivasLund University,Lunds universitet,Avdelningen för translationell cancerforskning,Institutionen för laboratoriemedicin,Medicinska fakulteten,Forskningsgrupp Lungcancer,Forskargrupper vid Lunds universitet,Bröst- och ovarialcancer,Bröst/lungcancer,Sektion I,Institutionen för kliniska vetenskaper, Lund,Division of Translational Cancer Research,Department of Laboratory Medicine,Faculty of Medicine,Research Group Lung Cancer,Lund University Research Groups,Breast and Ovarian Cancer Genomics,Breast/lungcancer,Section I,Department of Clinical Sciences, Lund,Breast/lung cancer(Swepub:lu)klin-sve (author)
Wejde, Johan (author)
Brosjö, OtteKarolinska Institutet (author)
Mandahl, NilsLund University,Lunds universitet,Avdelningen för klinisk genetik,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Clinical Genetics,Department of Laboratory Medicine,Faculty of Medicine(Swepub:lu)kgen-nma (author)
Mertens, FredrikLund University,Lunds universitet,Avdelningen för klinisk genetik,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Clinical Genetics,Department of Laboratory Medicine,Faculty of Medicine(Swepub:lu)kgen-fme (author)
Avdelningen för klinisk genetikInstitutionen för laboratoriemedicin (creator_code:org_t)

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In:Neoplasia: Elsevier BV14:9, s. 807-U1561522-8002
In:Neoplasia (New York, N.Y.): Elsevier BV14:9, s. 807-U1561476-5586

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By the author/editor: Hansén Nord, Kar ...; Paulsson, Kajsa; Veerla, Srinivas; Wejde, Johan; Brosjö, Otte; Mandahl, Nils; show more...; Mertens, Fredrik; show less...

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