The molecular classification of multiple myeloma

To better define the molecular basis of multiple myeloma (MM), we performed unsupervised hierarchic clustering of mRNA expression profiles in CD138-enriched plasma cells from 414 newly diagnosed patients who went on to receive high-dose therapy and tandem stem cell transplants. Seven disease subtype...

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Vydáno v:	Blood Ročník 108; číslo 6; s. 2020
Hlavní autoři:	Zhan, Fenghuang, Huang, Yongsheng, Colla, Simona, Stewart, James P, Hanamura, Ichiro, Gupta, Sushil, Epstein, Joshua, Yaccoby, Shmuel, Sawyer, Jeffrey, Burington, Bart, Anaissie, Elias, Hollmig, Klaus, Pineda-Roman, Mauricio, Tricot, Guido, van Rhee, Frits, Walker, Ronald, Zangari, Maurizio, Crowley, John, Barlogie, Bart, Shaughnessy, Jr, John D
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States 15.09.2006
Témata:	Chromosome Mapping Cluster Analysis Cyclin D Cyclins - genetics Data Interpretation, Statistical Gene Expression Profiling - statistics & numerical data Humans Membrane Glycoproteins - genetics Multiple Myeloma - classification Multiple Myeloma - genetics Multiple Myeloma - immunology Oligonucleotide Array Sequence Analysis - statistics & numerical data Plasma Cells - immunology Prognosis Proteoglycans - genetics RNA, Messenger - genetics RNA, Neoplasm - genetics Syndecan-1 Syndecans
ISSN:	0006-4971
On-line přístup:	Zjistit podrobnosti o přístupu
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Abstract	To better define the molecular basis of multiple myeloma (MM), we performed unsupervised hierarchic clustering of mRNA expression profiles in CD138-enriched plasma cells from 414 newly diagnosed patients who went on to receive high-dose therapy and tandem stem cell transplants. Seven disease subtypes were validated that were strongly influenced by known genetic lesions, such as c-MAF- and MAFB-, CCND1- and CCND3-, and MMSET-activating translocations and hyperdiploidy. Indicative of the deregulation of common pathways by gene orthologs, common gene signatures were observed in cases with c-MAF and MAFB activation and CCND1 and CCND3 activation, the latter consisting of 2 subgroups, one characterized by expression of the early B-cell markers CD20 and PAX5. A low incidence of focal bone disease distinguished one and increased expression of proliferation-associated genes of another novel subgroup. Comprising varying fractions of each of the other 6 subgroups, the proliferation subgroup dominated at relapse, suggesting that this signature is linked to disease progression. Proliferation and MMSET-spike groups were characterized by significant overexpression of genes mapping to chromosome 1q, and both exhibited a poor prognosis relative to the other groups. A subset of cases with a predominating myeloid gene expression signature, excluded from the profiling analyses, had more favorable baseline characteristics and superior prognosis to those lacking this signature.
AbstractList	To better define the molecular basis of multiple myeloma (MM), we performed unsupervised hierarchic clustering of mRNA expression profiles in CD138-enriched plasma cells from 414 newly diagnosed patients who went on to receive high-dose therapy and tandem stem cell transplants. Seven disease subtypes were validated that were strongly influenced by known genetic lesions, such as c-MAF- and MAFB-, CCND1- and CCND3-, and MMSET-activating translocations and hyperdiploidy. Indicative of the deregulation of common pathways by gene orthologs, common gene signatures were observed in cases with c-MAF and MAFB activation and CCND1 and CCND3 activation, the latter consisting of 2 subgroups, one characterized by expression of the early B-cell markers CD20 and PAX5. A low incidence of focal bone disease distinguished one and increased expression of proliferation-associated genes of another novel subgroup. Comprising varying fractions of each of the other 6 subgroups, the proliferation subgroup dominated at relapse, suggesting that this signature is linked to disease progression. Proliferation and MMSET-spike groups were characterized by significant overexpression of genes mapping to chromosome 1q, and both exhibited a poor prognosis relative to the other groups. A subset of cases with a predominating myeloid gene expression signature, excluded from the profiling analyses, had more favorable baseline characteristics and superior prognosis to those lacking this signature. To better define the molecular basis of multiple myeloma (MM), we performed unsupervised hierarchic clustering of mRNA expression profiles in CD138-enriched plasma cells from 414 newly diagnosed patients who went on to receive high-dose therapy and tandem stem cell transplants. Seven disease subtypes were validated that were strongly influenced by known genetic lesions, such as c-MAF- and MAFB-, CCND1- and CCND3-, and MMSET-activating translocations and hyperdiploidy. Indicative of the deregulation of common pathways by gene orthologs, common gene signatures were observed in cases with c-MAF and MAFB activation and CCND1 and CCND3 activation, the latter consisting of 2 subgroups, one characterized by expression of the early B-cell markers CD20 and PAX5. A low incidence of focal bone disease distinguished one and increased expression of proliferation-associated genes of another novel subgroup. Comprising varying fractions of each of the other 6 subgroups, the proliferation subgroup dominated at relapse, suggesting that this signature is linked to disease progression. Proliferation and MMSET-spike groups were characterized by significant overexpression of genes mapping to chromosome 1q, and both exhibited a poor prognosis relative to the other groups. A subset of cases with a predominating myeloid gene expression signature, excluded from the profiling analyses, had more favorable baseline characteristics and superior prognosis to those lacking this signature.To better define the molecular basis of multiple myeloma (MM), we performed unsupervised hierarchic clustering of mRNA expression profiles in CD138-enriched plasma cells from 414 newly diagnosed patients who went on to receive high-dose therapy and tandem stem cell transplants. Seven disease subtypes were validated that were strongly influenced by known genetic lesions, such as c-MAF- and MAFB-, CCND1- and CCND3-, and MMSET-activating translocations and hyperdiploidy. Indicative of the deregulation of common pathways by gene orthologs, common gene signatures were observed in cases with c-MAF and MAFB activation and CCND1 and CCND3 activation, the latter consisting of 2 subgroups, one characterized by expression of the early B-cell markers CD20 and PAX5. A low incidence of focal bone disease distinguished one and increased expression of proliferation-associated genes of another novel subgroup. Comprising varying fractions of each of the other 6 subgroups, the proliferation subgroup dominated at relapse, suggesting that this signature is linked to disease progression. Proliferation and MMSET-spike groups were characterized by significant overexpression of genes mapping to chromosome 1q, and both exhibited a poor prognosis relative to the other groups. A subset of cases with a predominating myeloid gene expression signature, excluded from the profiling analyses, had more favorable baseline characteristics and superior prognosis to those lacking this signature.
Author	Zhan, Fenghuang Huang, Yongsheng Epstein, Joshua Zangari, Maurizio Shaughnessy, Jr, John D Hollmig, Klaus Stewart, James P Walker, Ronald Sawyer, Jeffrey van Rhee, Frits Yaccoby, Shmuel Barlogie, Bart Gupta, Sushil Hanamura, Ichiro Pineda-Roman, Mauricio Colla, Simona Burington, Bart Tricot, Guido Anaissie, Elias Crowley, John
Author_xml	– sequence: 1 givenname: Fenghuang surname: Zhan fullname: Zhan, Fenghuang organization: Donna D. and Donald M. Lambert Laboratory of Myeloma Genetics, Myeloma Institute for Research and Therapy, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA – sequence: 2 givenname: Yongsheng surname: Huang fullname: Huang, Yongsheng – sequence: 3 givenname: Simona surname: Colla fullname: Colla, Simona – sequence: 4 givenname: James P surname: Stewart fullname: Stewart, James P – sequence: 5 givenname: Ichiro surname: Hanamura fullname: Hanamura, Ichiro – sequence: 6 givenname: Sushil surname: Gupta fullname: Gupta, Sushil – sequence: 7 givenname: Joshua surname: Epstein fullname: Epstein, Joshua – sequence: 8 givenname: Shmuel surname: Yaccoby fullname: Yaccoby, Shmuel – sequence: 9 givenname: Jeffrey surname: Sawyer fullname: Sawyer, Jeffrey – sequence: 10 givenname: Bart surname: Burington fullname: Burington, Bart – sequence: 11 givenname: Elias surname: Anaissie fullname: Anaissie, Elias – sequence: 12 givenname: Klaus surname: Hollmig fullname: Hollmig, Klaus – sequence: 13 givenname: Mauricio surname: Pineda-Roman fullname: Pineda-Roman, Mauricio – sequence: 14 givenname: Guido surname: Tricot fullname: Tricot, Guido – sequence: 15 givenname: Frits surname: van Rhee fullname: van Rhee, Frits – sequence: 16 givenname: Ronald surname: Walker fullname: Walker, Ronald – sequence: 17 givenname: Maurizio surname: Zangari fullname: Zangari, Maurizio – sequence: 18 givenname: John surname: Crowley fullname: Crowley, John – sequence: 19 givenname: Bart surname: Barlogie fullname: Barlogie, Bart – sequence: 20 givenname: John D surname: Shaughnessy, Jr fullname: Shaughnessy, Jr, John D
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/16728703$$D View this record in MEDLINE/PubMed
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Snippet	To better define the molecular basis of multiple myeloma (MM), we performed unsupervised hierarchic clustering of mRNA expression profiles in CD138-enriched...
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SubjectTerms	Chromosome Mapping Cluster Analysis Cyclin D Cyclins - genetics Data Interpretation, Statistical Gene Expression Profiling - statistics & numerical data Humans Membrane Glycoproteins - genetics Multiple Myeloma - classification Multiple Myeloma - genetics Multiple Myeloma - immunology Oligonucleotide Array Sequence Analysis - statistics & numerical data Plasma Cells - immunology Prognosis Proteoglycans - genetics RNA, Messenger - genetics RNA, Neoplasm - genetics Syndecan-1 Syndecans
Title	The molecular classification of multiple myeloma
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