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Gene expression pro...
Gene expression profiling of isolated tumour cells from anaplastic large cell lymphomas : insights into its cellular origin, pathogenesis and relation to Hodgkin lymphoma
- Article/chapterEnglish2009
Publisher, publication year, extent ...
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2009-08-06
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Springer Science and Business Media LLC,2009
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printrdacarrier
Numbers
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LIBRIS-ID:oai:DiVA.org:uu-125757
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-125757URI
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https://doi.org/10.1038/leu.2009.161DOI
Supplementary language notes
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Language:English
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Summary in:English
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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Anaplastic large cell lymphoma (ALCL) is a main type of T-cell lymphomas and comprises three distinct entities: systemic anaplastic lymphoma kinase (ALK) positive, systemic ALK(-) and cutaneous ALK(-) ALCL (cALCL). Little is known about their pathogenesis and their cellular origin, and morphological and immunophenotypical overlap exists between ALK(-) ALCL and classical Hodgkin lymphoma (cHL). We conducted gene expression profiling of microdissected lymphoma cells of five ALK(+) and four ALK(-) systemic ALCL, seven cALCL and sixteen cHL, and of eight subsets of normal T and NK cells. The analysis supports a derivation of ALCL from activated T cells, but the lymphoma cells acquired a gene expression pattern hampering an assignment to a CD4(+), CD8(+) or CD30(+) T-cell origin. Indeed, ALCL display a down-modulation of many T-cell characteristic molecules. All ALCL types show significant expression of NFkappaB target genes and upregulation of genes involved in oncogenesis (e.g. EZH2). Surprisingly, few genes are differentially expressed between systemic and cALCL despite their different clinical behaviour, and between ALK(-) ALCL and cHL despite their different cellular origin. ALK(+) ALCL are characterized by expression of genes regulated by pathways constitutively activated by ALK. This study provides multiple novel insights into the molecular biology and pathogenesis of ALCL.
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Added entries (persons, corporate bodies, meetings, titles ...)
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Brune, V.
(author)
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Döring, C.
(author)
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Tiacci, E.
(author)
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Bohle, V.
(author)
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Sundström, ChristerUppsala universitet,Institutionen för genetik och patologi(Swepub:uu)chrisund
(author)
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Kodet, R.
(author)
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Paulli, M.
(author)
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Falini, B.
(author)
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Klapper, W.
(author)
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Chaubert, A. B.
(author)
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Willenbrock, K.
(author)
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Metzler, D.
(author)
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Bräuninger, A.
(author)
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Küppers, Ralf
(author)
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Hansmann, M-L.
(author)
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Uppsala universitetInstitutionen för genetik och patologi
(creator_code:org_t)
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In:Leukemia: Springer Science and Business Media LLC23:11, s. 2129-21380887-69241476-5551
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Eckerle, S.
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Brune, V.
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Döring, C.
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Tiacci, E.
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Bohle, V.
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Sundström, Chris ...
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Kodet, R.
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Paulli, M.
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Falini, B.
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Klapper, W.
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Chaubert, A. B.
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Willenbrock, K.
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Metzler, D.
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Bräuninger, A.
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Küppers, Ralf
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Hansmann, M-L.
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Leukemia
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Uppsala University