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Titolo:
A deletion in the gene for transforming growth factor beta type I receptorabolishes growth regulation by transforming growth factor beta in a cutaneous T-cell lymphoma
Autore:
Schiemann, WP; Pfeifer, WM; Levi, E; Kadin, ME; Lodish, HF;
Indirizzi:
Whitehead Inst Biomed Res, Cambridge, MA 02142 USA Whitehead Inst Biomed Res Cambridge MA USA 02142 Cambridge, MA 02142 USA Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA USA Beth Israel Deaconess Med Ctr Boston MA USA Dept Pathol, Boston, MA USA Harvard Med Sch, Boston, MA USA Harvard Med Sch Boston MA USAHarvard Med Sch, Boston, MA USA MIT, Dept Biol, Cambridge, MA USA MIT Cambridge MA USAMIT, Dept Biol, Cambridge, MA USA
Titolo Testata:
BLOOD
fascicolo: 8, volume: 94, anno: 1999,
pagine: 2854 - 2861
SICI:
0006-4971(19991015)94:8<2854:ADITGF>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
TGF-BETA; SMAD PROTEINS; CANCER CELLS; RETINOBLASTOMA CELLS; PANCREATIC-CANCER; EXPRESSION; CLONING; KINASE; INHIBITION; CARCINOMA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
63
Recensione:
Indirizzi per estratti:
Indirizzo: Lodish, HF Whitehead Inst Biomed Res, 9 Cambridge Ctr, Cambridge, MA 02142USA Whitehead Inst Biomed Res 9 Cambridge Ctr Cambridge MA USA 02142
Citazione:
W.P. Schiemann et al., "A deletion in the gene for transforming growth factor beta type I receptorabolishes growth regulation by transforming growth factor beta in a cutaneous T-cell lymphoma", BLOOD, 94(8), 1999, pp. 2854-2861

Abstract

Spontaneous regression of skin lesions is characteristic of lymphomatoid papulosis (LyP), a clonal cutaneous lymphoproliferative disorder. A minorityof LyP patients progress to anaplastic large cell lymphoma (ALCL) in whichskin lesions no longer regress and extracutaneous dissemination often occurs. In 1 such case, we developed a tumor cell line, JK cells, and show thatthese cells are resistant to the growth inhibitory effects of transforminggrowth factor beta (TGF-beta) due to the loss of cell surface expression of the TGF-beta type I receptor (T beta R-I). Reverse transcriptase-polymerase chain reaction (RI-PCR) and sequencing of JK cell T beta R-I cDNA clonesidentified a deletion that spanned the last 178 bp of exon 1, including the initiating methionine. Hybridization of a radiolabeled fragment internal to the deletion was detected in the genomes of TGF-beta-responsive cells, but not in JK cells, indicating that they contain no wild-type T beta R-I gene. PCR primers that flanked the deleted T beta R-I region amplified a single hand from JK cell genomic DNA that lacked the last 178 bp of exon 1 and all of the approximate to 5 kb of intron 1. This JK cell-specific genomic Tbeta R-I PCR product was distinct from products amplified from TGF-beta-responsive cells and was also readily detected in tumor biopsies obtained before the establishment of the JK cell line. Our results identify the first inactivating mutation in T beta R-I gene in a human lymphoma that renders itinsensitive to growth inhibition by TGF-beta. (C) 1999 by The American Society of Hematology.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 20:52:46