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Titolo:
Quantitative effects of Nf1 inactivation on in vivo hematopoiesis
Autore:
Zhang, YY; Taylor, BR; Shannon, K; Clapp, DW;
Indirizzi:
Indiana Univ, Sch Med, Wells Ctr Pediat Res, Indianapolis, IN 46223 USA Indiana Univ Indianapolis IN USA 46223 at Res, Indianapolis, IN 46223 USA Indiana Univ, Sch Med, Dept Pediat, Indianapolis, IN 46223 USA Indiana Univ Indianapolis IN USA 46223 Pediat, Indianapolis, IN 46223 USA Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Indiana Univ, Sch Med, Dept Microbiol & Immunol, Indianapolis, IN 46202 USA Indiana Univ Indianapolis IN USA 46202 mmunol, Indianapolis, IN 46202 USA
Titolo Testata:
JOURNAL OF CLINICAL INVESTIGATION
fascicolo: 5, volume: 108, anno: 2001,
pagine: 709 - 715
SICI:
0021-9738(200109)108:5<709:QEONIO>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
JUVENILE MYELOMONOCYTIC LEUKEMIA; MALIGNANT MYELOID DISORDERS; CHRONIC MYELOGENOUS LEUKEMIA; COLONY-STIMULATING FACTOR; NEUROFIBROMATOSIS TYPE-1; STEM-CELL; BONE-MARROW; IN-VIVO; RAS; CHILDREN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Clapp, DW Inst Canc Res, 1044 W Walnut St, Indianapolis, IN 46202 USA InstCanc Res 1044 W Walnut St Indianapolis IN USA 46202 202 USA
Citazione:
Y.Y. Zhang et al., "Quantitative effects of Nf1 inactivation on in vivo hematopoiesis", J CLIN INV, 108(5), 2001, pp. 709-715

Abstract

The NF1 tumor-suppressor gene is frequently inactivated in juvenile myelomonocytic leukemia, and Nf1 mutant mice model this myeloproliferative disorder (MPD). Competitive repopulation assays were performed to quantify the proliferative advantage of Nf1(-/-) hematopoietic cells in vivo. Nf1 mutant stem cells demonstrated a growth advantage that was greatest in myeloid lineage cells and least pronounced in T lymphocytes. Surprisingly, although lownumbers of Nf1-deficient cells consistently outcompeted wild-type cells, levels of chimerism were stable over months of observation, and MPD was not observed unless threshold numbers of mutant cells were injected. These datashowing that normal competitor cells can strongly modulate the growth of mutant populations in vivo have general implications for modeling cancer in the mouse. In particular, strains in which cancer-associated mutations are expressed in fields of target cells may not accurately model early events in tumorigenesis because they eliminate the requirement for a mutant clone to outcompete resident normal cells.

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Documento generato il 01/12/20 alle ore 06:46:17