It's T-ALL about Notch

R. M. Demarest, F. Ratti, Anthony J Capobianco

Research output: Contribution to journalArticle

85 Citations (Scopus)

Abstract

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subset of ALL with poor clinical outcome compared to B-ALL. Therefore, to improve treatment, it is imperative to delineate the molecular blueprint of this disease. This review describes the central role that the Notch pathway plays in T-ALL development. We also discuss the interactions between Notch and the tumor suppressors Ikaros and p53. Loss of Ikaros, a direct repressor of Notch target genes, and suppression of p53-mediated apoptosis are essential for development of this neoplasm. In addition to the activating mutations of Notch previously described, this review will outline combinations of mutations in pathways that contribute to Notch signaling and appear to drive T-ALL development by 'mimicking' Notch effects on cell cycle and apoptosis.

Original languageEnglish
Pages (from-to)5082-5091
Number of pages10
JournalOncogene
Volume27
Issue number38
DOIs
StatePublished - Sep 1 2008
Externally publishedYes

Fingerprint

Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
Apoptosis
Mutation
p53 Genes
Neoplasms
Cell Cycle

Keywords

  • C-myc
  • CSL
  • Fbw7
  • Ikaros
  • p53
  • PTEN

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research
  • Genetics

Cite this

Demarest, R. M., Ratti, F., & Capobianco, A. J. (2008). It's T-ALL about Notch. Oncogene, 27(38), 5082-5091. https://doi.org/10.1038/onc.2008.222

It's T-ALL about Notch. / Demarest, R. M.; Ratti, F.; Capobianco, Anthony J.

In: Oncogene, Vol. 27, No. 38, 01.09.2008, p. 5082-5091.

Research output: Contribution to journalArticle

Demarest, RM, Ratti, F & Capobianco, AJ 2008, 'It's T-ALL about Notch', Oncogene, vol. 27, no. 38, pp. 5082-5091. https://doi.org/10.1038/onc.2008.222
Demarest RM, Ratti F, Capobianco AJ. It's T-ALL about Notch. Oncogene. 2008 Sep 1;27(38):5082-5091. https://doi.org/10.1038/onc.2008.222
Demarest, R. M. ; Ratti, F. ; Capobianco, Anthony J. / It's T-ALL about Notch. In: Oncogene. 2008 ; Vol. 27, No. 38. pp. 5082-5091.
@article{0eb7ec4deb834cac8fd0ec4322768e61,
title = "It's T-ALL about Notch",
abstract = "T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subset of ALL with poor clinical outcome compared to B-ALL. Therefore, to improve treatment, it is imperative to delineate the molecular blueprint of this disease. This review describes the central role that the Notch pathway plays in T-ALL development. We also discuss the interactions between Notch and the tumor suppressors Ikaros and p53. Loss of Ikaros, a direct repressor of Notch target genes, and suppression of p53-mediated apoptosis are essential for development of this neoplasm. In addition to the activating mutations of Notch previously described, this review will outline combinations of mutations in pathways that contribute to Notch signaling and appear to drive T-ALL development by 'mimicking' Notch effects on cell cycle and apoptosis.",
keywords = "C-myc, CSL, Fbw7, Ikaros, p53, PTEN",
author = "Demarest, {R. M.} and F. Ratti and Capobianco, {Anthony J}",
year = "2008",
month = "9",
day = "1",
doi = "10.1038/onc.2008.222",
language = "English",
volume = "27",
pages = "5082--5091",
journal = "Oncogene",
issn = "0950-9232",
publisher = "Nature Publishing Group",
number = "38",

}

TY - JOUR

T1 - It's T-ALL about Notch

AU - Demarest, R. M.

AU - Ratti, F.

AU - Capobianco, Anthony J

PY - 2008/9/1

Y1 - 2008/9/1

N2 - T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subset of ALL with poor clinical outcome compared to B-ALL. Therefore, to improve treatment, it is imperative to delineate the molecular blueprint of this disease. This review describes the central role that the Notch pathway plays in T-ALL development. We also discuss the interactions between Notch and the tumor suppressors Ikaros and p53. Loss of Ikaros, a direct repressor of Notch target genes, and suppression of p53-mediated apoptosis are essential for development of this neoplasm. In addition to the activating mutations of Notch previously described, this review will outline combinations of mutations in pathways that contribute to Notch signaling and appear to drive T-ALL development by 'mimicking' Notch effects on cell cycle and apoptosis.

AB - T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subset of ALL with poor clinical outcome compared to B-ALL. Therefore, to improve treatment, it is imperative to delineate the molecular blueprint of this disease. This review describes the central role that the Notch pathway plays in T-ALL development. We also discuss the interactions between Notch and the tumor suppressors Ikaros and p53. Loss of Ikaros, a direct repressor of Notch target genes, and suppression of p53-mediated apoptosis are essential for development of this neoplasm. In addition to the activating mutations of Notch previously described, this review will outline combinations of mutations in pathways that contribute to Notch signaling and appear to drive T-ALL development by 'mimicking' Notch effects on cell cycle and apoptosis.

KW - C-myc

KW - CSL

KW - Fbw7

KW - Ikaros

KW - p53

KW - PTEN

UR - http://www.scopus.com/inward/record.url?scp=50849085425&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=50849085425&partnerID=8YFLogxK

U2 - 10.1038/onc.2008.222

DO - 10.1038/onc.2008.222

M3 - Article

C2 - 18758476

AN - SCOPUS:50849085425

VL - 27

SP - 5082

EP - 5091

JO - Oncogene

JF - Oncogene

SN - 0950-9232

IS - 38

ER -