Burkitt Lymphoma: Much More than MYC

David Dominguez-Sola; Riccardo Dalla-Favera

doi:10.1016/j.ccr.2012.07.018

Burkitt Lymphoma: Much More than MYC

David Dominguez-Sola, Riccardo Dalla-Favera

Research output: Contribution to journal › Short survey › peer-review

13 Scopus citations

Abstract

Chromosomal translocations causing deregulated c-MYC expression are detectable in most Burkitt lymphoma cases. However, little is known about the additional lesions necessary for lymphomagenesis. Now, two independent studies, one of which was performed by Sander et al. in this issue of Cancer Cell, identify constitutive PI3K signaling and CyclinD3 mutations as cooperating lesions in both mice and humans. The results have directly actionable therapeutic implications.

Original language	English
Pages (from-to)	141-142
Number of pages	2
Journal	Cancer Cell
Volume	22
Issue number	2
DOIs	https://doi.org/10.1016/j.ccr.2012.07.018
State	Published - 14 Aug 2012
Externally published	Yes

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title = "Burkitt Lymphoma: Much More than MYC",

abstract = "Chromosomal translocations causing deregulated c-MYC expression are detectable in most Burkitt lymphoma cases. However, little is known about the additional lesions necessary for lymphomagenesis. Now, two independent studies, one of which was performed by Sander et al. in this issue of Cancer Cell, identify constitutive PI3K signaling and CyclinD3 mutations as cooperating lesions in both mice and humans. The results have directly actionable therapeutic implications.",

author = "David Dominguez-Sola and Riccardo Dalla-Favera",

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T2 - Much More than MYC

AU - Dominguez-Sola, David

AU - Dalla-Favera, Riccardo

PY - 2012/8/14

Y1 - 2012/8/14

N2 - Chromosomal translocations causing deregulated c-MYC expression are detectable in most Burkitt lymphoma cases. However, little is known about the additional lesions necessary for lymphomagenesis. Now, two independent studies, one of which was performed by Sander et al. in this issue of Cancer Cell, identify constitutive PI3K signaling and CyclinD3 mutations as cooperating lesions in both mice and humans. The results have directly actionable therapeutic implications.

AB - Chromosomal translocations causing deregulated c-MYC expression are detectable in most Burkitt lymphoma cases. However, little is known about the additional lesions necessary for lymphomagenesis. Now, two independent studies, one of which was performed by Sander et al. in this issue of Cancer Cell, identify constitutive PI3K signaling and CyclinD3 mutations as cooperating lesions in both mice and humans. The results have directly actionable therapeutic implications.

UR - https://www.scopus.com/pages/publications/84865148346

U2 - 10.1016/j.ccr.2012.07.018

DO - 10.1016/j.ccr.2012.07.018

M3 - Short survey

C2 - 22897844

AN - SCOPUS:84865148346

SN - 1535-6108

VL - 22

SP - 141

EP - 142

JO - Cancer Cell

JF - Cancer Cell

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ER -

Burkitt Lymphoma: Much More than MYC

Abstract

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