Leukemia propagating cells Akt up

Alejandro Gutierrez; Justine E Roderick; Michelle A Kelliher

doi:10.1016/j.ccr.2014.02.022

Leukemia propagating cells Akt up

Cancer Cell. 2014 Mar 17;25(3):263-5. doi: 10.1016/j.ccr.2014.02.022.

Authors

Alejandro Gutierrez¹, Justine E Roderick², Michelle A Kelliher³

Affiliations

¹ Division of Hematology/Oncology, Boston Children's Hospital, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA 02115, USA. Electronic address: alejandro.gutierrez@childrens.harvard.edu.
² Department of Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
³ Department of Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA. Electronic address: michelle.kelliher@umassmed.edu.

PMID: 24651006
DOI: 10.1016/j.ccr.2014.02.022

Abstract

Individual cancer cells can exhibit striking differences in tumorigenic potential following experimental transplantation, but the molecular pathways that regulate this activity remain poorly understood. In this issue of Cancer Cell, Blackburn and colleagues report that Akt signaling regulates both leukemia-propagating potential and proliferation rate via distinct pathways in T-ALL.

Publication types

Comment

MeSH terms

Animals
Clonal Evolution / genetics*
Humans
Mechanistic Target of Rapamycin Complex 1
Multiprotein Complexes / metabolism*
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / metabolism*
Proto-Oncogene Proteins c-akt / metabolism*
Proto-Oncogene Proteins c-myc / metabolism*
TOR Serine-Threonine Kinases / metabolism*

Substances

Multiprotein Complexes
Proto-Oncogene Proteins c-myc
Mechanistic Target of Rapamycin Complex 1
Proto-Oncogene Proteins c-akt
TOR Serine-Threonine Kinases

Grants and funding

R01 CA096899/CA/NCI NIH HHS/United States