PMID- 20587590
OWN - NLM
STAT- MEDLINE
DCOM- 20101202
LR  - 20100813
IS  - 1557-3265 (Electronic)
IS  - 1078-0432 (Linking)
VI  - 16
IP  - 16
DP  - 2010 Aug 15
TI  - NF1 inactivation revs up Ras in adult acute myelogenous leukemia.
PG  - 4074-6
LID - 10.1158/1078-0432.CCR-10-1438 [doi]
AB  - Mutations in the Ras pathway are common in myeloid malignancies. NF1, a tumor 
      suppressor and negative regulator of Ras, is inactivated in a subset of adult 
      acute myelogenous leukemia (AML) cases. Loss of NF1 function sensitizes cells to 
      inhibition of mammalian target of rapamycin (mTOR), a downstream effector of Ras 
      activation, highlighting a potential therapeutic opportunity for some AML 
      patients.
FAU - Mullally, Ann
AU  - Mullally A
AD  - Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 
      Boston, MA, USA.
FAU - Ebert, Benjamin L
AU  - Ebert BL
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20100629
PL  - United States
TA  - Clin Cancer Res
JT  - Clinical cancer research : an official journal of the American Association for 
      Cancer Research
JID - 9502500
RN  - EC 3.6.5.2 (ras Proteins)
SB  - IM
CIN - Clin Cancer Res. 2010 Aug 15;16(16):4135-47. PMID: 20505189
MH  - Adult
MH  - Gene Expression
MH  - Gene Expression Regulation, Neoplastic/*genetics
MH  - Gene Silencing
MH  - *Genes, Neurofibromatosis 1
MH  - Humans
MH  - Leukemia, Myeloid, Acute/*genetics
MH  - Signal Transduction/*genetics
MH  - ras Proteins/*biosynthesis
EDAT- 2010/07/01 06:00
MHDA- 2010/12/14 06:00
CRDT- 2010/07/01 06:00
PHST- 2010/07/01 06:00 [entrez]
PHST- 2010/07/01 06:00 [pubmed]
PHST- 2010/12/14 06:00 [medline]
AID - 1078-0432.CCR-10-1438 [pii]
AID - 10.1158/1078-0432.CCR-10-1438 [doi]
PST - ppublish
SO  - Clin Cancer Res. 2010 Aug 15;16(16):4074-6. doi: 10.1158/1078-0432.CCR-10-1438. 
      Epub 2010 Jun 29.