PMID- 26892781
OWN - NLM
STAT- MEDLINE
DCOM- 20160812
LR  - 20181113
IS  - 1420-9071 (Electronic)
IS  - 1420-682X (Linking)
VI  - 73
IP  - 9
DP  - 2016 May
TI  - The renewed battle against RAS-mutant cancers.
PG  - 1845-58
LID - 10.1007/s00018-016-2155-8 [doi]
AB  - The RAS genes encode for members of a large superfamily of 
      guanosine-5'-triphosphate (GTP)-binding proteins that control diverse 
      intracellular signaling pathways to promote cell proliferation. Somatic mutations 
      in the RAS oncogenes are the most common activating lesions found in human 
      cancers. These mutations invariably result in the gain-of-function of RAS by 
      impairing GTP hydrolysis and are frequently associated with poor responses to 
      standard cancer therapies. In this review, we summarize key findings of past and 
      present landmark studies that have deepened our understanding of the RAS biology 
      in the context of oncogenesis. We also discuss how emerging areas of research 
      could further bolster a renewed global effort to target the largely undruggable 
      oncogenic RAS and/or its activated downstream effector signaling cascades to 
      achieve better treatment outcomes for RAS-mutant cancer patients.
FAU - Zhang, Fuquan
AU  - Zhang F
AD  - Programme in Cancer and Stem Cell Biology, Duke-NUS Medical School, 8 College 
      Road, Singapore, 169857, Singapore.
FAU - Cheong, Jit Kong
AU  - Cheong JK
AUID- ORCID: 0000-0002-2658-5436
AD  - Programme in Cancer and Stem Cell Biology, Duke-NUS Medical School, 8 College 
      Road, Singapore, 169857, Singapore. jitkong.cheong@duke-nus.edu.sg.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20160218
PL  - Switzerland
TA  - Cell Mol Life Sci
JT  - Cellular and molecular life sciences : CMLS
JID - 9705402
RN  - 86-01-1 (Guanosine Triphosphate)
RN  - EC 3.6.5.2 (ras Proteins)
SB  - IM
MH  - Animals
MH  - Autophagy
MH  - Cell Transformation, Neoplastic
MH  - Guanosine Triphosphate/metabolism
MH  - Humans
MH  - Mutation
MH  - Neoplasms/metabolism/*pathology
MH  - Signal Transduction
MH  - ras Proteins/genetics/*metabolism
OTO - NOTNLM
OT  - Autophagy
OT  - Cancer therapeutics
OT  - HRAS
OT  - KRAS
OT  - Kinases
OT  - NRAS
OT  - Signaling
OT  - Small GTPases
EDAT- 2016/02/20 06:00
MHDA- 2016/08/16 06:00
CRDT- 2016/02/20 06:00
PHST- 2015/11/27 00:00 [received]
PHST- 2016/02/01 00:00 [accepted]
PHST- 2016/01/28 00:00 [revised]
PHST- 2016/02/20 06:00 [entrez]
PHST- 2016/02/20 06:00 [pubmed]
PHST- 2016/08/16 06:00 [medline]
AID - 10.1007/s00018-016-2155-8 [pii]
AID - 10.1007/s00018-016-2155-8 [doi]
PST - ppublish
SO  - Cell Mol Life Sci. 2016 May;73(9):1845-58. doi: 10.1007/s00018-016-2155-8. Epub 
      2016 Feb 18.