PMID- 20035814
OWN - NLM
STAT- MEDLINE
DCOM- 20100907
LR  - 20201222
IS  - 1879-1166 (Electronic)
IS  - 0198-8859 (Linking)
VI  - 71
IP  - 3
DP  - 2010 Mar
TI  - A census of predicted mutational epitopes suitable for immunologic cancer 
      control.
PG  - 245-54
LID - 10.1016/j.humimm.2009.12.007 [doi]
AB  - The adaptive immune system can protect against spontaneously arising tumors, and 
      the potential exists to reduce cancer incidence by priming adaptive immune 
      responses with vaccines. Immunologic cancer control has been implemented for 
      cancers caused by infectious agents, but not for spontaneous cancers caused by 
      mutation. This is largely due to the high cost of preventative clinical trials 
      and the lack of validated tumor epitopes. Here we evaluate, computationally, all 
      known somatic mutations in human tumors for their antigenic potential. All 
      possible human leukocyte antigen (HLA) class I presented peptides containing 
      recurrent somatic cancer mutations with frequency > 5% were screened by three 
      independent epitope prediction algorithms (SYFPEITHI, BIMAS, and IEDB). Using 
      stringent filters, a total of 20 genes, 35 mutations, and 159 candidate epitopes 
      were identified, each presented by up to four distinct HLA class I alleles. The 
      top-ranking gene from our survey was KRAS, which figures prominently because 
      there are frequent hotspot mutations in numerous, prevalent cancers, and mutant 
      peptides are predicted to be presented by several common HLA alleles. From our 
      data, we estimate that prophylactic vaccination could provide meaningful levels 
      of prevention of tumors associated with common recurrent mutations.
CI  - (c) 2010 American Society for Histocompatibility and Immunogenetics. Published by 
      Elsevier Inc. All rights reserved.
FAU - Warren, Rene L
AU  - Warren RL
AD  - British Columbia Cancer Agency, Genome Sciences Centre, Vancouver, British 
      Columbia, Canada.
FAU - Holt, Robert A
AU  - Holt RA
LA  - eng
GR  - Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100109
PL  - United States
TA  - Hum Immunol
JT  - Human immunology
JID - 8010936
RN  - 0 (Antigens, Neoplasm)
RN  - 0 (Cancer Vaccines)
RN  - 0 (Epitopes, T-Lymphocyte)
RN  - 0 (HLA Antigens)
RN  - 0 (KRAS protein, human)
RN  - 0 (Peptide Fragments)
RN  - 0 (Proto-Oncogene Proteins)
RN  - EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras))
RN  - EC 3.6.5.2 (ras Proteins)
SB  - IM
MH  - Adaptive Immunity
MH  - Algorithms
MH  - Antigen Presentation
MH  - Antigens, Neoplasm/genetics/*metabolism
MH  - *Cancer Vaccines
MH  - Computational Biology
MH  - Epitope Mapping
MH  - Epitopes, T-Lymphocyte/genetics/*metabolism
MH  - HLA Antigens/metabolism
MH  - Humans
MH  - Mutation
MH  - Peptide Fragments/genetics/*metabolism
MH  - Protein Binding/immunology
MH  - Proto-Oncogene Proteins/genetics/*metabolism
MH  - Proto-Oncogene Proteins p21(ras)
MH  - ras Proteins/genetics/*metabolism
EDAT- 2009/12/29 06:00
MHDA- 2010/09/08 06:00
CRDT- 2009/12/29 06:00
PHST- 2009/10/02 00:00 [received]
PHST- 2009/12/09 00:00 [revised]
PHST- 2009/12/17 00:00 [accepted]
PHST- 2009/12/29 06:00 [entrez]
PHST- 2009/12/29 06:00 [pubmed]
PHST- 2010/09/08 06:00 [medline]
AID - S0198-8859(09)00661-2 [pii]
AID - 10.1016/j.humimm.2009.12.007 [doi]
PST - ppublish
SO  - Hum Immunol. 2010 Mar;71(3):245-54. doi: 10.1016/j.humimm.2009.12.007. Epub 2010 
      Jan 9.