PMID- 24377085
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20140624
LR  - 20211021
IS  - 2234-943X (Print)
IS  - 2234-943X (Electronic)
IS  - 2234-943X (Linking)
VI  - 3
DP  - 2013 Dec 12
TI  - Genetic variation in the extended major histocompatibility complex and 
      susceptibility to childhood acute lymphoblastic leukemia: a review of the 
      evidence.
PG  - 300
LID - 10.3389/fonc.2013.00300 [doi]
LID - 300
AB  - The enduring suspicion that infections and immunologic response may play a role 
      in the etiology of childhood leukemia, particularly acute lymphoblastic leukemia 
      (ALL), is now supported, albeit still indirectly, by numerous epidemiological 
      studies. The cumulative evidence includes, for example, descriptive observations 
      of a peculiar peak incidence at age 2-5 years for ALL in economically developed 
      countries, clustering of cases in situations of population mixing associated with 
      unusual patterns of personal contacts, associations with various proxy measures 
      for immune modulatory exposures early in life, and genetic susceptibility 
      conferred by variation in genes involved in the immune system. In this review, 
      our focus is the extended major histocompatibility complex (MHC), an 
      approximately 7.6 Mb region that is well-known for its high-density of expressed 
      genes, extensive polymorphisms exhibiting complex linkage disequilibrium 
      patterns, and its disproportionately large number of immune-related genes, 
      including human leukocyte antigen (HLA). First discovered through the role they 
      play in transplant rejection, the classical HLA class I (HLA-A, -B, and -C) and 
      class II (HLA-DR, HLA-DQ, and HLA-DP) molecules reside at the epicenter of the 
      immune response pathways and are now the targets of many disease susceptibility 
      studies, including those for childhood leukemia. The genes encoding the HLA 
      molecules are only a minority of the over 250 expressed genes in the xMHC, and a 
      growing number of studies are beginning to evaluate other loci through targeted 
      investigations or utilizing a mapping approach with a comprehensive screen of the 
      entire region. Here, we review the current epidemiologic evidence available to 
      date regarding genetic variation contained within this highly unique region of 
      the genome and its relationship with childhood ALL risk.
FAU - Urayama, Kevin Y
AU  - Urayama KY
AD  - School of Public Health, University of California , Berkeley, CA , USA ; Center 
      for Clinical Epidemiology, St. Luke's Life Science Institute , Tokyo , Japan.
FAU - Thompson, Pamela D
AU  - Thompson PD
AD  - Cancer Immunogenetics, St. Mary's Hospital, University of Manchester , Manchester 
      , UK.
FAU - Taylor, Malcolm
AU  - Taylor M
AD  - Handforth , Cheshire , UK.
FAU - Trachtenberg, Elizabeth A
AU  - Trachtenberg EA
AD  - Center for Genetics, Children's Hospital Oakland Research Institute , Oakland, CA 
      , USA.
FAU - Chokkalingam, Anand P
AU  - Chokkalingam AP
AD  - School of Public Health, University of California , Berkeley, CA , USA.
LA  - eng
GR  - P01 CA111412/CA/NCI NIH HHS/United States
GR  - R01 ES009137/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20131212
PL  - Switzerland
TA  - Front Oncol
JT  - Frontiers in oncology
JID - 101568867
PMC - PMC3859964
OTO - NOTNLM
OT  - childhood leukemia
OT  - epidemiology
OT  - genetic susceptibility
OT  - human leukocyte antigen
OT  - major histocompatibility complex
EDAT- 2014/01/01 06:00
MHDA- 2014/01/01 06:01
PMCR- 2013/01/01
CRDT- 2013/12/31 06:00
PHST- 2013/08/06 00:00 [received]
PHST- 2013/11/26 00:00 [accepted]
PHST- 2013/12/31 06:00 [entrez]
PHST- 2014/01/01 06:00 [pubmed]
PHST- 2014/01/01 06:01 [medline]
PHST- 2013/01/01 00:00 [pmc-release]
AID - 10.3389/fonc.2013.00300 [doi]
PST - epublish
SO  - Front Oncol. 2013 Dec 12;3:300. doi: 10.3389/fonc.2013.00300.