PMID- 27115168
OWN - NLM
STAT- MEDLINE
DCOM- 20171102
LR  - 20181113
IS  - 1944-7930 (Electronic)
IS  - 1539-6509 (Print)
IS  - 1539-6509 (Linking)
VI  - 21
IP  - 115
DP  - 2016 Mar
TI  - Integrating understanding of epidemiology and genomics in B-cell non-Hodgkin 
      lymphoma as a pathway to novel management strategies.
PG  - 181-8
AB  - Non-Hodgkin lymphomas include a biologically and clinically heterogeneous group 
      of cancers distinguished by genetics, histology, and treatment outcomes. New 
      discoveries regarding the genomic alterations and epidemiological exposures 
      associated with these lymphomas have enhanced our understanding of factors that 
      contribute to lymphomagenesis for specific subtypes. We explore the impact of 
      normal B-cell biology engineered for recognizing a wide variety of antigens on 
      the development of specific lymphoma subtypes, review lymphoma genetics, and 
      examine the epidemiology of B-cell NHLs including recent investigations of risk 
      factors for particular lymphoma subtypes based on large pooled analyses. Burkitt 
      lymphoma, an aggressive form of B-cell NHL involving translocation of the MYC 
      gene and an immunoglobulin gene has been associated with a history of eczema, 
      hepatitis C, and occupation as a cleaner. Increased risk of diffuse large B-cell 
      lymphoma has been associated with increased young adult body mass index, history 
      of B-cell-activating autoimmune diseases, hepatitis C, and several single 
      nucleotide variants involving the human leukocyte antigen (HLA) region of 
      chromosome 6 and non-HLA loci near EXOC2, PVT1, MYC, and NCOA1. Tumor sequencing 
      studies suggest that multiple pathways are involved in the development of DLBCL. 
      Additional studies of epidemiological exposures, genome wide associations, and 
      tumor sequencing in follicular, lymphoplasmacytic, marginal zone, and mantle cell 
      lymphoma demonstrate overlapping areas of increased risk factors and unique 
      factors for specific subtypes. Integrating these findings is important for 
      constructing comprehensive models of NHL pathogenesis, which could yield novel 
      targets for therapy and strategies for lymphoma prevention in certain 
      populations.
FAU - Glass, Samantha
AU  - Glass S
AD  - University of Illinois at Chicago School of Medicine, Chicago, IL 60607, USA.
FAU - Phan, Anh
AU  - Phan A
AD  - Lymphoma Program, Department of Hematology/Oncology, Winship Cancer Institute, 
      Emory University School of Medicine, Atlanta, GA 30322, USA.
FAU - Williams, Jessica N
AU  - Williams JN
AD  - Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
FAU - Flowers, Christopher R
AU  - Flowers CR
AD  - Lymphoma Program, Department of Hematology/Oncology, Winship Cancer Institute, 
      Emory University School of Medicine, Atlanta, GA 30322, USA.
FAU - Koff, Jean L
AU  - Koff JL
AD  - Lymphoma Program, Department of Hematology/Oncology, Winship Cancer Institute, 
      Emory University School of Medicine, Atlanta, GA 30322, USA.
LA  - eng
GR  - R21 CA158686/CA/NCI NIH HHS/United States
GR  - U01 CA195568/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Discov Med
JT  - Discovery medicine
JID - 101250006
RN  - 0 (EXOC2 protein, human)
RN  - 0 (HLA Antigens)
RN  - 0 (MYC protein, human)
RN  - 0 (PVT1 long-non-coding RNA, human)
RN  - 0 (Proto-Oncogene Proteins c-myc)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (Vesicular Transport Proteins)
RN  - EC 2.3.1.48 (NCOA1 protein, human)
RN  - EC 2.3.1.48 (Nuclear Receptor Coactivator 1)
SB  - IM
MH  - Adaptive Immunity
MH  - B-Lymphocytes/*immunology
MH  - Cell Transformation, Neoplastic/genetics
MH  - Chromosomes, Human, Pair 6/genetics
MH  - Exome
MH  - Genomics
MH  - HLA Antigens/genetics
MH  - Humans
MH  - Lymphoma, B-Cell/*epidemiology/*genetics/therapy
MH  - Lymphoma, Non-Hodgkin/*epidemiology/*genetics/therapy
MH  - Mutation
MH  - Nuclear Receptor Coactivator 1/genetics
MH  - Polymorphism, Single Nucleotide
MH  - Proto-Oncogene Proteins c-myc/genetics
MH  - RNA, Long Noncoding/genetics
MH  - Risk Factors
MH  - Sequence Analysis, DNA
MH  - Translocation, Genetic
MH  - Vesicular Transport Proteins/genetics
PMC - PMC5754270
MID - NIHMS927149
COIS- Disclosure The authors report no conflicts of interest.
EDAT- 2016/04/27 06:00
MHDA- 2017/11/03 06:00
PMCR- 2018/01/05
CRDT- 2016/04/27 06:00
PHST- 2016/04/27 06:00 [entrez]
PHST- 2016/04/27 06:00 [pubmed]
PHST- 2017/11/03 06:00 [medline]
PHST- 2018/01/05 00:00 [pmc-release]
PST - ppublish
SO  - Discov Med. 2016 Mar;21(115):181-8.