PMID- 23603458
OWN - NLM
STAT- MEDLINE
DCOM- 20130730
LR  - 20161126
IS  - 0006-3002 (Print)
IS  - 0006-3002 (Linking)
VI  - 1836
IP  - 1
DP  - 2013 Aug
TI  - Importance of epigenetic changes in cancer etiology, pathogenesis, clinical 
      profiling, and treatment: what can be learned from hematologic malignancies?
PG  - 90-104
LID - S0304-419X(13)00021-8 [pii]
LID - 10.1016/j.bbcan.2013.04.001 [doi]
AB  - Epigenetic alterations represent a key cancer hallmark, even in hematologic 
      malignancies (HMs) or blood cancers, whose clinical features display a high 
      inter-individual variability. Evidence accumulated in recent years indicates that 
      inactivating DNA hypermethylation preferentially targets the subset of polycomb 
      group (PcG) genes that are regulators of developmental processes. Conversely, 
      activating DNA hypomethylation targets oncogenic signaling pathway genes, but 
      outcomes of both events lead in the overexpression of oncogenic signaling 
      pathways that contribute to the stem-like state of cancer cells. On the basis of 
      recent evidence from population-based, clinical and experimental studies, we 
      hypothesize that factors associated with risk for developing a HM, such as 
      metabolic syndrome and chronic inflammation, trigger epigenetic mechanisms to 
      increase the transcriptional expression of oncogenes and activate oncogenic 
      signaling pathways. Among others, signaling pathways associated with such risk 
      factors include pro-inflammatory nuclear factor kappaB (NF-kappaB), and mitogenic, 
      growth, and survival Janus kinase (JAK) intracellular non-receptor tyrosine 
      kinase-triggered pathways, which include signaling pathways such as transducer 
      and activator of transcription (STAT), Ras GTPases/mitogen-activated protein 
      kinases (MAPKs)/extracellular signal-related kinases (ERKs), phosphatidylinositol 
      3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR), and beta-catenin pathways. 
      Recent findings on epigenetic mechanisms at work in HMs and their importance in 
      the etiology and pathogenesis of these diseases are herein summarized and 
      discussed. Furthermore, the role of epigenetic processes in the determination of 
      biological identity, the consequences for interindividual variability in disease 
      clinical profile, and the potential of epigenetic drugs in HMs are also 
      considered.
CI  - Copyright (c) 2013 Elsevier B.V. All rights reserved.
FAU - Vecchio, Lorella
AU  - Vecchio L
AD  - Laboratory of Cytometry, Institute of Molecular Genetics, CNR, University of 
      Pavia, 27100 Pavia, Italy.
FAU - Seke Etet, Paul Faustin
AU  - Seke Etet PF
FAU - Kipanyula, Maulilio John
AU  - Kipanyula MJ
FAU - Krampera, Mauro
AU  - Krampera M
FAU - Nwabo Kamdje, Armel Herve
AU  - Nwabo Kamdje AH
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20130417
PL  - Netherlands
TA  - Biochim Biophys Acta
JT  - Biochimica et biophysica acta
JID - 0217513
SB  - IM
MH  - Animals
MH  - Cell Transformation, Neoplastic/*pathology
MH  - *Epigenomics
MH  - *Gene Expression Profiling
MH  - Hematologic Neoplasms/*etiology/pathology/*therapy
MH  - Humans
EDAT- 2013/04/23 06:00
MHDA- 2013/07/31 06:00
CRDT- 2013/04/23 06:00
PHST- 2012/10/25 00:00 [received]
PHST- 2013/01/25 00:00 [revised]
PHST- 2013/04/10 00:00 [accepted]
PHST- 2013/04/23 06:00 [entrez]
PHST- 2013/04/23 06:00 [pubmed]
PHST- 2013/07/31 06:00 [medline]
AID - S0304-419X(13)00021-8 [pii]
AID - 10.1016/j.bbcan.2013.04.001 [doi]
PST - ppublish
SO  - Biochim Biophys Acta. 2013 Aug;1836(1):90-104. doi: 10.1016/j.bbcan.2013.04.001. 
      Epub 2013 Apr 17.