PMID- 27636224
OWN - NLM
STAT- MEDLINE
DCOM- 20170721
LR  - 20180328
IS  - 1098-2264 (Electronic)
IS  - 1045-2257 (Linking)
VI  - 56
IP  - 2
DP  - 2017 Feb
TI  - Pediatric T-cell acute lymphoblastic leukemia.
PG  - 89-116
LID - 10.1002/gcc.22416 [doi]
AB  - The most common pediatric malignancy is acute lymphoblastic leukemia (ALL), of 
      which T-cell ALL (T-ALL) comprises 10-15% of cases. T-ALL arises in the thymus 
      from an immature thymocyte as a consequence of a stepwise accumulation of genetic 
      and epigenetic aberrations. Crucial biological processes, such as 
      differentiation, self-renewal capacity, proliferation, and apoptosis, are 
      targeted and deranged by several types of neoplasia-associated genetic 
      alteration, for example, translocations, deletions, and mutations of genes that 
      code for proteins involved in signaling transduction, epigenetic regulation, and 
      transcription. Epigenetically, T-ALL is characterized by gene expression changes 
      caused by hypermethylation of tumor suppressor genes, histone modifications, and 
      miRNA and lncRNA abnormalities. Although some genetic and gene expression 
      patterns have been associated with certain clinical features, such as 
      immunophenotypic subtype and outcome, none has of yet generally been implemented 
      in clinical routine for treatment decisions. The recent advent of massive 
      parallel sequencing technologies has dramatically increased our knowledge of the 
      genetic blueprint of T-ALL, revealing numerous fusion genes as well as novel gene 
      mutations. The challenges now are to integrate all genetic and epigenetic data 
      into a coherent understanding of the pathogenesis of T-ALL and to translate the 
      wealth of information gained in the last few years into clinical use in the form 
      of improved risk stratification and targeted therapies. Here, we provide an 
      overview of pediatric T-ALL with an emphasis on the acquired genetic alterations 
      that result in this disease. (c) 2016 Wiley Periodicals, Inc.
CI  - (c) 2016 Wiley Periodicals, Inc.
FAU - Karrman, Kristina
AU  - Karrman K
AD  - Department of Clinical Genetics, Office for Medical Services, Division of 
      Laboratory Medicine, Lund, Sweden.
AD  - Division of Clinical Genetics, Department of Laboratory Medicine, Lund 
      University, Lund, Sweden.
FAU - Johansson, Bertil
AU  - Johansson B
AD  - Department of Clinical Genetics, Office for Medical Services, Division of 
      Laboratory Medicine, Lund, Sweden.
AD  - Division of Clinical Genetics, Department of Laboratory Medicine, Lund 
      University, Lund, Sweden.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20161025
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
SB  - IM
MH  - Child
MH  - *DNA Methylation
MH  - *Epigenesis, Genetic
MH  - Humans
MH  - Mutation/*genetics
MH  - Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/diagnosis/*genetics/therapy
MH  - Prognosis
EDAT- 2016/10/26 06:00
MHDA- 2017/07/22 06:00
CRDT- 2016/09/17 06:00
PHST- 2016/07/01 00:00 [received]
PHST- 2016/09/06 00:00 [accepted]
PHST- 2016/10/26 06:00 [pubmed]
PHST- 2017/07/22 06:00 [medline]
PHST- 2016/09/17 06:00 [entrez]
AID - 10.1002/gcc.22416 [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2017 Feb;56(2):89-116. doi: 10.1002/gcc.22416. Epub 
      2016 Oct 25.