PMID- 34386081
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210814
IS  - 1792-1082 (Electronic)
IS  - 1792-1074 (Print)
IS  - 1792-1074 (Linking)
VI  - 22
IP  - 3
DP  - 2021 Sep
TI  - Role of CXCL12, TP53 and CYP1A1 gene polymorphisms in susceptibility to pediatric 
      acute lymphoblastic leukemia.
PG  - 659
LID - 10.3892/ol.2021.12920 [doi]
LID - 659
AB  - Acute lymphoblastic leukemia (ALL) is the most common type of childhood leukemia 
      and represents one third of all pediatric malignancies. Epidemiological studies 
      have shown that various genetic factors play a crucial role in leukemogenesis. 
      Recent genetic association studies on cancer risk have focused on the effects of 
      single-nucleotide polymorphisms (SNPs) in genes that regulate inflammation and 
      tumor suppression, such as chemokines, TP53 and cytochrome P450s (CYPs). Genetic 
      polymorphisms in the 3' untranslated region of the C-X-C motif chemokine ligand 
      12 (CXCL12; rs1801157) and TP53 (rs1042522) genes have been suggested to 
      influence the risk of ALL in children, while other studies have indicated an 
      association between the CYP1 subfamily A member 1 (CYP1A1)*2C (rs1048943) allele 
      and leukemia risk. The aim of the present study was to investigate the possible 
      association of rs1801157 (CXCL12), rs1042522 (TP53) and rs1048943 (CYP1A1*2C) 
      SNPs with an increased susceptibility of developing ALL. These SNPs were analyzed 
      in 86 children or adolescent patients with ALL and 125 control subjects by 
      PCR-restriction fragment length polymorphism and allelic-specific chain reaction 
      techniques. A higher frequency of CYP1A1*2C heterozygotes and TP53 rare 
      homozygotes, which include the proline (Pro)/Pro genotype, was observed among 
      children with ALL and control subjects, whereas no significant differences were 
      observed for the CXCL12 SNP. Furthermore, the analysis of various allelic 
      combinations of the aforementioned gene polymorphisms demonstrated a markedly 
      increased risk of developing ALL in children. In conclusion, the present study 
      demonstrated that there was a strong association between CYP1A1*2C heterozygotes, 
      as well as the TP53 Pro/Pro genotype, and an increased susceptibility for 
      pediatric ALL in Caucasians.
CI  - Copyright (c) 2021, Spandidos Publications.
FAU - Kampouraki, Eleni
AU  - Kampouraki E
AD  - Department of Pediatric Hematology-Oncology, University Hospital of Heraklion and 
      Laboratory of Blood Diseases and Childhood Cancer Biology, Medical School, 
      University of Crete, 71003 Heraklion, Greece.
FAU - Lourou, Marilena
AU  - Lourou M
AD  - Department of Pediatric Hematology-Oncology, University Hospital of Heraklion and 
      Laboratory of Blood Diseases and Childhood Cancer Biology, Medical School, 
      University of Crete, 71003 Heraklion, Greece.
FAU - Zervou, Maria I
AU  - Zervou MI
AD  - Section of Molecular Pathology and Human Genetics, Department of Internal 
      Medicine, Medical School of Crete, University of Crete, 71003 Heraklion, Greece.
FAU - Ampazoglou, Evangelia-Dimitra
AU  - Ampazoglou ED
AD  - Department of Pediatric Hematology-Oncology, University Hospital of Heraklion and 
      Laboratory of Blood Diseases and Childhood Cancer Biology, Medical School, 
      University of Crete, 71003 Heraklion, Greece.
FAU - Yachnakis, Emmanuel
AU  - Yachnakis E
AD  - Laboratory of Bio-Medical Data Analyses, Digital Applications and 
      Interdisciplinary Approaches, University of Crete, 71003 Heraklion, Greece.
FAU - Katzilakis, Nikolaos
AU  - Katzilakis N
AD  - Department of Pediatric Hematology-Oncology, University Hospital of Heraklion and 
      Laboratory of Blood Diseases and Childhood Cancer Biology, Medical School, 
      University of Crete, 71003 Heraklion, Greece.
FAU - Goulielmos, George N
AU  - Goulielmos GN
AD  - Section of Molecular Pathology and Human Genetics, Department of Internal 
      Medicine, Medical School of Crete, University of Crete, 71003 Heraklion, Greece.
FAU - Stiakaki, Eftichia
AU  - Stiakaki E
AD  - Department of Pediatric Hematology-Oncology, University Hospital of Heraklion and 
      Laboratory of Blood Diseases and Childhood Cancer Biology, Medical School, 
      University of Crete, 71003 Heraklion, Greece.
LA  - eng
PT  - Journal Article
DEP - 20210713
PL  - Greece
TA  - Oncol Lett
JT  - Oncology letters
JID - 101531236
PMC - PMC8299027
OTO - NOTNLM
OT  - CXCL12
OT  - CYP1A1
OT  - TP53
OT  - acute lymphoblastic leukemia
OT  - pediatric
OT  - polymorphisms
COIS- The authors declare that they have no competing interests.
EDAT- 2021/08/14 06:00
MHDA- 2021/08/14 06:01
PMCR- 2021/07/13
CRDT- 2021/08/13 07:07
PHST- 2021/03/22 00:00 [received]
PHST- 2021/05/26 00:00 [accepted]
PHST- 2021/08/13 07:07 [entrez]
PHST- 2021/08/14 06:00 [pubmed]
PHST- 2021/08/14 06:01 [medline]
PHST- 2021/07/13 00:00 [pmc-release]
AID - OL-0-0-12920 [pii]
AID - 10.3892/ol.2021.12920 [doi]
PST - ppublish
SO  - Oncol Lett. 2021 Sep;22(3):659. doi: 10.3892/ol.2021.12920. Epub 2021 Jul 13.