PMID- 21745313
OWN - NLM
STAT- MEDLINE
DCOM- 20120312
LR  - 20131121
IS  - 1478-3231 (Electronic)
IS  - 1478-3223 (Linking)
VI  - 31
IP  - 9
DP  - 2011 Oct
TI  - Hepatic aflatoxin B1-DNA adducts and TP53 mutations in patients with 
      hepatocellular carcinoma despite low exposure to aflatoxin B1 in southern Japan.
PG  - 1366-72
LID - 10.1111/j.1478-3231.2011.02572.x [doi]
AB  - BACKGROUND & AIMS: Hepatitis B or C virus infection is considered to be the main 
      cause of hepatocellular carcinoma (HCC) in Japan. Aflatoxin B1 (AFB1) is a 
      carcinogen associated with HCC in regions with high exposure. Mutations in codon 
      249, exon 7 are a hallmark of AFB1 exposure. Therefore, to clarify the role of 
      AFB1 in hepatocarcinogenesis, we examined AFB1-DNA in liver tissue and sequenced 
      TP53 in Japanese patients with HCC. METHODS: Hepatocyte AFB1-DNA adducts were 
      determined immunohistochemically and direct sequencing of TP53 was done to 
      determine mutations in 188 of 279 patients who underwent hepatic resection for 
      HCC. We assessed hepatitis C virus antibodies (HCV Ab) and HBSAg expression; 
      patients without either were defined as having non-B non-C hepatocellular 
      carcinoma (NBNC HCC). RESULTS: AFB1-DNA adducts were detected in hepatocyte 
      nuclei in 18/279 patients (6%), including 13/83 patients (16%) with NBNC HCC and 
      5/51 patients (10%) expressing hepatitis B surface antigen. None of the patients 
      with HCV Ab (n=136) were positive for AFB1-DNA. The incidence of the G-T 
      transversion and mutations in exon 7 of TP53 in patients with AFB1-DNA adducts 
      were significantly higher in patients with than in patients without AFB1-DNA 
      adducts. All three patients with the codon 249 AGG-AGT mutation had AFB1-DNA 
      adducts. CONCLUSION: Although exposure to AFB1 is thought to be low in Japan, it 
      is still associated with hepatocarcinogenesis, particularly in NBNC HCC and 
      hepatitis B individuals.
CI  - (c) 2011 John Wiley & Sons A/S.
FAU - Shirabe, Ken
AU  - Shirabe K
AD  - Department of Surgery and Science, Graduate School of Medical Sciences, Kyushu 
      University, Fukuoka, Japan. kshirabe@surg2.med.kyushu-u.ac.jp
FAU - Toshima, Takeo
AU  - Toshima T
FAU - Taketomi, Akinobu
AU  - Taketomi A
FAU - Taguchi, Kennichi
AU  - Taguchi K
FAU - Yoshizumi, Tomoharu
AU  - Yoshizumi T
FAU - Uchiyama, Hideaki
AU  - Uchiyama H
FAU - Harimoto, Norifumi
AU  - Harimoto N
FAU - Kajiyama, Kiyoshi
AU  - Kajiyama K
FAU - Egashira, Akinori
AU  - Egashira A
FAU - Maehara, Yoshihiko
AU  - Maehara Y
LA  - eng
PT  - Journal Article
PT  - Multicenter Study
DEP - 20110628
PL  - United States
TA  - Liver Int
JT  - Liver international : official journal of the International Association for the 
      Study of the Liver
JID - 101160857
RN  - 0 (DNA Adducts)
RN  - 0 (Hepatitis B Surface Antigens)
RN  - 0 (Hepatitis C Antibodies)
RN  - 0 (TP53 protein, human)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 0 (aflatoxin B1-DNA adduct)
RN  - 9N2N2Y55MH (Aflatoxin B1)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aflatoxin B1/adverse effects/*analysis
MH  - Aged
MH  - Aged, 80 and over
MH  - Carcinoma, Hepatocellular/*chemistry/epidemiology/*genetics/pathology
MH  - Chi-Square Distribution
MH  - DNA Adducts/adverse effects/*analysis
MH  - DNA Mutational Analysis
MH  - Female
MH  - Hepatitis B Surface Antigens/blood
MH  - Hepatitis C Antibodies/blood
MH  - Humans
MH  - Immunohistochemistry
MH  - Japan/epidemiology
MH  - Liver Neoplasms/*chemistry/epidemiology/*genetics/pathology
MH  - Male
MH  - Middle Aged
MH  - *Mutation
MH  - Risk Assessment
MH  - Risk Factors
MH  - Tumor Suppressor Protein p53/*genetics
MH  - Young Adult
EDAT- 2011/07/13 06:00
MHDA- 2012/03/13 06:00
CRDT- 2011/07/13 06:00
PHST- 2011/07/13 06:00 [entrez]
PHST- 2011/07/13 06:00 [pubmed]
PHST- 2012/03/13 06:00 [medline]
AID - 10.1111/j.1478-3231.2011.02572.x [doi]
PST - ppublish
SO  - Liver Int. 2011 Oct;31(9):1366-72. doi: 10.1111/j.1478-3231.2011.02572.x. Epub 
      2011 Jun 28.