PMID- 26284269
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20150818
LR  - 20190722
IS  - 1532-8392 (Electronic)
IS  - 0046-8177 (Linking)
VI  - 46
IP  - 7
DP  - 2015 Jul
TI  - ARID2, p110alpha, p53, and beta-catenin protein expression in hepatocellular carcinoma 
      and clinicopathologic implications.
PG  - 1068-77
AB  - ARID2 (ARID2), CTNNB1 (beta catenin), tumor protein 53 (p53), and PIK3CA (p110alpha) 
      mutations are implicated in hepatocellular carcinoma (HCC); and previous work has 
      contributed to thorough molecular characterization of these events. However, 
      studies that assess the impact of these mutations on downstream protein 
      expression, especially those that evaluate all 4 cancer markers simultaneously, 
      are relatively lacking. Hence, the present study uses immunohistochemistry to 
      assess protein expression patterns of ARID2, beta-catenin, p53, and p110alpha in HCCs 
      and adjacent nonneoplastic cirrhotic tissues from 58 explanted livers. Notably, 
      this study is the first to our knowledge to investigate ARID2 protein expression 
      in the liver. The frequency of ARID2 mutations detected using our 
      immunohistochemistry method was similar to that reported in previous molecular 
      studies. Furthermore, we found that loss of ARID2 protein expression may be 
      associated with recurrence, although further studies must be done to validate 
      these findings in a larger population. We found that expression patterns of the 4 
      cancer markers were independent of each other, suggesting separate pathways of 
      hepatocarcinogenesis. We also did not observe an association between viral 
      etiology and protein expression. Consistent with previous studies, overexpression 
      of p53 correlated with poor differentiation. Lastly, 17.5% of HCCs paradoxically 
      had diffuse loss of the oncoprotein p110alpha compared with strong expression in 
      background cirrhotic liver. The exact mechanism is unclear, but enigmatic loss of 
      oncoprotein function has been described in other carcinomas and could potentially 
      have significant implications for the use of mechanistic target of rapamycin 
      (mTOR) drug therapies.
FAU - You, Jason
AU  - You J
FAU - Yang, Hushan
AU  - Yang H
FAU - Lai, Yinzhi
AU  - Lai Y
FAU - Simon, Lindsay
AU  - Simon L
FAU - Au, Jen
AU  - Au J
FAU - Burkart, Ashlie L
AU  - Burkart AL
LA  - eng
GR  - R03 CA153099/CA/NCI NIH HHS/United States
GR  - R21 CA159047/CA/NCI NIH HHS/United States
PT  - Published Erratum
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Hum Pathol
JT  - Human pathology
JID - 9421547
EFR - Hum Pathol. 2015 Apr;46(4):583-92. PMID: 25701229
EDAT- 2015/08/19 06:00
MHDA- 2015/08/19 06:01
CRDT- 2015/08/19 06:00
PHST- 2015/08/19 06:00 [entrez]
PHST- 2015/08/19 06:00 [pubmed]
PHST- 2015/08/19 06:01 [medline]
AID - S0046-8177(15)00162-8 [pii]
AID - 10.1016/j.humpath.2015.05.005 [doi]
PST - ppublish
SO  - Hum Pathol. 2015 Jul;46(7):1068-77. doi: 10.1016/j.humpath.2015.05.005.