PMID- 21156243
OWN - NLM
STAT- MEDLINE
DCOM- 20110104
LR  - 20101215
IS  - 1873-4456 (Electronic)
IS  - 0165-4608 (Linking)
VI  - 203
IP  - 2
DP  - 2010 Dec
TI  - Correlation between clinical characteristics, survival and genetic alterations in 
      patients with hepatocellular carcinoma from Saudi Arabia.
PG  - 269-77
LID - 10.1016/j.cancergencyto.2010.08.011 [doi]
AB  - Amplification of the two oncogenes ERBB2 and MYC and deletion of the tumor 
      suppressor gene TP53 are frequently encountered in cancerous tissues. The purpose 
      of this study was to use the fluorescence in situ hybridization (FISH) technique 
      for the assessment of ERBB2 and MYC amplification and TP53 deletion, and to 
      relate these molecular markers to clinical and pathologic factors in Saudi 
      patients with hepatocellular carcinoma. The study was conducted on 40 
      paraffin-embedded tissue samples originally taken from either hepatitis C virus 
      (HCV)- or HBV-infected patients using the FISH technique. The level of ERBB2, 
      MYC, and TP53 in the malignant group was significantly increased as compared to 
      the control group. Of the 40 patients, 3 (7.5%) had amplification of ERBB2 gene, 
      4 (10%) different patients had amplification of MYC, and 26 patients (65%) had 
      evidence of deletion of at least one allele on chromosome 17 for the TP53 gene in 
      a high proportion of cells. There was a significant correlation between 
      amplification of MYC oncogene and the number of tumor masses. Moreover, 
      significant correlation was observed between poorly differentiated tumors when 
      compared with moderate or well-differentiated tumors when MYC was analyzed. On 
      the other hand, MYC failed to reveal any significant association between oncogene 
      amplification and other clinicopathologic variables examined. Univariate analysis 
      revealed a strong association between deletion of TP53 and multiple tumor mass 
      (P< 0.001). No statistical correlation could be detected between deletion of TP53 
      and tumor size, grade, stage, and tumor differentiation. No significant 
      difference could be detected in the mean survival time of patients positive for 
      the alteration of the genes compared to the patients who showed no alterations 
      for the same genes. However, when the stage of the tumor was analyzed, there was 
      a significant difference in the mean survival time between patients who showed 
      gene alterations compared to patients with no changes in the studied genes. When 
      overall survival was analyzed, only patients with MYC amplification had a lower 
      median survival (20.75 months) than patients without MYC amplification (35.82, P 
      = 0.009). Genetic alterations of ERBB2 and TP53 genes had no effect on survival 2 
      (see Results). The combination of ERBB2, MYC, and TP53 could be useful markers to 
      stratify patients into different risk groups.
CI  - Copyright (c) 2010 Elsevier Inc. All rights reserved.
FAU - Al-Qahtani, Ahmed
AU  - Al-Qahtani A
AD  - Biological and Medical Research MBC 03, King Faisal Specialist Hospital and 
      Research Centre, Box 3344 MBC-03, Riyadh 11211, Saudi Arabia.
FAU - Al-Hazzani, Tahani
AU  - Al-Hazzani T
FAU - Al-hussain, Turki
AU  - Al-hussain T
FAU - Al-Ghamdi, Abdulmonem
AU  - Al-Ghamdi A
FAU - Al-Mana, Hadeel
AU  - Al-Mana H
FAU - Al-Arifi, Saud
AU  - Al-Arifi S
FAU - Al-Ahdal, Mohammed
AU  - Al-Ahdal M
FAU - Aly, Magdy
AU  - Aly M
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Cancer Genet Cytogenet
JT  - Cancer genetics and cytogenetics
JID - 7909240
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Alleles
MH  - Biopsy
MH  - Carcinoma, Hepatocellular/ethnology/*genetics/mortality
MH  - Gene Deletion
MH  - Genes, myc
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Liver/pathology
MH  - Liver Neoplasms/ethnology/*genetics/mortality
MH  - Middle Aged
MH  - Saudi Arabia
MH  - Treatment Outcome
EDAT- 2010/12/16 06:00
MHDA- 2011/01/05 06:00
CRDT- 2010/12/16 06:00
PHST- 2010/06/16 00:00 [received]
PHST- 2010/07/30 00:00 [revised]
PHST- 2010/08/08 00:00 [accepted]
PHST- 2010/12/16 06:00 [entrez]
PHST- 2010/12/16 06:00 [pubmed]
PHST- 2011/01/05 06:00 [medline]
AID - S0165-4608(10)00453-X [pii]
AID - 10.1016/j.cancergencyto.2010.08.011 [doi]
PST - ppublish
SO  - Cancer Genet Cytogenet. 2010 Dec;203(2):269-77. doi: 
      10.1016/j.cancergencyto.2010.08.011.