PMID- 10616527
OWN - NLM
STAT- MEDLINE
DCOM- 20000113
LR  - 20190816
IS  - 0165-4608 (Print)
IS  - 0165-4608 (Linking)
VI  - 116
IP  - 1
DP  - 2000 Jan 1
TI  - Allelic loss at chromosome band 6q14 correlates with favorable prognosis in 
      hepatocellular carcinoma.
PG  - 23-7
AB  - Cytogenetic and molecular studies have frequently shown chromosome 6q deletions 
      in non-Hodgkin lymphoma and several human cancers. There have been few studies 
      concerning chromosome 6q deletion in hepatocellular carcinoma (HCC), and most of 
      these studies have focused on region 6q26-27. We previously described frequent 
      allelic loss at 6q14 in HCC. As a step toward narrowing the scope of search for 
      tumor suppressor genes, we used a series of yeast artificial chromosome clones 
      that map to the long arm of chromosome 6 (6q14-6q22) by fluorescence in situ 
      hybridization (FISH) to define the minimal common region of allelic loss in 25 
      cases of HCC. Altogether, 12 tumors had allelic loss on 6q (48%). Eleven of the 
      12 tumors had polysomy of chromosome 6 with evident intratumor cytogenetic 
      heterogeneity. The minimal common region of allelic loss lies within a 2-cM 
      region at 6q14, flanked by D6S458 (849_d_8) and D6S275 (911_a_3). 
      Clinicopathologic correlation between the 12 patients with allelic loss at 6q and 
      the 13 patients without allelic loss showed no significant differences in any 
      basic characteristics except survival. Patients with allelic loss at 6q had a 
      much longer median survival time than those without allelic loss (50 months vs. 
      11 months, P = 0.0019). Only 5 of the 25 HCC patients were still alive at the 
      time of this study, and all of them had allelic loss at 6q, which is also 
      statistically significant (P = 0.037, alive vs. dead). The association of allelic 
      loss at 6q with polysomy implies that this may be a progression-associated event 
      in HCC. The correlation of allelic loss at 6q with long survival suggests a 
      complex mechanism of tumorigenesis in HCC and is worthy of further investigation.
FAU - Huang, S F
AU  - Huang SF
AD  - Department of Pathology, National Taiwan University Hospital National Taiwan 
      University College of Medicine, Taipei, Taiwan.
FAU - Hsu, H C
AU  - Hsu HC
FAU - Cheng, Y M
AU  - Cheng YM
FAU - Chang, T C
AU  - Chang TC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer Genet Cytogenet
JT  - Cancer genetics and cytogenetics
JID - 7909240
SB  - IM
MH  - Adult
MH  - Aged
MH  - Alleles
MH  - Aneuploidy
MH  - Carcinoma, Hepatocellular/*genetics/pathology
MH  - Chromosome Mapping
MH  - Chromosomes, Artificial, Yeast
MH  - *Chromosomes, Human, Pair 6
MH  - Female
MH  - *Gene Deletion
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Liver Neoplasms/*genetics/pathology
MH  - Male
MH  - Middle Aged
MH  - Prognosis
EDAT- 2000/01/05 00:00
MHDA- 2000/01/05 00:01
CRDT- 2000/01/05 00:00
PHST- 2000/01/05 00:00 [pubmed]
PHST- 2000/01/05 00:01 [medline]
PHST- 2000/01/05 00:00 [entrez]
AID - S0165-4608(99)00111-9 [pii]
AID - 10.1016/s0165-4608(99)00111-9 [doi]
PST - ppublish
SO  - Cancer Genet Cytogenet. 2000 Jan 1;116(1):23-7. doi: 
      10.1016/s0165-4608(99)00111-9.