PMID- 17239935
OWN - NLM
STAT- MEDLINE
DCOM- 20070404
LR  - 20070216
IS  - 0046-8177 (Print)
IS  - 0046-8177 (Linking)
VI  - 38
IP  - 3
DP  - 2007 Mar
TI  - An assessment of chromosomal alterations detected by fluorescence in situ 
      hybridization and p16 expression in sporadic and primary sclerosing 
      cholangitis-associated cholangiocarcinomas.
PG  - 491-9
AB  - The objective of this study was to assess and compare the chromosome 
      abnormalities present in sporadic and primary sclerosing cholangitis 
      (PSC)-associated cholangiocarcinomas (CCAs) and biliary dysplasias. Histologic 
      sections from 22 patients with CCA (16 sporadic and 6 PSC associated), 5 of whom 
      had associated dysplasia, and 2 PSC patients with biliary dysplasia alone were 
      assessed for chromosomal alterations with fluorescence in situ hybridization 
      (FISH). FISH involved the use of a multiprobe set consisting of 
      centromere-specific probes for chromosomes 3, 7, and 17 and a locus-specific 
      probe for 9p21. The number of signals for each of these probes was enumerated in 
      50 nonoverlapping interphase nuclei, and the percentage of nuclei containing 0, 
      1, 2, and 3 or more signals was recorded for each probe. p16 expression was 
      assessed using immunohistochemistry. Gain of at least 1 chromosome was identified 
      in 19 of 22 (86%) invasive tumors and in 4 of 7 (57%) biliary dysplasias. Gain of 
      2 or more chromosomes (polysomy) was observed in 17 of 22 (77%) invasive tumors 
      and in 3 of 7 (43%) biliary dysplasias. Homozygous loss of 9p21 was identified in 
      11 of 22 (50%) invasive tumors and in 3 of 7 (43%) biliary dysplasias. The 
      patterns of chromosomal abnormalities detected by FISH in PSC-associated and 
      sporadic CCAs were similar. Nine of 13 (69%) invasive tumors and 2 of 5 (40%) 
      biliary dysplasias with complete loss of p16 expression by immunohistochemistry 
      showed allelic loss of 9p21 by FISH. Polysomy and homozygous 9p21 deletion are 
      common in both sporadic and PSC-associated CCAs and are frequently detectable in 
      PSC-associated biliary dysplasia.
FAU - DeHaan, Ryan D
AU  - DeHaan RD
AD  - Department of Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, 
      Rochester, MN 55905, USA.
FAU - Kipp, Benjamin R
AU  - Kipp BR
FAU - Smyrk, Thomas C
AU  - Smyrk TC
FAU - Abraham, Susan C
AU  - Abraham SC
FAU - Roberts, Lewis R
AU  - Roberts LR
FAU - Halling, Kevin C
AU  - Halling KC
LA  - eng
PT  - Journal Article
DEP - 20070119
PL  - United States
TA  - Hum Pathol
JT  - Human pathology
JID - 9421547
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p16)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Bile Ducts, Intrahepatic/pathology
MH  - Cholangiocarcinoma/*complications/genetics
MH  - Cholangitis, Sclerosing/*complications/genetics
MH  - *Chromosome Aberrations
MH  - Cyclin-Dependent Kinase Inhibitor p16/*biosynthesis
MH  - Female
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Male
MH  - Middle Aged
EDAT- 2007/01/24 09:00
MHDA- 2007/04/05 09:00
CRDT- 2007/01/24 09:00
PHST- 2006/07/13 00:00 [received]
PHST- 2006/09/05 00:00 [revised]
PHST- 2006/09/06 00:00 [accepted]
PHST- 2007/01/24 09:00 [pubmed]
PHST- 2007/04/05 09:00 [medline]
PHST- 2007/01/24 09:00 [entrez]
AID - S0046-8177(06)00572-7 [pii]
AID - 10.1016/j.humpath.2006.09.004 [doi]
PST - ppublish
SO  - Hum Pathol. 2007 Mar;38(3):491-9. doi: 10.1016/j.humpath.2006.09.004. Epub 2007 
      Jan 19.