PMID- 9656121
OWN - NLM
STAT- MEDLINE
DCOM- 19980917
LR  - 20061115
IS  - 0277-1691 (Print)
IS  - 0277-1691 (Linking)
VI  - 17
IP  - 3
DP  - 1998 Jul
TI  - Primary carcinoma of the fallopian tube: comparative genomic hybridization 
      reveals high genetic instability and a specific, recurring pattern of chromosomal 
      aberrations.
PG  - 245-54
AB  - Primary fallopian tube carcinoma (PFTC) is a rare and highly aggressive tumor. 
      Twelve cases of PFTC (stages IA to IV) were analyzed by comparative genomic 
      hybridization. The most consistent DNA gain was mapped to chromosome arm 3q in 11 
      of 12 cases. In six cases, the gain of 3q was present as a high level copy number 
      increase (amplification) with a consensus region mapped to 3q26.2-qter. In the 12 
      cases, other frequent gains were located on chromosome arms 1q (in 11 cases), 2q 
      (in 10), 7q (in 9), 8q (in 9), 5p (in 8), 6p (in 7), 12p (in 7), and 14q (in 6). 
      Frequent copy number losses occurred on chromosome arms 16q (in 8 cases), 22q 
      (in7), 6q (in 6). 8p (in 6), 18q (in 6), Xq (in 6), 1p (in 5), and 17p (in 5). 
      All chromosomes were involved in chromosomal aberrations and the average number 
      of copy alterations per case was 19.7. None of the 12 carcinomas revealed the 
      presence of human papillomavirus (HPV) genomes. All of the cases exhibited crude 
      aneuploidy. Strong p53 immunoreactivity could be observed in 10 of 12 cases while 
      p21/WAF1 expression was low or undetectable. These results indicate that PFTC is 
      a genomically highly unstable cancer, an observation that is in agreement with 
      the poor prognosis associated with this tumor. A high frequency of 3q-gains has 
      also been observed in HPV-related carcinomas of the uterine cervix. However, none 
      of the PFTC was HPV related, suggesting that the 3q-gain is independent from HPV 
      DNA.
FAU - Heselmeyer, K
AU  - Heselmeyer K
AD  - Genome Technology Branch, National Human Genome Research Institute, National 
      Institutes of Health, Bethesda Maryland 20892-4470, USA.
FAU - Hellstrom, A C
AU  - Hellstrom AC
FAU - Blegen, H
AU  - Blegen H
FAU - Schrock, E
AU  - Schrock E
FAU - Silfversward, C
AU  - Silfversward C
FAU - Shah, K
AU  - Shah K
FAU - Auer, G
AU  - Auer G
FAU - Ried, T
AU  - Ried T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Int J Gynecol Pathol
JT  - International journal of gynecological pathology : official journal of the 
      International Society of Gynecological Pathologists
JID - 8214845
RN  - 0 (CDKN1A protein, human)
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p21)
RN  - 0 (Cyclins)
RN  - 0 (Ki-67 Antigen)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Aneuploidy
MH  - Carcinoma/chemistry/*genetics
MH  - Cell Division
MH  - Chromosome Aberrations
MH  - Cyclin-Dependent Kinase Inhibitor p21
MH  - Cyclins/analysis
MH  - DNA/analysis
MH  - Fallopian Tube Neoplasms/chemistry/*genetics
MH  - Female
MH  - Humans
MH  - Immunohistochemistry
MH  - Karyotyping
MH  - Ki-67 Antigen/analysis
MH  - Middle Aged
MH  - Nucleic Acid Hybridization/methods
MH  - Tumor Suppressor Protein p53/analysis
EDAT- 1998/07/10 00:00
MHDA- 1998/07/10 00:01
CRDT- 1998/07/10 00:00
PHST- 1998/07/10 00:00 [pubmed]
PHST- 1998/07/10 00:01 [medline]
PHST- 1998/07/10 00:00 [entrez]
PST - ppublish
SO  - Int J Gynecol Pathol. 1998 Jul;17(3):245-54.