title: Primary carcinoma of the fallopian tube: comparative genomic hybridization reveals high genetic instability and a specific, recurring pattern of chromosomal aberrations.
abstract: 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.
authors.affiliation: Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda Maryland 20892-4470, USA.
authors.forename: K
authors.initials: K
authors.lastname: Heselmeyer
authors.forename: A C
authors.initials: AC
authors.lastname: Hellström
authors.forename: H
authors.initials: H
authors.lastname: Blegen
authors.forename: E
authors.initials: E
authors.lastname: Schröck
authors.forename: C
authors.initials: C
authors.lastname: Silfverswärd
authors.forename: K
authors.initials: K
authors.lastname: Shah
authors.forename: G
authors.initials: G
authors.lastname: Auer
authors.forename: T
authors.initials: T
authors.lastname: Ried
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000782:Aneuploidy; D002277:Carcinoma / Q000737:chemistry / Q000235:genetics*; D002455:Cell Division; D002869:Chromosome Aberrations; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000032:analysis; D004247:DNA / Q000032:analysis; D005185:Fallopian Tube Neoplasms / Q000737:chemistry / Q000235:genetics*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007621:Karyotyping; D019394:Ki-67 Antigen / Q000032:analysis; D008875:Middle Aged; D009693:Nucleic Acid Hybridization / Q000379:methods; D016159:Tumor Suppressor Protein p53 / Q000032:analysis
chemical_list: C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D019394:Ki-67 Antigen; D016159:Tumor Suppressor Protein p53; D004247:DNA