TY - JOUR
T1 - Primary carcinoma of the fallopian tube
T2 - Comparative genomic hybridization reveals high genetic instability and a specific, recurring pattern of chromosomal aberrations
AU - Heselmeyer, Kerstin
AU - Hellström, Ann Cathrin
AU - Blegen, Harald
AU - Schröck, Evelin
AU - Silfverswärd, Claes
AU - Shah, Keerti
AU - Auer, Gert
AU - Ried, Thomas
PY - 1998/7
Y1 - 1998/7
N2 - 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 lq (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 (in 7), 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.
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 lq (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 (in 7), 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.
KW - Cancer
KW - Chromosome aberrations
KW - Comparative genomic hybridization (CGH)
KW - DNA ploidy
KW - Fallopian tube
KW - Human papillomavirus (HPV)
KW - P53
KW - Proliferation
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U2 - 10.1097/00004347-199807000-00009
DO - 10.1097/00004347-199807000-00009
M3 - Article
C2 - 9656121
AN - SCOPUS:0031863236
SN - 0277-1691
VL - 17
SP - 245
EP - 254
JO - International Journal of Gynecological Pathology
JF - International Journal of Gynecological Pathology
IS - 3
ER -