Micropapillary serous carcinoma of the ovary has distinct patterns of chromosomal imbalances by comparative genomic hybridization compared with atypical proliferative serous tumors and serous carcinomas.
Recent studies have subdivided serous borderline tumors into 2 categories: atypical proliferative serous tumors (APSTs), which have a relatively benign course, and micropapillary serous carcinomas (MPSCs), which behave like low-grade carcinoma. This study was undertaken to determine, using comparative genomic hybridization (CGH), whether cytogenetic changes support this hypothesis. Nine cases of APST, 10 of MPSC, and 11 of invasive serous carcinoma (SC) were analyzed by CGH. Tumor DNA was extracted from frozen or paraffin-embedded tissue from the primary ovarian tumor, using either sections with at least 70% tumor cells or tissue after relative enrichment by microdissection. Chromosomal imbalances were identified in 3 of 9 APST, 6 of 10 MPSC, and 11 of 11 SC. Three or more chromosomal imbalances were found in 0 of 9 APST, 4 of 10 MPSC, and 9 of 11 SC. Recurrent copy number alterations were grouped into 4 classes correlating with the different tumor types. Class I changes were present in APST and in MPSC or SC and included +8q (7 of 11 SC, 2 of 10 MPSC, 2 of 9 APST), -9p (5 of 11 SC, 0 of 10 MPSC, 1 of 9 APST), and +12 (+12p in 3/11 SC, +12 in 2 of 10 MPSC, +12 in 1 of 9 APST). Class II changes were found only in MPSC and SC, but not in APST. The most frequent examples were +3q (10 of 11 SC, 1 of 10 MPSC), -4q (5 of 11 SC, 1 of 10 MPSC), and -17p (5 of 11 SC, 1 of 10 MPSC). Class III changes were limited to SC, like -16q (7 of 11 SC) and -18q (6 of 11 SC). Class VI changes were unique to MPSC. Gain of 16p (3 of 10 MPSC) was the only aberration in this group. This aberration was not only unique to MPSC but was also the most frequent finding in MPSC. These data support the hypothesis that noninvasive serous tumors of the ovary can be subdivided into 2 categories: APST and MPSC. The number of imbalances in MPSC is substantially higher than in APST and lower than in SC. Some changes in MPSC are shared with SC and APST and others with SC only, suggesting that a subset of MPSC may represent a stage in progression from APST to SC. Other cases of MPSC with independent genetic alterations may represent another subset of tumors that are a distinct entity from APST and SC.
Staebler
Annette
A
Department of Pathology, The Johns Hopkins Hospital, Baltimore, MD 21231, USA.
Heselmeyer-Haddad
Kerstin
K
Bell
Karen
K
Riopel
Maureen
M
Perlman
Elizabeth
E
Ried
Thomas
T
Kurman
Robert J
RJ
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002869:Chromosome Aberrations; D018283:Cystadenocarcinoma, Papillary / Q000145:classification / Q000235:genetics* / Q000473:pathology; D018284:Cystadenocarcinoma, Serous / Q000145:classification / Q000235:genetics* / Q000473:pathology; D018293:Cystadenoma, Serous / Q000145:classification / Q000235:genetics* / Q000473:pathology; D004273:DNA, Neoplasm / Q000032:analysis; D004210:Dissection; D005260:Female; D018628:Gene Dosage; D006801:Humans; D007091:Image Processing, Computer-Assisted; D017403:In Situ Hybridization; D007621:Karyotyping; D008846:Micromanipulation; D008875:Middle Aged; D009367:Neoplasm Staging; D010051:Ovarian Neoplasms / Q000145:classification / Q000235:genetics* / Q000473:pathology
D004273:DNA, Neoplasm