Ovarian Papillary Serous Carcinoma Research Articles

Molecular similarities between primary peritoneal and primary ovarian carcinomas.

The objective of this paper was to characterize expression patterns of biologic markers to distinguish papillary serous peritoneal carcinoma (PPC) from papillary serous ovarian carcinoma (POC). Immunohistochemical analysis of HER-2/neu, p53, bcl-2, and nm23-H1 expression was performed on archival paraffin-embedded tissues. Antigen expression was compared at ovarian and extra-ovarian sites. Thirty-two PPC cases were compared to 18 POC cases. Mean age, stage, grade, and survival outcome were comparable between the two groups. Antigen expression patterns were not significantly different between PPC and POC for the four markers studied. In all cases, nm23-H1 was expressed. Conversely, bcl-2 was expressed at only a single tissue site in three of 32 (9.4%) PPC cases and in one of 18 (5.6%) POC cases. Eleven of 32 (34.4%) PPC cases overexpressed HER-2/neu, vs. four of 18 (22.2%) POC cases. P53 staining results were positive in 23 of 32 (71.9%) PPC and 13 of 18 (72.2%) POC cases. Intrapatient antigen expression was identical at primary and metastatic tumor sites in 50% of the POC and 48.4% of the PPC cases. We conclude that PPC and POC have a comparable immunohistochemical phenotype for these four molecular markers, which is reflected by their similar clinical courses.

Molecular similarities between primary peritoneal and primary ovarian carcinomas

The objective of this paper was to characterize expression patterns of biologic markers to distinguish papillary serous peritoneal carcinoma (PPC) from papillary serous ovarian carcinoma (POC). Immunohistochemical analysis of HER-2/neu, p53, bcl-2, and nm23-H1 expression was performed on archival paraffin-embedded tissues. Antigen expression was compared at ovarian and extra-ovarian sites. Thirty-two PPC cases were compared to 18 POC cases. Mean age, stage, grade, and survival outcome were comparable between the two groups. Antigen expression patterns were not significantly different between PPC and POC for the four markers studied. In all cases, nm23-H1 was expressed. Conversely, bcl-2 was expressed at only a single tissue site in three of 32 (9.4%) PPC cases and in one of 18 (5.6%) POC cases. Eleven of 32 (34.4%) PPC cases overexpressed HER-2/neu, vs. four of 18 (22.2%) POC cases. P53 staining results were positive in 23 of 32 (71.9%) PPC and 13 of 18 (72.2%) POC cases. Intrapatient antigen expression was identical at primary and metastatic tumor sites in 50% of the POC and 48.4% of the PPC cases. We conclude that PPC and POC have a comparable immunohistochemical phenotype for these four molecular markers, which is reflected by their similar clinical courses.

Extraovarian peritoneal serous papillary carcinoma: a phase II trial of cisplatin and cyclophosphamide with comparison to a cohort with papillary serous ovarian carcinoma—a Gynecologic Oncology Group Study

Objectives The goals of this study were first, to assess the clinical effectiveness of cisplatin and cyclophosphamide in a phase II study involving a well-defined group of women with extraovarian peritoneal serous papillary carcinoma (EPSPC); and second, to compare these results with those of a group of patients with papillary serous ovarian carcinoma (PSOC) who received identical therapy. Methods After primary surgery, patients were treated with cisplatin 75 mg/m 2 and cyclophosphamide 750 mg/m 2 every 21 days for six cycles. Patient demographics, tumor characteristics, clinical and surgical response to treatment, progression-free survival, and overall survival were evaluated. These patients were then compared with patients with PSOC who received identical treatment on a separate protocol. Results Women with a diagnosis of EPSPC tended to be older than those with PSOC (median age: 65.8 years vs 60.3 years, P = 0.04). The estimated probability of clinical response (complete and partial) to the treatment regimen for EPSPC was 65% (95% confidence interval [CI]: 41–85%) compared with 59% (95% CI: 47–71%) for women with PSOC. Surgical complete responses were similar (20% vs 19%) in the two patient groups. Additionally, the death rates did not significantly differ between the two groups (hazard ratio: 1.25, 95% CI: 0.834–1.88). Conclusion Women with EPSPC and PSOC exhibit a similar probability of response to cisplatin and cyclophosphamide and a similar overall survival. Based on these findings and the fact that results of ovarian cancer trials are frequently extrapolated to patients with EPSPC, it is reasonable to include EPSPC patients in future large-scale treatment trials involving patients with advanced ovarian cancer.

Molecular determinants of tumor differentiation in papillary serous ovarian carcinoma.

In epithelial ovarian cancer, tumor grade is an independent prognosticator whose molecular determinants remain unknown. We investigated patterns of gene expression in well- and poorly differentiated serous papillary ovarian and peritoneal carcinomas with cDNA microarrays. A 6500-feature cDNA microarray was used for comparison of the molecular profiles of eight grade III and four grade I stage III serous papillary adenocarcinomas. With a modified F-test in conjunction with random permutations, 99 genes whose expression was significantly different between grade I and grade III tumors were identified (P < 0.01). A disproportionate number of these differentially expressed genes were located on the chromosomal regions 20q13 and all exhibited higher expression in grade III tumors. Interphase fluorescent in situ hybridization demonstrated 20q13 amplification in two of the four grade III and none of the three grade I tumors available for evaluation. Several centrosome-related genes also showed higher expression in grade III tumors. We propose a model in which tumor differentiation is inversely correlated with the overexpression of several oncogenes located on 20q13, a common amplicon in ovarian and numerous other cancers. Dysregulation of centrosome function is one potential mechanistic link between genetic/epigenetic changes and the poorly differentiated phenotype in ovarian cancer.

Infiltrating Micropapillary Carcinoma of the Breast

To examine the cytologic features of infiltrating micropapillary carcinoma (IMPC). Using the histopathology files of one of the authors (I.J.B.), we retrospectively identified 20 IMPC cases (pure, 12; partial micropapillary carcinoma differentiation, 8) with corresponding cytology. We evaluated the cases for cellularity, atypia, architecture and background. All cases were diagnostic of malignancy, characterized by atypical cells present predominantly in three-dimensional clusters and single cells, facilitating the diagnosis. The clusters had cell ball and papillarylike arrangements, like the morular growth pattern seen on histopathology. Apocrine cytology was present in 12 cases, focal mucin background in 5 and psamomma bodies in 2. The differential diagnosis includes primary papillary neoplasms of the breast, metastatic ovarian papillary serous carcinoma, apocrine and colloid carcinoma of the breast, and intraductal carcinoma (micropapillary type). As in histopathology, the cytologic features of IMPC are unique and should be recognized due to its aggressive behavior.

Lymphatic spread among women with primary peritoneal carcinoma.

Our knowledge regarding the pathologic lymphatic spread pattern of primary peritoneal carcinoma (PPC) is limited. The aim of this study was to compare the incidence and the pathologic patterns of pelvic and para-aortic lymph node metastases among women with PPC and those with papillary serous ovarian carcinoma (PSOC). We conducted a prospective study over the last 4 years among women with FIGO stage III and IV PPC and PSOC who had optimal primary cytoreductive surgery (<1 cm residual). The same surgeon performed pelvic and para-aortic lymphadenectomy on all the patients using a similar technique. The same pathologist reviewed all lymph nodes and recorded nodal involvement with cancer, diameter of the largest nodal tumor, capsular integrity, and pattern of immune response (lymphocyte predominant, germinal cell predominant, unstimulated, or lymphocyte depletion). Both groups were compared in their characteristics, FIGO stage, tumor grade, number of lymph nodes, proportion of lymph nodes with metastases, and the pathologic characteristics of the positive lymph nodes. Eleven women had PPC and 27 had PSOC. Patients with PPC were older than those with PSOC (mean age: 63.2 years +/- 11.0 vs. 57.4 +/- 13.4, P = 0.181). There was no difference in FIGO stage or tumor grade between both groups. There was no difference among the mean numbers of pelvic and para-aortic lymph nodes between women with PPC and those with PSOC (10.8 +/- 7.3 vs. 11.0 +/- 6.7 and 3.0 +/- 3.3 vs. 3.4 +/- 2.1, P = 0.768 and 0.706, respectively). The incidences of pelvic, para-aortic, and pelvic and/or para-aortic lymph node metastases were similar among women with PPC and those with PSOC (72.7% vs. 66.6%, P = 0.701, 72.7% vs. 48.1%, P = 0.172, and 72.7% vs. 77.8%, P = 0.736, respectively). Similarly, pelvic and para-aortic nodal tumor size, capsular integrity, and immune response were similar in both groups. The incidence of significant complications related to lymphadenectomy was low among women with PPC and those with PSOC (9.1% vs. 7.4%, respectively). PPC and PSOC exhibit similar pathologic lymphatic spread patterns. Pelvic and para-aortic lymphadenectomy should be considered among women with PPC in whom the tumor could be optimally cytoreduced.

Malignant mullerian mixed tumor arising from ovarian serous carcinoma: a clinicopathologic and molecular study of two cases.

The clinical, histologic, and molecular pathologic features of two cases of malignant mullerian mixed tumor (MMMT) arising from ovarian papillary serous carcinoma are presented. Identical p53 mutations were detected in the primary ovarian carcinoma and the subsequent MMMT in each case.

Value of mesothelial and epithelial antibodies in distinguishing diffuse peritoneal mesothelioma in females from serous papillary carcinoma of the ovary and peritoneum.

To evaluate the role of mesothelial markers (calretinin, thrombomodulin, cytokeratin 5/6, and CD44H) and carcinoma markers (polyclonal and monoclonal carcinoembryonic antigen, Leu-M1, CA-125 and Ber-EP4) in distinguishing diffuse peritoneal malignant mesothelioma from primary serous papillary adenocarcinoma of the ovary and peritoneum. Paraffin-embedded formalin-fixed blocks from 32 diffuse peritoneal mesotheliomas of epithelial subtype (all females), 20 serous papillary ovarian carcinomas and three primary peritoneal serous papillary carcinomas were studied. Calretinin and Ber-EP4 appeared to be the best positive mesothelial and carcinoma marker, respectively. Nuclear calretinin expression was identified in 28 of 32 malignant mesotheliomas with no nuclear immunoreactivity in the cohorts of serous papillary ovarian and peritoneal carcinomas, thus yielding 88% sensitivity and 100% specificity. Ber-EP4 showed 95% sensitivity and 91% specificity for serous papillary ovarian carcinoma. Thrombomodulin, cytokeratin 5/6 and CD44H immunoreactivities were seen in 18 (56%), 17 (53%) and 15 (47%) of peritoneal mesotheliomas, respectively, and in six (30%), five (25%) and five (25%) of the ovarian tumours, respectively. None of the three primary peritoneal serous papillary carcinomas expressed calretinin, thrombomodulin, cytokeratin 5/6 or CD44H. Polyclonal and monoclonal CEA, and Leu-M1 were expressed by two (10%), one (5%) and seven (35%) serous papillary ovarian carcinomas, respectively. None of the serous papillary peritoneal carcinomas expressed polyclonal CEA, monoclonal CEA or Leu-M1. CA-125 was positive in 19 (95%) and two (67%) ovarian and peritoneal carcinomas, respectively, and in eight (25%) peritoneal mesotheliomas. Calretinin and Ber-EP4 are useful discriminant markers in distinguishing peritoneal mesothelioma in women from serous papillary ovarian and peritoneal carcinoma. The other mesothelial markers (thrombomodulin, cytokeratin 5/6, and CD44H) and carcinoma markers (polyclonal and monoclonal CEA, and Leu-M1) yielded a too low sensitivity for practical use.

Carcinoma papilar de la superficie serosa del ovario

Summary We present the case of a 74 year-old woman with bronchiectasis, concomitantly with abdominal distension and ascites. Vaginal ecography and CT scan showed a solid mass of 10 × 8 cm, suggestive of an ovarian neoplasm. During vaginal surgery a peritoneal carcinomatosis was found. The patient died within a month of the procedure, without receiving radiotherapy. The tumour was an ovarian serous surface papillary carcinoma.

Evaluation of a Region on Chromosome 1p in Ovarian Serous Carcinoma That Is Frequently Deleted in Uterine Papillary Serous Carcinoma

Objective. The goal of this study was to assess the involvement of chromosome 1p deletion in ovarian papillary serous carcinoma (OPSC) via high-resolution physical mapping to detect a candidate tumor suppressor gene previously implicated in uterine papillary serous carcinoma (UPSC) tumorigenesis.Methods. Previous studies have demonstrated a high rate of loss of heterozygosity (LOH) within a critical region of chromosome 1p in UPSC, suggesting the presence of a putative tumor suppressor gene important in the development of UPSC. To compare the genetic changes in OPSC with those in UPSC, seven microsatellite repeat polymorphisms were used to evaluate LOH in primary OPSC specimens. Allelic intensity was compared between normal and tumor DNA from microdissected, formalin-fixed, paraffin-embedded specimens. In addition to the same seven 1p markers used for UPSC, three additional non-1p markers for chromosomes 1q, 11q, and 2p were tested to determine a baseline rate of LOH.Results. Overall, 26.6% (8/30) of OPSC (vs 63.2% of UPSC) were characterized by loss at either of the two loci that define the critical region for UPSC. Rates of LOH at each of the 1p loci in the OPSC tumors ranged from 5.6 to 38.9%, which are compatible with background rates of loss for OPSC. LOH at non-1p loci was 29.2%.Conclusion. While a tumor suppressor gene on 1p appears to be an important genetic event in the development of UPSC, a similar rate and pattern of loss on 1p are not identified in OPSC. Thus, despite the striking clinical similarities between UPSC and OPSC, tumorigenesis in these carcinomas appears to occur via distinctly different pathways.

Allelotype of Papillary Serous Peritoneal Carcinomas

Objective. Papillary serous peritoneal carcinoma (PSPC) is histologically indistinguishable from papillary serous ovarian carcinoma (PSOC) with a similar clinical presentation, yet may differ in its carcinogenesis. The purpose of this study was to determine the incidence of allelic loss and the frequency of p53 mutation by p53 overexpression in PSPC compared to PSOC.Methods. An allelotype analysis of 26 patients with PSPC was performed using 39 microsatellite markers from 25 chromosomal arms. Thirty-seven previously studied patients with PSOC served as the comparison. P53 mutations were detected by immunohistochemical protein overexpression.Results. There was significantly less LOH in PSPC than PSOC. Both the number of chromosomes with LOH and the proportion of tumors with allelic loss were less frequent. Significant LOH, defined as ≥30% of informative tumors having loss at a chromosome locus, was seen on 4 chromosome arms in PSPC: 12p, 17p, 17q, and 18q, compared to 18 arms in PSOC: 4q, 5q, 6p, 6q, 9p, 9q, 12p, 12q, 13q, 15q, 16q, 17p, 17q, 18q, 19p, 19q, 22q, and Xq (P < 0.001). The median LOH frequency was higher in PSOC than PSPC, 43% versus 33%, respectively (P = 0.013), and more PSOC tumors had LOH than PSPC tumors, 91% versus 65% (P = 0.042). P53 overexpression was detected in 80% of PSPC tumors.Conclusions. LOH occurs less frequently in PSPC compared to PSOC. Chromosomal regions with high frequencies of LOH common to PSPC and PSOC, such as 12p, 17p, 17q, and 18q, may harbor tumor suppressor genes important in the carcinogenesis of both malignancies and likely include p53.

Gene expression profiles of low- and high-grade papillary serous ovarian carcinomas using cDNA microarray analysis

Gene expression profiles of low- and high-grade papillary serous ovarian carcinomas using cDNA microarray analysis

Primary papillary serous carcinoma of the peritoneum in a man

Primary papillary serous carcinoma of the peritoneum is a well-known entity in women. The tumour is derived from the extraovarian mesothelium and the pelvis and lower abdomen mesothelia. The treatment strategies are similar to ovarian serous papillary carcinoma. A case of primary serous papillary carcinoma of the peritoneum in a man is presented. The patient, 53 years old, died 2 months after diagnosis. The histologic and immunohistochemical studies of the tumour will be presented. These studies, made during lifetime and at autopsy of the patient, confirm a diagnosis of primary serous papillary carcinoma of the peritoneum. primary serous papillary carcinoma of the peritoneum can occur in men, and should be considered in the differential diagnosis in cases of abdominal carcinomatosis of unknown origin. Treatment options remain to be determined.

Primary Papillary Serous Carcinoma of the Peritoneum: A Case Report

Primary papillary serous carcinoma of the peritoneum is a rare primary tumor involving the peritoneum. Histologically, it is indistinguishable from serous ovarian papillary carcinoma, although it either spares the o-varies or only microscopically involves their surface. The characteristic features of this tumor are extensive peritoneal and omental masses or implants with psammomatous calcification, and ascites. In addition, it can occur focally in the pelvic peritoneum. We report the CT findings, with histopathologic correlation of primary papillary serous carcinoma of the peritoneum occurring in the upper mesorectum.

MICROPAPILLARY BLADDER CARCINOMA: A CLINICOPATHOLOGICAL STUDY OF 20 CASES

Purpose Micropapillary bladder carcinoma is rare, with only 18 cases reported to date. We report 20 additional cases with long-term followup. Materials and Methods A total of 680 patients with an initial diagnosis of bladder carcinoma in western Sweden in 1987 and 1989 were prospectively registered. The clinical records of all 816 patients with bladder cancer treated at Sahlgrenska University Hospital with external beam irradiation between 1962 and 1989 were reviewed. The histopathological material was reviewed and immunohistochemical analyses were performed on 20 cases identified with micropapillary bladder carcinoma. Results The incidence of micropapillary bladder carcinoma was 0.7%. Mean patient age at diagnosis was 69 years (range 45 to 82) and the male-to-female ratio was 2.3:1. All but 5 patients had stage T3a disease or higher. There was no difference in stage or prognosis between the 5 prospectively identified patients and those treated with external beam irradiation. Only 2 patients had micropapillary bladder carcinoma as the only pattern, while 1 had 10% and the remainder had 20 to 95% micropapillary bladder carcinoma. Transitional cell carcinoma was noted in 17 patients and 5 had areas of gland forming adenocarcinoma. Carcinoma in situ was noted in 13 patients and 15 had lymphatic invasion. Only 5 patients survived 5 years, 1 of whom died of bladder cancer after 7 years. Radiation and chemotherapy did not seem to be effective. Conclusions The light microscopic appearance, which is strikingly similar to ovarian papillary serous carcinoma, and immunohistochemical staining pattern lend some support to the theory that micropapillary bladder carcinoma is a variant of adenocarcinoma. Since even the focal presence of micropapillary bladder carcinoma is associated with a poor prognosis, recognition of this entity is important. Due to its rarity, the optimal treatment of micropapillary bladder carcinoma needs to be determined in a multicenter study.

Trisomy 8 in Stage I and Stage III Ovarian Cancer Detected by Fluorescencein SituHybridization

Ovarian cancer is the leading cause of death from gynecologic maligancy among women in the United States. In 1997, there were nearly 27,000 ovarian cancer cases with over 14,000 deaths. Recent attempts at early detection of ovarian cancer have been aimed at the identification of biomarkers that would indicate an underlining malignant process or reflect the biological behavior of the tumor. Our previous studies revealed that chromosome 8 copy number abnormality, especially trisomy, is common in several cancers. Archival tissues from 24 cases of papillary serous ovarian carcinoma (10 stage I and 14 stage III) were analyzed by fluorescencein situhybridization (FISH) with a chromosome 8-specific α-satellite probe (Oncor, Gaithersburg, MD). The analysis was done according to standard protocols of the Lifespan Academic Medical Center Cytogenetics Laboratory at Rhode Island Hospital. Twenty-one of 24 cases (87.5%) were found to be trisomic for chromosome 8, if a cutoff point of ≥15% cells with three signals is adopted. Overall, 80% of stage I and 93% of stage III tumors had trisomy 8. This study confirms the presence of a high frequency of trisomy 8 in both early and late stages of the disease and suggests that trisomy 8 may be an early event in the multistep process leading to ovarian cancer. It is of interest to note that a higher frequency of trisomy 8 was found in a higher stage of disease, consistent with our previous results on breast cancer. Thus, additional FISH studies of ovarian tumors for chromosome 8 copy number assessment may be warranted.

Trisomy 8 in papillary serous carcinoma of the ovary studied by FISH

Ovarian cancer is the leading cause of death from gynecologic malignancy among women in the United States. In 1997, there were nearly 27,000 ovarian cancer cases with over 14,000 deaths. Recent attempts at early detection of ovarian cancer have been aimed at the identification of biomarkers that would indicate an underlining malignant process or reflect the biological behavior of the tumor. Our previous studies revealed that chromosome 8 copy number abnormality, especially trisomy, is common in several cancers. Archival tissues from 24 cases of papillary serous ovarian carcinoma (10 stage I and 14 stage III) were analyzed by FISH with a chromsome 8 α-satellite probe (Oncor, Gaithersburg, MD). The analysis was done according to standard protocols of the Lifespan Academic Medical Center Cytogenetics Laboratory at Rhode Island Hospital. Twenty-one out of 24 cases (87.5%) were found to be trisomic for chromosome 8, if a cutoff point of ≥15% cells with three signals is adopted. Overall 80% of stage I and 93% of stage III tumors had trisomy 8. This study confirms the presence of a high frequency of trisomy 8 in both early and late stages of the disease and suggests that trisomy 8 may be an early event in the multi-step process leading to ovarian cancer. (This study was funded in part by Vysis, Inc., Downers Grove, IL.)

BRCA1 gene mutations in women with papillary serous carcinoma of the peritoneum

Objective: To compare BRCA1 mutations in papillary serous carcinoma of the peritoneum and papillary serous ovarian carcinoma. Methods: Germline DNA from 17 consecutive patients with peritoneal carcinoma was screened for mutations in the BRCA1 gene using single-strand conformation polymorphism analysis. Shifted DNA bands were sequenced. Patients with germline BRCA1 mutations were screened for allelic loss in tumor DNA at the BRCA1 locus. Results: Two of the 17 patients (11%, 95% confidence interval 0.07, 0.37) exhibited the 185 delAG germline BRCA1 mutation described in the Ashkenazi Jewish population. The family history of one patient was notable for a mother and five aunts with breast or ovarian cancer. The other patient had a personal history of breast cancer. Both patients exhibited allelic loss of the normal BRCA1 allele in their tumor. A third patient was found to have a previously undescribed exon 11 single base pair substitution at nucleotide 1239 (CAG to CAC) resulting in a missense mutation (Gln to His). The patient had no family or personal history of breast or ovarian cancer, and her tumor did not exhibit loss of heterozygosity. Conclusion: Germline BRCA1 mutations occur in papillary serous carcinoma of the peritoneum with a frequency comparable to the BRCA1 mutation rate in ovarian cancer. Although the penetrance is unknown, peritoneal carcinoma should be considered a malignancy expressed in the familial breast ovarian cancer syndrome.

Expression of γ-glutamyl transpeptidase in stage III and IV ovarian surface epithelial carcinomas does not alter response to primary cisplatin-based chemotherapy

OBJECTIVE: γ-Glutamyl transpeptidase activity has been shown to be essential for the nephrotoxicity of cisplatin. The purpose of this study was to determine whether expression of γ-glutamyl transpeptidase in ovarian carcinomas is necessary for the antitumor effect of cisplatin. STUDY DESIGN: Tumor tissue from 18 patients with stage III or IV ovarian serous papillary carcinoma or poorly differentiated adenocarcinoma was analyzed for expression of γ-glutamyl transpeptidase by histochemical or immunohistochemical staining. Response to cisplatin-based combination chemotherapy was evaluated on the basis of clinical response, progression-free interval, and survival. RESULTS: γ-Glutamyl transpeptidase expression in the tumors ranged from 0% to 100% of the tumor cells γ-glutamyl transpeptidase positive. Patient survival ranged from 15 months to 9 years. Twelve of the 18 patients had a complete response to the initial course of cisplatin-based combination chemotherapy. There was no statistically significant correlation between either response or time to relapse and γ-glutamyl transpeptidase expression. However, there was a correlation between high levels of γ-glutamyl transpeptidase in the tumor and acute ototoxicity in patients treated with cisplatin. Expression of high levels of γ-glutamyl transpeptidase in the tumor was also found to be associated with shorter patient survival, suggesting that γ-glutamyl transpeptidase might have a role in resistance to drugs used in second- and third-line therapy. CONCLUSIONS: Expression of γ-glutamyl transpeptidase in ovarian serous papillary or poorly differentiated adenocarcinomas is not necessary for the antitumor activity of cisplatin. A correlation was found between high levels of γ-glutamyl transpeptidase in the tumor and both increased ototoxicity from cisplatin and decreased patient survival. These data suggest that administering an inhibitor of γ-glutamyl transpeptidase activity to block the nephrotoxicity of cisplatin would not interfere with its therapeutic effect. (Am J Obstet Gynecol 1998;179:363-7.)

Uterine papillary serous carcinoma: study of 19 cases

Objective: Uterine papillary serous carcinoma (UPSC) is an uncommon highly malignant variant of endometrial carcinoma that histologically and clinically resembles ovarian papillary serous carcinoma. The purpose of this study was to present the conjoined experience of two regional hospitals in the south of Israel (Soroka Medical Center, Beer-Sheva and Kaplan Hospital, Rehovot) of handling this tumour. Study Design: Data from the files of 19 patients with UPSC who were managed at these hospitals between July 1991 and June 1997 were evaluated. Results: The three-year survival rate was 57.3% overall; 83.3% for Stage I and 21.2% for Stages II, III, and IV combined ( P<0.02). Eighteen patients had primary surgery which included total abdominal hysterectomy and bilateral salpingo-oophorectomy and 15 (83.3%) of them received postoperative adjuvant therapy which included radiotherapy and/or systemic chemotherapy. Conclusions: The prognosis of patients with UPSC is worse than that of patients with other forms of endometrial carcinoma. Primary surgery comprised of total abdominal hysterectomy, bilateral salpingo-oophorectomy and staging is the mainstay of treatment. The type of postoperative treatment is not consistent. By and large, adjuvant pelvic radiotherapy is usually given in early-stage disease and adjuvant systemic chemotherapy is usually prescribed in advanced-stage disease.