Uterine papillary serous carcinoma (UPSC): a single institution review of 129 cases

Slomovitz, Brian M.; Burke, Thomas W.; Eifel, Patricia J.; Ramondetta, Lois M.; Silva, Elvio G.; Jhingran, Anuja; Oh, Jonathan C.; Atkinson, E. Neely; Broaddus, Russell R.; Gershenson, David M.; Lu, Karen H.

doi:10.1016/j.ygyno.2003.08.018

Cited by 318 publications

(254 citation statements)

References 25 publications

Supporting

Mentioning

221

Contrasting

Unclassified

Order By: Relevance

“…14,41 Similarly, the 3-year disease-specific survival of morphologically ambiguous endometrial carcinomas with p53 overexpression (54%) was similar to uterine serous carcinomas (43-62%). 10,14,41 Although multivariate analysis was a C, censored; two patients lost to follow up after surgery; 33 patients (maximum) were included in the analyses. b 3-year PFS and DSS were estimated by the Kaplan-Meier method and comparisons of survival curves between variable categories were performed using the log-rank test.…”

Section: Discussionmentioning

confidence: 75%

p53 overexpression in morphologically ambiguous endometrial carcinomas correlates with adverse clinical outcomes

et al. 2010

View full text Add to dashboard Cite

The distinction between uterine serous and endometrioid carcinomas can usually be achieved by morphologic examination alone. However, there are occasional 'morphologically ambiguous endometrial carcinomas' that show overlapping serous and endometrioid features and defy histologic classification. The primary aim of this study was to assess the clinical significance of p53 overexpression using immunohistochemistry in such tumors. Related aims included (1) assessing interobserver diagnostic concordance for histologic subclassification of these tumors using a panel of pathologists with and without gynecologic pathology expertise and (2) elucidating the histologic features that correlate with p53 status. Thirty-five such cases were identified during the study period. p53 overexpression was seen in 17 of 35 cases. Tumors with p53 overexpression were associated with a significantly inferior progression-free survival and disease-specific survival compared with those that lacked p53 overexpression (3-year progression-free survival and disease-specific survival were 94 and 100% in patients with no p53 overexpression, and 52 and 54% in patients with p53 overexpression; P ¼ 0.02 and 0.003, respectively). The consensus diagnosis rendered by gynecologic pathologists was predictive of disease-specific survival (P ¼ 0.002), but not progression-free survival (P ¼ 0.11). Although the interobserver diagnostic concordance (kappa ¼ 0.70) was substantial for gynecologic pathologists, and highly associated with p53 status (77% of 'favor serous' cases showed p53 overexpression, whereas only 25% of 'favor endometrioid' cases showed p53 overexpression; P ¼ 0.005), the concordance between the consensus diagnosis of the two specialized pathologists versus each of three non-specialized pathologists was poor (kappa ¼ 0.13-0.25). The histologic feature that correlated most with p53 overexpression was the presence of diffuse high nuclear grade. p53 immunohistochemistry assays in morphologically ambiguous endometrial carcinomas are roughly as clinically informative as gynecologic pathology consultation and can be helpful for prognostic assessment and therapeutic decision making in difficult endometrial carcinomas.

show abstract

Section: Discussionmentioning

confidence: 75%

p53 overexpression in morphologically ambiguous endometrial carcinomas correlates with adverse clinical outcomes

et al. 2010

View full text Add to dashboard Cite

show abstract

“…12,13 In reported series of serous endometrial intraepithelial carcinoma, the incidence of extrauterine disease or pelvic serous carcinoma ranged from 33-67% (average approximately 50%). [12][13][14] The exact origin of extrauterine serous carcinoma has yet to be established. Extrauterine disease was previously thought to be derived from transtubal metastasis.…”

mentioning

confidence: 99%

Primary sources of pelvic serous cancer in patients with endometrial intraepithelial carcinoma

Zeng

Wang

et al. 2015

Modern Pathology

View full text Add to dashboard Cite

Serous endometrial intraepithelial carcinoma is often associated with extrauterine disease. It is currently unclear where does the extrauterine disease come from. This study addressed this issue. A total of 135 samples from 21 serous endometrial intraepithelial carcinoma patients were studied. Cellular lineage relationships between intrauterine and extrauterine serous carcinomas were determined by TP53-mutation analysis and correlated to the clinicopathologic features. There were three conditions contributing the extrauterine disease: metastasis from serous endometrial intraepithelial carcinoma (n ¼ 10) showed identical TP53 mutation between intrauterine lesions and extrauterine disease, cases of adnexal origin (n ¼ 5) had discordant TP53 mutations, and the mixed cellular origin cases (n ¼ 6) with both identical and discordant mutation status. Patients with extrauterine disease from serous endometrial intraepithelial carcinoma metastasis typically had small tumor masses (o2 cm) in extrauterine sites and without finding of serous tubal intraepithelial carcinoma, while extrauterine disease with adnexal or tubal origin commonly had larger tumor masses in extrauterine sites including ovary and omentum and serous tubal intraepithelial carcinoma. The majority of extrauterine diseases associated with serous endometrial intraepithelial carcinoma are metastasized from the endometrium. Serous endometrial intraepithelial carcinoma is frequently associated with serous cancers of adnexal or tubal origin, indicating that endometrial and adnexal or tubal serous cancers may share similar etiologies. TP53-mutation analysis provides a strong linkage for cellular lineage analysis. Tumor size in extrauterine disease and presence of serous tubal intraepithelial carcinoma or not are useful clinicopathologic features to determine primary cancer site, which helps in clinical management.

show abstract

“…Endometrioid or Type I EC, represents the majority of EC cases, is oestrogen-related, usually arises in the setting of endometrial hyperplasia, and tends to be biologically less aggressive (Hecht and Mutter, 2006). Nonendometrioid or Type II EC, predominantly uterine serous papillary carcinoma and clear cell endometrial carcinoma, accounts for approximately 10% of ECs, is not oestrogen-related, arises from atrophic endometrium, and frequently presents in advanced stages with 5-year survival rates, on average, between 30 and 40% (Abeler and Kjorstad, 1991;Goff et al, 1994;Slomovitz et al, 2003). Extra-uterine disease is often found in these patients even in the absence of myometrial invasion (Abeler 1991;Goff et al, 1994;Bristow et al, 2001).…”

mentioning

confidence: 99%

HER2 gene amplification and EGFR expression in a large cohort of surgically staged patients with nonendometrioid (type II) endometrial cancer

et al. 2008

View full text Add to dashboard Cite

Type II endometrial cancers (uterine serous papillary and clear cell histologies) represent rare but highly aggressive variants of endometrial cancer (EC). HER2 and EGFR may be differentially expressed in type II EC. Here, we evaluate the clinical role of HER2 and EGFR in a large cohort of surgically staged patients with type II (nonendometrioid) EC and compare the findings with those seen in a representative cohort of type I (endometrioid) EC. In this study HER2 gene amplification was studied by fluorescence in situ hybridisation (FISH) and EGFR expression by immunohistochemistry. Tissue microarrays were constructed from 279 patients with EC (145 patients with type I and 134 patients with type II EC). All patients were completely surgically staged and long-term clinical follow up was available for 258 patients. The rate of HER2 gene amplification was significantly higher in type II EC compared with type I EC (17 vs 1%, Po0.001). HER2 gene amplification was detected in 17 and 16% of the cases with uterine serous papillary and clear cell type histology, respectively. In contrast, EGFR expression was significantly lower in type II compared with type I EC (34 vs 46%, P ¼ 0.041). EGFR expression but not HER2 gene amplification was significantly associated with poor overall survival in patients with type II EC, (EGFR, median survival 20 vs 33 months, P ¼ 0.028; HER2, median survival 18 vs 29 months, P ¼ 0.113) and EGFR expression retained prognostic independence when adjusting for histology, stage, grade, and age (EGFR, P ¼ 0.0197; HER2, P ¼ 0.7855). We conclude that assessment of HER2 gene amplification and/or EGFR expression may help to select type II EC patients who could benefit from therapeutic strategies targeting both HER2 and EGFR.

show abstract

Uterine papillary serous carcinoma (UPSC): a single institution review of 129 cases

Cited by 318 publications

References 25 publications

p53 overexpression in morphologically ambiguous endometrial carcinomas correlates with adverse clinical outcomes

p53 overexpression in morphologically ambiguous endometrial carcinomas correlates with adverse clinical outcomes

Primary sources of pelvic serous cancer in patients with endometrial intraepithelial carcinoma

HER2 gene amplification and EGFR expression in a large cohort of surgically staged patients with nonendometrioid (type II) endometrial cancer

Contact Info

Product

Resources

About