National Cancer Data Base report of associations, patterns, and survival benefit of lymphadenectomy in endometrial cancer
J.C. CripeElizabeth A. HandorfJennifer BrownScott E. WoodmanStephen C. RubinAngela JainGina Mantia-Smaldone
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Lymphadenectomy
Serous carcinoma
Clear cell carcinoma
There are several morphologic types of ovarian carcinoma. It has been shown that p16 is overexpressed in high-grade serous carcinoma but there has been little detailed comparison of p16 expression in the common types of ovarian carcinoma. The aim of this study was to compare p16 expression in ovarian carcinomas of serous, endometrioid, clear cell, and mucinous type with a view to ascertaining whether high expression in a primary ovarian carcinoma is specific for a serous neoplasm. We included problematic cases, which are difficult to type, such as poorly differentiated and undifferentiated carcinomas and serous carcinomas with clear cells. In these problematic groups, we compared p16 expression with that of WT1, which is known to be relatively specific for a serous phenotype. Cases of ovarian high-grade serous carcinoma (n=38), endometrioid carcinoma (n=15), clear cell carcinoma (n=12), and mucinous carcinoma (n=10) were stained with p16. Cases were scored both with respect to distribution of immunoreactivity (0–5) and intensity (0–3). An immunohistochemical composite score was also calculated (0–15) by multiplying the distribution and intensity scores. Serous carcinomas typically exhibited high p16 expression; there was statistically significant higher p16 expression in serous carcinomas compared with the other morphologic types. There was high p16 and WT1 expression in most undifferentiated carcinomas and in serous carcinomas with clear cells, suggesting that these represent variants of serous carcinoma. We have demonstrated that p16 is highly expressed in high-grade serous and undifferentiated carcinomas compared with other morphologic types of ovarian carcinoma. This may be useful, in conjunction with WT1, in the classification of problematic neoplasms. p16 may be involved in the pathogenesis of high-grade ovarian serous carcinomas, possibly through inactivation of retinoblastoma protein.
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A review of the pathology and cytopathology of 295 endometrial adenocarcinomas treated surgically at King Edward Memorial Hospital for Women, with full 5-year follow-up, revealed 16 cases of pure serous carcinoma (USC), 10 cases of mixed serous and endometrioid carcinoma with a predominant serous component (mixed USC-EAC) and six cases of mixed serous and endometrioid carcinoma with a predominant endometrioid component (mixed EAC-USC). The mixed carcinomas may be characterized microscopically by classical serous features side by side with classical endometrioid features, or additionally by features intermediate between the two. Many of these features are reproduced in preoperative cervicovaginal smears. USC and mixed USC-EAC were found to be indistinguishable clinically and prognostically, with an identical corrected 5-year survival of 40%, although numbers are small. Mixed EAC-USC (which contained 10-25% serous differentiation in this series), however, were similar in many respects to a control population of 95 EAC of Grade 2 and 3. The corrected 5-year survival in these two groups was 67% and 79%, respectively, which is not statistically significant in this small series. This study suggests that the behavior of a mixed tumor containing 50% or more serous differentiation is similar to that of pure serous carcinoma, and that the behavior of a mixed tumor containing less than 25% serous differentiation is similar to that of the other component. Given the poor correlation between pathologic findings in curettage and subsequent hysterectomy specimens, however, identification of any significant serous element in curettage material may prove vital in optimizing surgical and adjuvant therapy.
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[Purpose] To investigate the relationship of preoperative serous CA125 with clinicopathological features and prognosis in patients with epithelial ovarian carcinoma.[Methods] The relationship of preoperative serous CA125 with histologic type,grade,FIGO stage,ascites and survival in 279 cases with epithelial ovarian carcinoma were analyzed retrospectively.[Results] The median CA125 value for all 279 patients was 339.2 U/ml(range 3.6～20 220.0U/ml).Preoperative serous CA125 in serous carcinoma was significantly higher than that in non-serous carcinoma(P0.05).For non-serous carcinoma with different histologic types,preoperative serous CA125 in mucinous /clear cell carcinoma was significantly lower than that in serous carcinoma(P0.01),and no significant difference was found between other types of non-serous carcinoma.Preoperative serous CA125 in early stage(stage Ⅰ) patient was significantly lower than that in advanced stage(stage Ⅱ～Ⅳ) patient(P=0.000).For non-mucinous/clear cell carcinoma patient,lower serous CA125 was usually associated with early disease and fairly good prognosis.As compared,higher serous CA125 was usually connected with advanced diseases,among which those with highest CA125 level displayed better survival than those with intermediate CA125 level.[Conclusion] Preoperative serous CA125 might reflect the tumor load for serous and other non-mucinous/clear cell carcinoma in epithelial ovarian carcinoma.
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Introduction The dualistic theory of ovarian carcinogenesis proposes that epithelial “ovarian” cancer is not one entity with several histological subtypes but a collection of different diseases arising from cells of different origin, some of which may not originate in the ovarian surface epithelium. Methods All cases referred to the Pan-Birmingham Gynaecological Cancer Centre with an ovarian, tubal, or primary peritoneal cancer between April 2006 and April 2012 were identified from the West Midlands Cancer Registry. Tumors were classified into type I (low-grade endometrioid, clear cell, mucinous, and low-grade serous) and type II (high-grade serous, high-grade endometrioid, carcinosarcoma, and undifferentiated) cancers. Results Ovarian (83.5%), tubal (4.3%), or primary peritoneal carcinoma (12.2%) were diagnosed in a total of 583 woman. The ovarian tumors were type I in 134 cases (27.5%), type II in 325 cases (66.7%), and contained elements of both type I and type II tumors in 28 cases (5.7%). Most tubal and primary peritoneal cases, however, were type II tumors: 24 (96.0%) and 64 (90.1%), respectively. Only 16 (5.8%) of the ovarian high-grade serous carcinomas were stage I at diagnosis, whereas 240 (86.6%) were stage III+. Overall survival varied between the subtypes when matched for stage. Stage III low-grade serous and high-grade serous carcinomas had a significantly better survival compared to clear cell and mucinous cases, P = 0.0134. There was no significant difference in overall survival between the high-grade serous ovarian, tubal, or peritoneal carcinomas when matched for stage (stage III, P = 0.3758; stage IV, P = 0.4820). Conclusions Type II tumors are more common than type I and account for most tubal and peritoneal cancers. High-grade serous carcinomas, whether classified as ovarian/tubal/peritoneal, seem to behave as one disease entity with no significant difference in survival outcomes, therefore supporting the proposition of a separate classification of “tubo-ovarian serous carcinoma”.
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Noninvasive micropapillary serous carcinoma of the ovary is also referred to as the micropapillary variant of serous borderline tumor and displays a characteristic pattern of papillary branching but lacks invasion. In contrast, invasive micropapillary serous carcinoma is the usual form of low-grade invasive serous carcinoma. There is a consensus that peritoneal "implants" associated with serous borderline tumors that display invasive features ("invasive implants") have a poor prognosis with a 7-year survival of 66%, and can also be referred to as invasive carcinoma. Evidence indicates that noninvasive micropapillary serous carcinoma has a strong association with invasive implants as compared with typical serous borderline tumors (49% vs. 7%, respectively, P < 0.0001). After excluding micropapillary serous borderline tumors and those with invasive implants, the remaining patients with serous borderline tumors have a survival of virtually 100%, thereby obviating the need for the serous borderline category.
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Although risk factors have been established for the development of serous carcinoma after a diagnosis of serous borderline tumor (SBT), comprising atypical proliferative serous tumor (APST) (ie, conventional SBT) and noninvasive low-grade serous carcinoma (niLGSC) (ie, micropapillary SBT), subsequent invasive carcinoma still occurs in a subset of women who are not at increased risk. Whether subsequent serous carcinoma in women with a prior SBT represents malignant progression/recurrence or an independent primary tumor is unclear, and the combined clinicopathologic and molecular features of SBTs and their subsequent carcinomas have not been fully characterized. In this study, we analyzed a cohort of 42 women initially diagnosed with SBT who subsequently developed serous carcinoma of a total of 1025 cases of ovarian SBT from a nationwide population-based cohort. Review of the diagnostic slides was performed from this subset of SBTs and matched metachronous invasive serous carcinomas (39 low grade, 3 high grade). DNA was extracted from tissue blocks available for 41 cases (both SBT and carcinoma, n=36; SBT only, n=3; carcinoma only, n=2). Samples were subjected to digital droplet PCR to analyze mutation hotspots in KRAS (codon 12) and BRAF (V600E), which are frequently found in low-grade serous tumors. Eighty-one percent of SBTs (34/42) were APST, and 19% (8/42) were niLGSC. Forty percent of cases (17/42) were FIGO stage I, the majority of which were APST (14/17; 82%). The median time to development of carcinoma was 9 years (range, 0.6 to 25 y). Mutations in SBTs were distributed as follows: 5/39 (13%) BRAF mutant, 22/39 (56%) KRAS mutant, and 12/39 (31%) wild-type for both genes. There was a significant relationship between SBT gene mutation and histologic type, with BRAF mutations occurring exclusively in APST and a higher frequency of niLGSC among SBTs wild-type for BRAF and KRAS ( P =0.01). The diffuse presence of tumor cells with abundant eosinophilic cytoplasm was significantly associated with the BRAF mutation ( P =0.001). Mutational analyses of matched SBT/carcinoma pairs revealed concordant profiles in 33/36 (92%) cases, of which 19 (53%) were KRAS mutant, 4 (11%) were BRAF mutant, and 10 (28%) were wild type for both genes. The 3 discordant cases consisted of a wild-type niLGSC with a subsequent BRAF -mutant invasive LGSC, a KRAS G12V -mutant APST with a KRAS G12C -mutant LGSC, and a BRAF -mutant APST with subsequent development of a KRAS G12D -mutant high-grade serous carcinoma. In conclusion, some women with SBTs can subsequently develop serous carcinoma, occasionally over 10 years later. Most subsequent carcinomas are low grade, but a small subset can be high grade. The type of gene mutation in SBT correlates with various histologic features. While most cases of serous carcinoma developing after a diagnosis of SBT probably represent tumor progression, a minority are independent primary tumors, presumably arising from endosalpingiosis.
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There are conflicting data about chemoresistance and prognosis in ovarian clear cell carcinoma (CCC). This could be due to significant interobserver variation in the diagnosis of CCC and other ovarian surface epithelial tumors containing clear cells. Thirty-two cases previously diagnosed as CCC, high-grade ovarian serous carcinoma (SC), and mixed surface epithelial carcinoma (SEC) with clear cell and serous components were reviewed by 4 gynecologic pathologists blinded to the original diagnoses. Interobserver reproducibility was evaluated. Each case was also assessed using immunohistochemical markers Wilm tumor 1, estrogen receptor, and p53. The interobserver reproducibility was greatest for pure CCC (kappa of 0.82), and lowest for the mixed SEC (kappa of 0.32). Moderate agreement was seen in the pure SC category (kappa of 0.59). All pure SC and most mixed SEC presented as stage III or IV diseases. Most pure CCC presented as stage I or II diseases. Immunoreactivities of the mixed SECs were similar to those of pure SC, but significantly different from those of pure CCC for Wilm tumor 1 (P=0.0011 for both components), estrogen receptor (P=0.0003 for clear cell component, P=0.0001 for serous component), and p53 (P=0.0062 for both components). The serous and clear cell components of mixed SEC showed higher mitotic rates than pure CCC (P=0.004 and P=0.023, respectively), but the mitotic rate of pure SC was similar to the mixed SEC. We conclude that (1) pure CCC is reproducibly diagnosed. (2) The diagnosis of mixed ovarian SEC with clear cell component is not reproducible. (3) Mixed SEC with clear cell and serous components show similar stage, mitotic activities, and immunoreactivities to those of pure SC, and likely represent SC with clear cell changes.
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