Malignant Mullerian Mixed Tumor Arising From Ovarian Serous Carcinoma: A Clinicopathologic and Molecular Study of Two Cases

Gallardo, Alberto; Matías‐Guiu, Xavier; Lagarda, Helena; Catasús, Lluis; Bussaglia, Elena; Gras, Esther; Suárez, Daniel; Prat, Jaime

doi:10.1097/00004347-200207000-00010

Cited by 40 publications

(28 citation statements)

References 20 publications

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“…Moreover, the presence of a heterologous component has been associated with poor prognosis [15,16]. More recent evidence, however, has shown that carcinosarcoma characteristics are more closely associated with the behavior of the carcinoma components [17]. Although heterologous ovarian carcinosarcomas have been associated with poorer prognosis than have homologous carcinosarcomas, other studies have reported no difference in overall survival [2].…”

Section: Discussionmentioning

confidence: 99%

Optimal Debulking Surgery Followed by Paclitaxel/Platinum Chemotherapy Is Very Effective in Treating Ovarian Carcinosarcomas: A Single Center Experience

Chun

Kim²,

Kim³

et al. 2011

Gynecol Obstet Invest

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Background: There have been only a few reports on the survival and management of patients with ovarian carcinosarcomas. We evaluated the clinical characteristics, outcomes and prognostic factors of ovarian carcinosarcomas. Methods: Retrospective analysis of data obtained from medical records of 40 patients treated at the Asan Medical Center, Seoul, Korea, between January 1989 and January 2008. Results: Median survival was significantly longer in patients <60 years of age than in those ≧60 (p = 0.001), patients with early-stage compared to advanced tumors (p = 0.035), those with optimally debulked tumors compared to suboptimally (p < 0.001) in the advanced stage, and patients treated with paclitaxel/platinum compared to patients treated with other chemotherapies (p < 0.001). The progression-free interval was longer in patients with early-stage (p = 0.003) and optimally debulked tumors (p = 0.001), as well as in those treated with paclitaxel/platinum (p = 0.049). Multivariate analysis showed that advanced-stage, non-optimal debulking and non-paclitaxel/platinum chemotherapy were significant independent predictors of a shorter progression-free interval, and that non-optimal debulking and non-paclitaxel/platinum chemotherapy were significant independent predictors of shorter overall survival. Conclusions: Early-stage optimal debulking and adequate chemotherapy can influence time to progression and survival, indicating that the most effective treatment for patients with ovarian carcinosarcomas consists of optimal debulking surgery followed by paclitaxel/platinum chemotherapy.

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Section: Discussionmentioning

confidence: 99%

Optimal Debulking Surgery Followed by Paclitaxel/Platinum Chemotherapy Is Very Effective in Treating Ovarian Carcinosarcomas: A Single Center Experience

Chun

Kim²,

Kim³

et al. 2011

Gynecol Obstet Invest

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“…It is well known that chromosomal aberrations occur commonly in carcinosarcomas of the female genital tract. Cytogenetic studies have shown that p53 and K-ras mutations, LOH, and microsatellite instability arise in both tumor components [1,14,15,25,38]. Wada et al [38] found identical mutations of p53 and K-ras in the two different tumor components.…”

Section: Discussionmentioning

confidence: 99%

Molecular genetic aberrations of ovarian and uterine carcinosarcomas—a CGH and FISH study

Schipf¹,

Mayr

Kirchner

et al. 2008

Virchows Arch

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The origin of carcinosarcomas of the ovary and uterus has long been discussed. In this study, we used a molecular-genetic approach to elucidate the tumorigenesis of carcinosarcomas of these organs correlating our findings with the specific biphasic pattern of these tumors. We analyzed a series of 30 paraffin-embedded carcinosarcomas of the ovary and the uterus using comparative genomic hybridization (CGH) and fluorescence in-situ hybridization (FISH). In general, gains (85%) were observed more frequently, than losses (30%). Characteristic and frequent chromosomal amplification was observed on chromosome 8q and 20q (42 and 70%). FISH revealed c-myc (8q24.12) and ZNF217 (20q13.2) amplification in 78 and 87%. Amplification of ZNF217 was mostly seen in both tumor components, whereas amplification of c-myc was observed less often in the sarcomatous than in the carcinomatous tumor component. Analysis of the proliferation index using Ki67 immunohistochemistry revealed a strong or moderate expression in all cases, wherein the carcinomatous tumor component showed significantly a higher proliferation index compared to the sarcomatous tumor areas. Although our results are in agreement with a monoclonal origin of ovarian and uterine carcinosarcomas, the carcinomatous component seems to be the more aggressive part of the tumor. Furthermore, the observed patterns of genetic aberrations are highly similar to those of serous carcinomas. This is compatible with the current opinion that these neoplasms should be considered as metaplastic carcinomas.

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“…Like high-grade serous carcinoma, other Type II tumors, specifically malignant mixed mesodermal tumors (carcinosarcomas) also demonstrate TP53 mutations in almost all cases analyzed (40)(41)(42). Moreover, when the carcinomatous and sarcomatous components of MMMTs are analyzed for TP53 mutation the identical mutation has been detected in both the epithelial and stromal component leading investigators to suggest that malignant mixed mesodermal tumors are in essence variants of carcinoma.…”

Section: Serous Tumorsmentioning

confidence: 99%

Pathogenesis of Ovarian Cancer

Kurman¹,

Shih²

2008

International Journal of Gynecological Pathology

218

176

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The received view of ovarian carcinogenesis is that carcinoma begins in the ovary, undergoes progressive "dedifferentiation" from a well to a poorly differentiated tumor and then spreads to the pelvic and abdominal cavities before metastasizing to distant sites. It has therefore been reasoned that survival for this highly lethal disease could be improved by developing screening methods that detect disease when it is confined to the ovary. To date, however, no prospective, randomized trial of any ovarian cancer screening test(s) has demonstrated a decrease in mortality. We believe that one of the main reasons for this is that the dogma underlying ovarian carcinogenesis is flawed. Based on studies performed in our laboratory over the last decade we have proposed a model of ovarian carcinogenesis that takes into account the diverse nature of "ovarian cancer" and correlates the clinical, pathologic and molecular features of the disease. In this model, ovarian tumors are divided into two groups designated Type I and Type II. Type I tumors are slow growing, generally confined to the ovary at diagnosis and develop from well established precursor lesions that are termed "borderline" tumors. Type I tumors include low-grade micropapillary serous carcinoma, mucinous, endometrioid, and clear cell carcinomas. They are genetically stable and are characterized by mutations in a number of different genes including KRAS, BRAF, PTEN, and beta-catenin. Type II tumors are rapidly growing, highly aggressive neoplasms for which well defined precursor lesions have not been described. Type II tumors include high-grade serous carcinoma, malignant mixed mesodermal tumors (carcinosarcomas) and undifferentiated carcinomas. This group of tumors has a high level of genetic instability and is characterized by mutation of TP53. The model helps to explain why current screening techniques, aimed at detecting stage I disease, have not been effective. Tumors that remain confined to the ovary for a long period of time belong to the Type I group but they account for only 25% of the malignant tumors. The vast majority of what is considered "ovarian cancer" belongs to the Type II category and these are only rarely confined to the ovary. Although the reasons for this are not entirely clear, it appears that some tumors evolve rapidly and spread to extra-ovarian sites early in their development. In addition, a significant number of Type II "ovarian carcinomas" develop outside the ovary, specifically, the peritoneum and fallopian tube, and involve the ovary secondarily. These tumors are advanced stage at their inception. Therefore, a more realistic endpoint for the early detection of ovarian carcinoma may be volume and not stage of disease. Thus, the model which correlates the clinical and pathologic features of "ovarian cancer" with the specific molecular genetic events that play a role in tumor progression can lead to a more rational approach to early detection and to more targeted therapeutic intervention.The received view of ovarian carcinogen...

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Malignant Mullerian Mixed Tumor Arising From Ovarian Serous Carcinoma: A Clinicopathologic and Molecular Study of Two Cases

Abstract: 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.

Cited by 40 publications

References 20 publications

Optimal Debulking Surgery Followed by Paclitaxel/Platinum Chemotherapy Is Very Effective in Treating Ovarian Carcinosarcomas: A Single Center Experience

Optimal Debulking Surgery Followed by Paclitaxel/Platinum Chemotherapy Is Very Effective in Treating Ovarian Carcinosarcomas: A Single Center Experience

Molecular genetic aberrations of ovarian and uterine carcinosarcomas—a CGH and FISH study

Pathogenesis of Ovarian Cancer

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