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1. Huang YD, Hung YC, Yeh LS, Chiang IP, Zeng GC, Chang WC: Synchronous ovarian endometrioid adenocarcinoma and endocervical mucinous adenocarcinoma. Taiwan J Obstet Gynecol; 2006 Sep;45(3):264-7
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  • [Title] Synchronous ovarian endometrioid adenocarcinoma and endocervical mucinous adenocarcinoma.
  • OBJECTIVE: We report a rare case of synchronous cancer consisting of ovarian endometrioid adenocarcinoma and endocervical mucinous adenocarcinoma.
  • Computed tomography showed an 18 x 16 cm right pelvic tumor, with both cystic and solid components, ascites and bilateral massive pleural effusion.
  • Cytology of the pleural effusion showed no malignant cells.
  • Histology showed moderately to poorly differentiated endometrioid adenocarcinoma of the right ovary with extensive lymphovascular permeation, as well as paraaortic and bilateral pelvic lymph node metastases.
  • Extensive tumor thrombi were observed in the lymphovascular channels of the left ovary, bilateral tubes and uterus.
  • Endocervical adenocarcinoma, < 3 mm in depth, was also identified on the cervix.
  • The final surgical-pathologic stage of ovarian endometrioid adenocarcinoma was stage IIIc and of endocervical mucinous adenocarcinoma was stage IA1.
  • Adjuvant chemotherapy with carboplatin and paclitaxel was prescribed postoperatively, but the malignancy was not controlled due to lung, brain and vulva metastases.
  • CONCLUSION: The coexistence of primary neoplasms in the ovary and cervix is rare.
  • Diagnosis should be based on histologic examination and requires appropriate treatment for both tumors.
  • [MeSH-major] Adenocarcinoma, Mucinous / epidemiology. Carcinoma, Endometrioid / epidemiology. Neoplasms, Multiple Primary / pathology. Ovarian Neoplasms / epidemiology. Uterine Cervical Neoplasms / epidemiology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / secondary. Carcinoembryonic Antigen / metabolism. Combined Modality Therapy. Female. Humans. Lung Neoplasms / secondary. Lymphatic Metastasis. Necrosis. Vulvar Neoplasms / secondary

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  • (PMID = 17175478.001).
  • [ISSN] 1875-6263
  • [Journal-full-title] Taiwanese journal of obstetrics & gynecology
  • [ISO-abbreviation] Taiwan J Obstet Gynecol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Carcinoembryonic Antigen
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2. Pan Y, Kao MS: Endometrioid ovarian carcinoma benefits from aromatase inhibitors: case report and literature review. Curr Oncol; 2010 Nov;17(6):82-5

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  • [Title] Endometrioid ovarian carcinoma benefits from aromatase inhibitors: case report and literature review.
  • Aromatase inhibitors have not been adequately assessed in treatment of ovarian cancer.
  • The aromatase inhibitor letrozole (2.5 mg daily) was administered in 2 cases of advanced endometrioid ovarian cancer with positive estrogen receptor.
  • CASE 1: A 52-year-old woman with a grade 2-3, stage iiic endometrioid ovarian cancer was optimally debulked and received 6 cycles of intravenous paclitaxel and intraperitoneal cisplatin-paclitaxel.
  • Post chemotherapy, one of several biopsies showed residual disease during the second-look laparoscopy.
  • CASE 2: A 47-year-old woman with a grade 3, stage iiic endometrioid ovarian cancer was optimally debulked and treated with intravenous carboplatin-paclitaxel.
  • Letrozole was administered after the chemotherapy.
  • CONCLUSIONS: Endometrioid ovarian carcinoma may benefit from aromatase inhibitors, especially when the tumour burden is low after primary chemotherapy or when the inhibitor is used as maintenance therapy between chemotherapies.

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  • (PMID = 21151415.001).
  • [ISSN] 1718-7729
  • [Journal-full-title] Current oncology (Toronto, Ont.)
  • [ISO-abbreviation] Curr Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC2993449
  • [Keywords] NOTNLM ; Aromatase inhibitor / endometrioid ovarian cancer / letrozole / maintenance therapy / recurrent ovarian cancer
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3. Pieretti-Vanmarcke R, Donahoe PK, Pearsall LA, Dinulescu DM, Connolly DC, Halpern EF, Seiden MV, MacLaughlin DT: Mullerian Inhibiting Substance enhances subclinical doses of chemotherapeutic agents to inhibit human and mouse ovarian cancer. Proc Natl Acad Sci U S A; 2006 Nov 14;103(46):17426-31
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  • [Title] Mullerian Inhibiting Substance enhances subclinical doses of chemotherapeutic agents to inhibit human and mouse ovarian cancer.
  • Mullerian Inhibiting Substance (MIS), a biological modifier that causes regression of Mullerian ducts in male embryos, is effective as a single agent in vitro and in vivo against human and mouse ovarian cancer cell lines expressing MIS type II receptor; however, little is known about how recombinant human MIS (rhMIS), now being scaled for preclinical trials, could be used in combination with cytotoxic or targeted chemotherapeutic agents.
  • Mouse serous and endometrioid ovarian carcinoma cell lines were tested in vitro against rhMIS alone and with doxorubicin, paclitaxel, or cisplatin as agents in clinical use.
  • MIS increases p16 protein levels, and 5'-Aza-2'-deoxycytidine (AzadC) induces p16 mRNA; therefore, they were used in combination in vitro and in vivo with a human ovarian cancer cell line.
  • A paclitaxel-resistant human ovarian cancer cell line and its parental line both respond to rhMIS in vitro.
  • Additivity, synergy, or competition was observed with MIS and rapamycin, AzadC, doxorubicin, cisplatin, and paclitaxel, suggesting that MIS in combination with selective targeted therapies might achieve greater activity against ovarian cancer than the use of each individual agent alone.

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  • (PMID = 17088539.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K24 CA109416; United States / NCI NIH HHS / CA / U01 CA084242; United States / NCI NIH HHS / CA / R01 CA017393; United States / NCI NIH HHS / CA / CA 17393; United States / NCI NIH HHS / CA / 1K24 CA109416; United States / NCI NIH HHS / CA / P50 CA083638; United States / NICHD NIH HHS / HD / HD 32212
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glycoproteins; 0 / Immunoglobulin G; 0 / Receptors, Peptide; 0 / Receptors, Transforming Growth Factor beta; 0 / Testicular Hormones; 0 / anti-Mullerian hormone receptor; 0 / antineoplastic agent K 18; 776B62CQ27 / decitabine; 80497-65-0 / Anti-Mullerian Hormone; M801H13NRU / Azacitidine; P88XT4IS4D / Paclitaxel; Q41OR9510P / Melphalan
  • [Other-IDs] NLM/ PMC1859945
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4. Tao X, Kavanagh JJ: Chemotherapy for gynecological malignancies in organ transplantation patients: report of two cases. Int J Gynecol Cancer; 2008 Nov-Dec;18(6):1376-80
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  • [Title] Chemotherapy for gynecological malignancies in organ transplantation patients: report of two cases.
  • Treatment, especially chemotherapy, in these patients should take into consideration their renal function and the effects of immunosuppressive agents.
  • We here present two case reports of patients with chemotherapy-treated gynecological malignancies who had previously received organ transplantation.
  • The first case, a rare occurrence of simultaneous carcinomas of the uterine corpus and ovary, is the first such report in the English literature describing chemotherapy for concurrent serous papillary ovarian carcinoma and endometrioid endometrial carcinoma in a renal transplant patient.
  • The second case report, describing chemotherapy for cervical cancer following two organ transplantation, also rare, is the first such report in the English literature and the first report of cervical cancer after heart-kidney transplantation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Adenosquamous / drug therapy. Heart Transplantation. Kidney Transplantation. Ovarian Neoplasms / drug therapy. Uterine Neoplasms / drug therapy
  • [MeSH-minor] Disease Progression. Female. Graft Survival / drug effects. Humans. Immunosuppressive Agents / pharmacology. Middle Aged


5. Abe A, Furumoto H, Yoshida K, Nishimura M, Irahara M, Kudo E, Sano T: A case of ovarian endometrioid adenocarcinoma with a yolk sac tumor component. Int J Gynecol Cancer; 2008 Jan-Feb;18(1):168-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of ovarian endometrioid adenocarcinoma with a yolk sac tumor component.
  • Endometrioid adenocarcinoma of the ovary coexists very rarely with yolk sac tumor (YST).
  • This unusual mixed tumor is thought to be a rare variant of endometrioid ovarian carcinoma because of its aggressive behavior, lack of response to chemotherapy, and unfavorable prognosis.
  • We report a case of ovarian endometrioid adenocarcinoma with a YST component in a postmenopausal woman.
  • Cytokeratin7 and epithelial membrane antigen were negative in YST, but positive in endometrioid adenocarcinoma.
  • [MeSH-major] Carcinoma, Endometrioid / pathology. Endodermal Sinus Tumor / pathology. Ovarian Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bleomycin / administration & dosage. Bridged Compounds / administration & dosage. Cisplatin / administration & dosage. Etoposide / administration & dosage. Female. Humans. Immunoenzyme Techniques. Middle Aged. Platinum / administration & dosage. Taxoids / administration & dosage. alpha-Fetoproteins / metabolism

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  • (PMID = 17466041.001).
  • [ISSN] 1525-1438
  • [Journal-full-title] International journal of gynecological cancer : official journal of the International Gynecological Cancer Society
  • [ISO-abbreviation] Int. J. Gynecol. Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bridged Compounds; 0 / Taxoids; 0 / alpha-Fetoproteins; 11056-06-7 / Bleomycin; 1605-68-1 / taxane; 49DFR088MY / Platinum; 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin
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6. Tohya T, Shimajiri S, Onoda C, Yoshimura T: Complete remission of ovarian endometrioid adenocarcinoma associated with hyperamylasemia and liver metastasis treated by paclitaxel and carboplatin chemotherapy: a case report. Int J Gynecol Cancer; 2004 Mar-Apr;14(2):378-80
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  • [Title] Complete remission of ovarian endometrioid adenocarcinoma associated with hyperamylasemia and liver metastasis treated by paclitaxel and carboplatin chemotherapy: a case report.
  • Complete remission in the case of a 45-year-old woman with ovarian endometrioid adenocarcinoma associated with hyperamylasemia and liver metastasis is described.
  • The serum amylase was 600 micro/l (normal value: 60-200 micro/l), and electrophoresis identified isoamylases of the salivary type.
  • A total abdominal hysterectomy with bilateral salpingo-oophorectomy was performed for invasive carcinoma of the left ovary.
  • The histology of the left ovary showed endometrioid adenocarcinoma.
  • Immunohistochemically, the adenocarcinoma cells were diffusely and strongly positive for amylase.
  • The patient received six courses of paclitaxel and carboplatin combination chemotherapy.
  • The prognosis of patients with ovarian cancer metastatic to the liver is uniformly poor.
  • [MeSH-major] Carcinoma, Endometrioid / diagnosis. Liver Neoplasms / diagnosis. Ovarian Neoplasms / diagnosis
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carboplatin / administration & dosage. Combined Modality Therapy. Diagnosis, Differential. Female. Humans. Hyperamylasemia / etiology. Hysterectomy. Immunohistochemistry. Middle Aged. Ovariectomy. Paclitaxel / administration & dosage

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  • (PMID = 15086742.001).
  • [ISSN] 1048-891X
  • [Journal-full-title] International journal of gynecological cancer : official journal of the International Gynecological Cancer Society
  • [ISO-abbreviation] Int. J. Gynecol. Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel
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7. Fu M, Maresh EL, Soslow RA, Alavi M, Mah V, Zhou Q, Iasonos A, Goodglick L, Gordon LK, Braun J, Wadehra M: Epithelial membrane protein-2 is a novel therapeutic target in ovarian cancer. Clin Cancer Res; 2010 Aug 1;16(15):3954-63
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  • [Title] Epithelial membrane protein-2 is a novel therapeutic target in ovarian cancer.
  • PURPOSE: The tetraspan protein epithelial membrane protein-2 (EMP2) has been shown to regulate the surface display and signaling from select integrin pairs, and it was recently identified as a prognostic biomarker in human endometrial cancer.
  • In this study, we assessed the role of EMP2 in human ovarian cancer.
  • EXPERIMENTAL DESIGN: We examined the expression of EMP2 within a population of women with ovarian cancer using tissue microarray assay technology.
  • We evaluated the efficacy of EMP2-directed antibody therapy using a fully human recombinant bivalent antibody fragment (diabody) in vitro and ovarian cancer xenograft models in vivo.
  • RESULTS: EMP2 was found to be highly expressed in >70% of serous and endometrioid ovarian tumors compared with nonmalignant ovarian epithelium using a human ovarian cancer tissue microarray.
  • Using anti-EMP2 diabody, we evaluated the in vitro response of nine human ovarian cancer cell lines with detectable EMP2 expression.
  • Treatment of human ovarian cancer cell lines with anti-EMP2 diabodies induced cell death and retarded cell growth, and these response rates correlated with cellular EMP2 expression.
  • We next assessed the effects of anti-EMP2 diabodies in mice bearing xenografts from the ovarian endometrioid carcinoma cell line OVCAR5.
  • CONCLUSIONS: These findings indicate that EMP2 is expressed in the majority of ovarian tumors and may be a feasible target in vivo.

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  • [Copyright] (c) 2010 AACR.
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  • (PMID = 20670949.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA016042; United States / NCI NIH HHS / CA / U24 CA086366; United States / NICHD NIH HHS / HD / R03 HD048540; United States / NCI NIH HHS / CA / R21 CA131756; United States / NCI NIH HHS / CA / P30 CA016042; United States / NCI NIH HHS / CA / NCI CA-86366; United States / NCI NIH HHS / CA / U54 CA119367; United States / NCI NIH HHS / CA / R21 CA131756-01A1; United States / NCI NIH HHS / CA / CA131756-01A1; United States / NICHD NIH HHS / HD / HD48540
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / EMP2 protein, human; 0 / Immunoglobulin Fragments; 0 / Membrane Glycoproteins
  • [Other-IDs] NLM/ NIHMS211285; NLM/ PMC2913478
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8. Ehara R, Koga T, You S, Natori H, Kamimura T, Nishimura M, Matsuo K: Pseudo-Meigs'syndrome as a cause of exertional dyspnea: a case report. Kurume Med J; 2009;56(3-4):85-7
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  • A 61-year-old otherwise healthy woman presented with gradually worsening exertional dyspnea.
  • Systemic examinations showed ascites and a pelvic tumor, which turned out to be right ovarian endometrioid adenocarcinoma.
  • Surgical removal and chemotherapy against the ovarian cancer resulted in disappearance of the ascites and pleural effusion, establishing a diagnosis of pseudo-Meigs'syndrome.
  • It is common for reported cases of pseudo-Meigs' syndrome to initially present with dyspnea, therefore it is important to consider this disorder when attempting a differential diagnosis in female patients presenting with dyspnea without other noticeable conditions.

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  • (PMID = 20505286.001).
  • [ISSN] 1881-2090
  • [Journal-full-title] The Kurume medical journal
  • [ISO-abbreviation] Kurume Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / CA-125 Antigen; 0 / MUC16 protein, human; 0 / Membrane Proteins
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9. Wu TI, Chang TC, Hsueh S, Lai CH: Ovarian endometrioid carcinoma with diffuse pigmented peritoneal keratin granulomas: a case report and review of the literature. Int J Gynecol Cancer; 2006 Jan-Feb;16(1):426-9
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  • [Title] Ovarian endometrioid carcinoma with diffuse pigmented peritoneal keratin granulomas: a case report and review of the literature.
  • The presence of keratin granulomas in peritoneal cavity associated with ovarian endometrioid carcinoma, which might be related to leakage from the ovarian tumor, is rarely reported.
  • Its clinical significance has not yet been well investigated.
  • The ovarian tumor was an endometrioid adenocarcinoma with squamous differentiation.
  • Since viable epithelial cells in the implants could be differentially identified against mesothelial or granulomatous components by CK-7 staining and DNA aneuploidy was demonstrated on primary ovarian tumor, four courses of chemotherapy were administered.
  • The patient has been free of disease for 18 months since diagnosis.
  • [MeSH-major] Carcinoma, Endometrioid / secondary. Granuloma / pathology. Lymph Nodes / pathology. Ovarian Neoplasms / pathology. Peritoneal Diseases / pathology
  • [MeSH-minor] Abdominal Pain / diagnosis. Abdominal Pain / etiology. Biopsy, Needle. Female. Flow Cytometry. Follow-Up Studies. Frozen Sections. Humans. Immunohistochemistry. Laparotomy. Middle Aged. Ovariectomy. Treatment Outcome


10. Kamoi S, Ohaki Y, Mori O, Okada S, Seto M, Matsushita N, Kawamura T, Araki T: A case of ovarian endometrioid adenocarcinoma with yolk sac tumor component in a postmenopausal woman. APMIS; 2002 Jun;110(6):508-14
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  • [Title] A case of ovarian endometrioid adenocarcinoma with yolk sac tumor component in a postmenopausal woman.
  • The co-existence of an endometrioid adenocarcinoma with an ovarian yolk sac tumor is very rare.
  • Microscopically, foci of endometrioid adenocarcinoma together with a yolk sac tumor component were observed within a large endometriotic cyst.
  • Since the tumor was clinically staged 1c, the patient was given 500 mg of intraperitoneal carboplatin postoperatively, followed by five courses of combination chemotherapy consisting of cisplatin, etoposide and peplomycin at 4-week intervals.
  • [MeSH-major] Carcinoma, Endometrioid / pathology. Endodermal Sinus Tumor / pathology. Neoplasms, Multiple Primary / pathology. Ovarian Neoplasms / pathology

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  • (PMID = 12193212.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, Tumor-Associated, Carbohydrate; 0 / Biomarkers, Tumor; 0 / alpha-Fetoproteins
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11. Bilir A, Altinoz MA, Attar E, Erkan M, Aydiner A: Acetaminophen modulations of chemotherapy efficacy in MDAH 2774 human endometrioid ovarian cancer cells in vitro. Neoplasma; 2002;49(1):38-42
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  • [Title] Acetaminophen modulations of chemotherapy efficacy in MDAH 2774 human endometrioid ovarian cancer cells in vitro.
  • Epidemiological data have correlated consumption of nonsteroidal antinflammatory drugs with lowered risk for many types of cancer, and some recent studies indicate a reverse correlation with acetaminophen consumption and ovarian malignancy.
  • In this study we examined effects of acetaminophen on plating, S-phase and colony growth of MDAH 2774 human endometrioid ovarian carcinoma, as well as sensitivity of this cell line to carboplatin in all three tests, and paclitaxel to clonogenic assay.
  • Acetaminophen significantly enhanced S-phase in first 72 hours and enhanced cell population in 96 hours of plating monitorization, but decreased one week colony growth by approximately 80%, which was in the range of cytotoxic drugs.
  • It did not effect paclitaxel colony growth inhibiting acitivity.
  • Thus, presence of lower doses of oxidizing drugs may help the induction of proliferative signals, but only their sustained presence may overcome such signals and ultimately bring to cell demise.
  • [MeSH-major] Acetaminophen / pharmacology. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Antineoplastic Agents / pharmacology. Carboplatin / pharmacology. Cell Division / drug effects. Ovarian Neoplasms / drug therapy. Paclitaxel / pharmacology
  • [MeSH-minor] Dose-Response Relationship, Drug. Drug Synergism. Female. Humans. Tumor Cells, Cultured / drug effects

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  • (PMID = 12044058.001).
  • [ISSN] 0028-2685
  • [Journal-full-title] Neoplasma
  • [ISO-abbreviation] Neoplasma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Slovakia
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Antineoplastic Agents; 362O9ITL9D / Acetaminophen; BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel
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12. Cryns P, Roofthooft NJ, Tjalma WA: Malignant mixed müllerian tumor of the ovary and false negative punctures. Eur J Gynaecol Oncol; 2003;24(1):70-2
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  • [Title] Malignant mixed müllerian tumor of the ovary and false negative punctures.
  • Malignant mixed müllerian tumour (MMMT) of the ovary is a rare and aggressive tumour with a poor prognosis.
  • We present a case of a 57-year-old woman with a large pelvic mass, omental cake, ascites and pleural effusions, clinically highly suspect of an ovarian neoplasm.
  • Paracentesis and ultrasound-guided biopsy of the ovary were negative for malignant disease.
  • The latter gave a histopathologic diagnosis of an endometrioid adenocarcinoma of the ovary.
  • However after cytoreductive surgery anatomopathologic examination revealed a malignant mixed müllerian tumour of the ovary with heterologous differentiation.
  • Adjuvant chemotherapy, active against the sarcomatous and the carcinomatous component, was given.
  • At present the patient is well and disease free 35 months after the initial diagnosis.
  • Cytological examination of ascites may be negative in the presence of malignant disease.
  • Punctures should be discouraged as a diagnostic tool in patients in whom an ovarian malignancy is suspected.
  • [MeSH-major] Adenocarcinoma / pathology. Mixed Tumor, Malignant / pathology. Mixed Tumor, Mullerian / pathology. Ovarian Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Biopsy, Needle. Combined Modality Therapy. Diagnosis, Differential. False Negative Reactions. Female. Follow-Up Studies. Humans. Immunohistochemistry. Middle Aged. Neoplasm Staging. Ovariectomy / methods. Risk Assessment. Treatment Outcome

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  • (PMID = 12691322.001).
  • [ISSN] 0392-2936
  • [Journal-full-title] European journal of gynaecological oncology
  • [ISO-abbreviation] Eur. J. Gynaecol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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13. Picone O, Lhommé C, Tournaire M, Pautier P, Camatte S, Vacher-Lavenue MC, Castaigne D, Morice P: Preservation of pregnancy in a patient with a stage IIIB ovarian epithelial carcinoma diagnosed at 22 weeks of gestation and treated with initial chemotherapy: case report and literature review. Gynecol Oncol; 2004 Aug;94(2):600-4
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  • [Title] Preservation of pregnancy in a patient with a stage IIIB ovarian epithelial carcinoma diagnosed at 22 weeks of gestation and treated with initial chemotherapy: case report and literature review.
  • BACKGROUND: To report a case of successful management of a FIGO stage III endometrioid carcinoma of the ovary diagnosed during pregnancy at 22 weeks of gestation and treated with initial chemotherapy while preserving the pregnancy.
  • At the same time, a radical hysterectomy, omentectomy, pelvic and paraaortic lymphadenectomies and peritonectomies were carried out.
  • The patient underwent seven postoperative courses of chemotherapy (carboplatin + paclitaxel regimen) after radical surgery.
  • CONCLUSION: Chemotherapy during pregnancy with preservation of the fetus could be considered and should be discussed in case of epithelial ovarian cancer (EOC) diagnosed during the second trimester of the pregnancy.
  • [MeSH-major] Ovarian Neoplasms / drug therapy. Pregnancy Complications, Neoplastic / drug therapy

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  • (PMID = 15297214.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 10
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14. Santillan A, Bristow RE: Paraneoplastic cerebellar degeneration in a woman with ovarian cancer. Nat Clin Pract Oncol; 2006 Feb;3(2):108-12; quiz 1 p following 112
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  • [Title] Paraneoplastic cerebellar degeneration in a woman with ovarian cancer.
  • During her initial admission, the patient improved to some degree and was discharged with a possible diagnosis of viral meningitis.
  • A general and gynecological examination was otherwise unremarkable.
  • INVESTIGATIONS: General physical and gynecological examinations, MRI of the brain, lumbar punctures, electroencephalogram, transvaginal ultrasound, mammogram, tumor markers, anti-neuronal antibodies, colonoscopy, whole-body positron emission tomography scan, laparoscopy and biopsies.
  • DIAGNOSIS: Stage IIIC endometrioid adenocarcinoma of the ovary with paraneoplastic cerebellar degeneration.
  • MANAGEMENT: Tumor cytoreduction, plasmapheresis, total abdominal hysterectomy, bilateral salpingo-oophorectomy, bilateral pelvic and para-aortic lymph-node dissection, total omentectomy, carboplatin and paclitaxel chemotherapy, rehabilitation, and speech therapy.
  • [MeSH-major] Carcinoma, Endometrioid / diagnosis. Ovarian Neoplasms / diagnosis. Paraneoplastic Cerebellar Degeneration / diagnosis


15. Akahira J, Konno R, Ito K, Sato S, Yajima A: Choroidal metastasis presented as the initial symptom of the recurrence from ovarian endometrioid adenocarcinoma: A case report. Gynecol Oncol; 2000 Apr;77(1):219-21
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  • [Title] Choroidal metastasis presented as the initial symptom of the recurrence from ovarian endometrioid adenocarcinoma: A case report.
  • Choroidal metastasis from recurrent ovarian cancer is extremely rare.
  • To our knowledge, this report is the first such case of endometrioid adenocarcinoma.
  • Ophthalmologic evaluation revealed a metastatic choroidal tumor from ovarian cancer which had been diagnosed 10 years ago.
  • After cesarean section, multiple metastases were found including the choroid, scalp, bone, and lung, and she received four courses of single agent carboplatin chemotherapy.
  • This case highlights the need to investigate the etiology of visual complaints in patients with a history of ovarian cancer even in the early stage.
  • [MeSH-major] Carcinoma, Endometrioid / secondary. Choroid Neoplasms / secondary. Ovarian Neoplasms / pathology. Pregnancy Complications, Neoplastic / pathology
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans. Neoplasm Metastasis / diagnosis. Neoplasm Recurrence, Local. Pregnancy. Vision Disorders / diagnosis

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  • [Copyright] Copyright 2000 Academic Press.
  • (PMID = 10739718.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] UNITED STATES
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16. Hong DG, Chong GO, Seong WJ, Lee YS, Cho YL, Park JY, Chae JM, Park IS: A case of ovarian endometrioid adenocarcinoma with yolk sac tumor in a 35-year-old woman. Eur J Gynaecol Oncol; 2010;31(4):471-4
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  • [Title] A case of ovarian endometrioid adenocarcinoma with yolk sac tumor in a 35-year-old woman.
  • Ovarian yolk sac tumor (YST) is a malignant ovarian neoplasm differentiated from primordial germ cells that occur in young age, while endometrioid carcinoma (ECA) is a müllerian epithelial tumor that usually occurs in older patients.
  • The coexistence of an ovarian ECA and YST component is very rare.
  • The parts of both ovaries that showed an endometrioid-like glandular pattern were positive for cytokeratin 7 and negative for AFP, but the YST component was negative for cytokeratin 7 and positive for AFP.
  • After completion of four courses of BEP chemotherapy, two courses of taxane and carboplatin chemotherapy were added.
  • [MeSH-major] Carcinoma, Endometrioid / pathology. Endodermal Sinus Tumor / pathology. Ovarian Neoplasms / pathology

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  • (PMID = 20882900.001).
  • [ISSN] 0392-2936
  • [Journal-full-title] European journal of gynaecological oncology
  • [ISO-abbreviation] Eur. J. Gynaecol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
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17. Yamamoto K, Oogi S, Inoue H, Kudoh K, Kita T, Kikuchi Y: Chronic administration of single weekly paclitaxel in heavily pretreated ovarian cancer patients. Curr Med Chem; 2004 Feb;11(4):425-8
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  • [Title] Chronic administration of single weekly paclitaxel in heavily pretreated ovarian cancer patients.
  • Ovarian cancer patients with paclitaxel-resistance have been reported to respond to a weekly schedule of the same drug.
  • After the surgery, the tumor was diagnosed as serous cystadenocarcinoma of the ovary (stage IV) and 6 cycles of treatment consisting of cyclophosphamide, adriamycin and cisplatin (CAP) were performed.
  • The CA 125 level (8400 U/ml) rapidly declined to 150 U/ml by this CAP therapy.
  • Therefore, treatment with single weekly T was performed and CA 125 levels remained between 70-90 U/ml during 13 cycles of this therapy (progression free interval; more than 1 year).
  • Computing tomography (CT) and magnetic resonance imaging (MRI) revealed large amount of ascite and pelvic mass (9 x 7 x 7 cm), and low density area (3 x 3 cm) suggesting metastasis in right lobe of liver.
  • The tumor was diagnosed as endometrioid adenocarcinoma of the ovary, stage IV and chemotherapy with CAP was initiated on September 5, 1998.
  • Thereafter, she received treatments with gamma knife and CAP for brain metastasis.
  • Side effects by weekly T were mild and tolerable despite of long term treatment.
  • In addition, weekly T can be safely used in outpatient setting and even in patients with poor performance status (PS), and warrant long time to progression.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / therapy. Carcinoma, Endometrioid / drug therapy. Cystadenocarcinoma, Serous / drug therapy. Neoplasm Recurrence, Local / drug therapy. Ovarian Neoplasms / drug therapy. Paclitaxel / administration & dosage
  • [MeSH-minor] Adult. Cisplatin / administration & dosage. Cyclophosphamide / administration & dosage. Disease-Free Survival. Doxorubicin / administration & dosage. Drug Administration Schedule. Drug Resistance, Neoplasm / drug effects. Fatal Outcome. Female. Humans. Middle Aged. Neoplasm, Residual / diagnosis. Neoplasm, Residual / drug therapy. Neoplasm, Residual / surgery. Reoperation

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  • (PMID = 14965223.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
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18. Ardavanis A, Karamouzis MV, Alexopoulos A, Rigatos G: Simultaneous endometrioid ovarian and uterine carcinoma diagnosed after an in vitro fertilization procedure--case report and review of the literature. Eur J Gynaecol Oncol; 2005;26(6):654-6
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  • [Title] Simultaneous endometrioid ovarian and uterine carcinoma diagnosed after an in vitro fertilization procedure--case report and review of the literature.
  • BACKGROUND: The presence of simultaneous carcinomas involving both the ovary and uterus is relatively uncommon, while the possible link between fertility drugs and carcinogenesis still remains controversial.
  • CASE: The case of a 40-year-old patient with simultaneous aggressive endometrioid carcinoma of the ovary and uterus a few months after the sixth attempt of in vitro fertilization is presented.
  • The patient had de novo lung disease at surgery and diffuse metastatic spread to adjacent bone, subcutaneous tissue and the central nervous system (CNS) soon after a spectacular response to the primary paclitaxel/carboplatinum chemotherapy and while on maintenance and second-line chemotherapy, respectively.
  • Definite conclusions about the possible association with the previously performed assisted reproduction cannot be drawn but close clinical surveillance of such patients before, during and after infertility treatment is strongly warranted.
  • [MeSH-major] Carcinoma, Endometrioid / pathology. Fertilization in Vitro / adverse effects. Lung Neoplasms / secondary. Neoplasms, Multiple Primary / pathology. Ovarian Neoplasms / pathology. Uterine Neoplasms / pathology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Fatal Outcome. Female. Humans

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  • (PMID = 16398231.001).
  • [ISSN] 0392-2936
  • [Journal-full-title] European journal of gynaecological oncology
  • [ISO-abbreviation] Eur. J. Gynaecol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 16
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19. Swiersz LM: Role of endometriosis in cancer and tumor development. Ann N Y Acad Sci; 2002 Mar;955:281-92; discussion 293-5, 396-406
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  • [Title] Role of endometriosis in cancer and tumor development.
  • Endometriosis, like cancer, is characterized by cell invasion and unrestrained growth.
  • Furthermore, endometriosis and cancer are similar in other aspects, such as the development of new blood vessels and a decrease in the number of cells undergoing apoptosis.
  • In spite of these similarities, endometriosis is not considered a malignant disorder.
  • The possibility that endometriosis could, however, transform and become cancer has been debated in the literature since 1925.
  • Mutations in the genes that encode for metabolic and detoxification enzymes, such as GALT and GSTM, have been implicated in the pathogenesis of endometriosis and in the progression to carcinoma of the ovary.
  • PTEN, a tumor suppressor commonly mutated (50%) in endometrial carcinoma, is found mutated in endometrioid carcinoma of the ovary, but not in other forms of ovarian cancer.
  • A recent study has shown that somatic mutations in the PTEN gene were identified in 20% of endometrioid carcinomas and 20.6% of solitary endometrial cysts, suggesting that inactivation of the PTEN tumor suppressor gene is an early event in the development of ovarian endometrioid carcinoma.
  • In addition to cancerous transformation at the site of endometriosis, there is recent evidence to indicate that having endometriosis itself may increase a woman's risk of developing non-Hodgkin's lymphoma, malignant melanoma, and breast cancer.
  • [MeSH-major] Breast Neoplasms / etiology. Endometriosis / complications. Melanoma / drug therapy. Ovarian Neoplasms / etiology


20. Messalli EM, Scaffa C, Mainini G, Rotondi M, Pecori E, Cobellis L: Third stage ovarian carcinoma--case report: the necessity of a multidisciplinary approach to treatment. Eur J Gynaecol Oncol; 2006;27(3):291-3
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  • [Title] Third stage ovarian carcinoma--case report: the necessity of a multidisciplinary approach to treatment.
  • Ovarian carcinoma, part of a heterogeneous group of tumours, is the main cause of death by gynaecological neoplasms.
  • The diagnosis, in general, is delayed.
  • Multiorgan diffusion, the necessity of a surgical operation and strong chemotherapy, and the eventual pathology due to patient age are all factors that require a multidisciplinary approach.
  • In fact the case, here reported, refers to a patient who came under our observation for a bilateral ovarian mass discovered casually during an abdominal ultrasound exam carried out for renal colic.
  • The histological report was G3, angioinvasive bilateral ovarian endometrioid adenocarcinoma.
  • It is concluded that the complexity of similar cases always requires a multidisciplinary approach as in our case, involving an oncologist, hematologist, surgeon, gynaecologist, radiologist, anaesthesiologist, and nursing staff in the management of third stage ovarian cancer patients to obtain the best treatment thus guaranteeing a higher survival rate and better quality of life.
  • [MeSH-major] Carcinoma, Endometrioid / surgery. Ovarian Neoplasms / surgery

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  • (PMID = 16800262.001).
  • [ISSN] 0392-2936
  • [Journal-full-title] European journal of gynaecological oncology
  • [ISO-abbreviation] Eur. J. Gynaecol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
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21. Tanaka T, Toujima S, Umesaki N: Growth-inhibitory signals by activin A do not affect anticancer drug-sensitivity and acquired multi-drug-resistance in human ovarian endometrioid adenocarcinoma OVK-18 cells. Oncol Rep; 2004 Mar;11(3):667-71
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  • [Title] Growth-inhibitory signals by activin A do not affect anticancer drug-sensitivity and acquired multi-drug-resistance in human ovarian endometrioid adenocarcinoma OVK-18 cells.
  • Using the human ovarian adenocarcinoma cell line, OVK-18, which is sensitive to activin A-mediated inhibition of growth and various anticancer drugs, we determined whether activin A altered the sensitivity of these cells to seven anticancer drugs.
  • The relationship between the sensitivity to activin and the resistance to anticancer drugs was also investigated in OVK-18 parent cells and OVK-18-derived CDDP-resistant cells.
  • Activin A inhibited proliferation of OVK-18 parent cells in a dose-dependent manner, although it did not affect the sensitivity of OVK-18 parent cells to the seven anticancer drugs, CDDP, CBDCA, adriamycin, paclitaxel, SN38, terarubicin and etoposide (VP16).
  • Both the sensitivity to activin A-mediated inhibition of growth and the sensitivity to anticancer drug-induced apoptosis were reduced in CDDP-resistant cells, while their sensitivity to the seven anticancer drugs was not affected by activin A.
  • Flow cytometric analysis revealed a significant reduction in type IIA activin receptor expression on the surface of CDDP-resistant cells.
  • These results indicate that the activin A-induced intracellular signals inhibiting cell growth are independent of the inhibition caused by the seven anticancer drugs, and suggest that the reduced sensitivity of CDDP-resistant cells to activin A is derived in part from reduced activin receptor expression and not acquired drug-resistance.
  • [MeSH-major] Activins / physiology. Antineoplastic Agents / pharmacology. Drug Resistance, Multiple. Inhibin-beta Subunits / physiology. Ovarian Neoplasms / drug therapy
  • [MeSH-minor] Cell Division. Cell Line, Tumor. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Female. Flow Cytometry. Humans. Sensitivity and Specificity

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  • (PMID = 14767519.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / activin A; 104625-48-1 / Activins; 93443-12-0 / Inhibin-beta Subunits
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22. Okugawa K, Hirakawa T, Ogawa S, Kaku T, Nakano H: Ovarian endometrioid adenocarcinoma arising from an endometriotic cyst in a postmenopausal woman under tamoxifen therapy for breast cancer: a case report. Gynecol Oncol; 2002 Nov;87(2):231-4
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  • [Title] Ovarian endometrioid adenocarcinoma arising from an endometriotic cyst in a postmenopausal woman under tamoxifen therapy for breast cancer: a case report.
  • BACKGROUND: Ovarian cancer arising from an endometriotic cyst in a postmenopausal woman under tamoxifen therapy is rare.
  • CASE: We herein report the case of a 67-year-old woman with a history of breast cancer, taking tamoxifen citrate 20 mg/day for 4 years, who underwent an operation for left ovarian tumor.
  • The postoperative histological diagnosis was endometrioid adenocarcinoma in an endometriotic cyst with a gradual transition of the degree of cellular atypia noted from typical endometriotic epithelium, to atypical endometriosis, and finally to adenocarcinoma.
  • CONCLUSION: Tamoxifen may cause malignant transformation of endometriosis through atypical endometriosis even in the postmenopausal state.
  • Atypical endometriosis may act as a precancerous lesion in the process of tamoxifen-induced malignant transformation of endometriosis.
  • [MeSH-major] Antineoplastic Agents, Hormonal / adverse effects. Breast Neoplasms / drug therapy. Carcinoma, Endometrioid / etiology. Neoplasms, Second Primary / etiology. Ovarian Cysts / complications. Ovarian Neoplasms / etiology. Tamoxifen / adverse effects
  • [MeSH-minor] Aged. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / pathology. Endometriosis / complications. Endometriosis / pathology. Female. Humans


23. Blumenfeld Z: Hormonal suppressive therapy for endometriosis may not improve patient health. Fertil Steril; 2004 Mar;81(3):487-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hormonal suppressive therapy for endometriosis may not improve patient health.
  • OBJECTIVE: To critically examine the possible association between hormonal treatment of endometriosis and ovarian cancer.
  • RESULT(S): The malignant potential of endometriosis has been suggested by several clinical studies.
  • Although controversial, ovarian carcinoma of the endometrioid and clear cell subtypes has been associated with endometriosis, particularly among subjects with a longstanding disease.
  • Furthermore, a significantly higher frequency of endometriosis has been found in patients undergoing surgery for endometrioid, clear cell, and mixed subtypes of ovarian carcinoma, as compared with the other subtypes.
  • Because hormonal ablative treatments may suppress the normal, eukaryotic cells more than the aneuploid cells bearing chromosomal aberrations, it may increase the rate of dyskaryotic cells in the endometriotic implants, possibly augmenting the risk of malignant transformation.
  • A recent published association between Danazol and ovarian cancer suggests that such a theoretical risk may occur.
  • CONCLUSION(S): The hormonal ablative treatment of endometriosis may increase the risk of malignant transformation in the endometriotic implants by causing a negative selection and increasing the rate of dyskaryosis and loss of heterozygosity.
  • [MeSH-major] Endometrial Neoplasms / chemically induced. Endometriosis / drug therapy. Estrogen Antagonists / adverse effects. Gonadotropin-Releasing Hormone / analogs & derivatives. Health. Patients

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  • (PMID = 15037387.001).
  • [ISSN] 0015-0282
  • [Journal-full-title] Fertility and sterility
  • [ISO-abbreviation] Fertil. Steril.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Antagonists; 0 / Progestins; 33515-09-2 / Gonadotropin-Releasing Hormone; 79561-22-1 / LHRH, Ala(6)-Gly(10)-ethylamide-; N29QWW3BUO / Danazol
  • [Number-of-references] 59
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24. Boruban MC, Jaishuen A, Sirisabya N, Li Y, Zheng HG, Deavers MT, Kavanagh JJ: Ovarian endometriosis associated with carcinoma and sarcoma: case report. Eur J Gynaecol Oncol; 2008;29(4):393-6
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  • [Title] Ovarian endometriosis associated with carcinoma and sarcoma: case report.
  • Endometriosis is a common clinical disorder that shares certain characteristics, metastasis and recurrence, with malignant neoplasms.
  • Most malignant ovarian tumors arising from endometriosis are clear cell carcinoma or endometrioid adenocarcinoma.
  • Few reports exist of sarcoma associated with endometriosis, and even fewer exist of multiple types of malignancies occurring simultaneously.
  • She was then referred to our institution for treatment recommendation.
  • The pathologic findings revealed bilateral endometrioid adenofibroma of low malignant potential, which was associated with endometrioid intraepithelial carcinoma in the left ovary and high-grade sarcoma in the right ovary.
  • The optimal treatment for endometriosis-associated ovarian cancer depends on the type of malignancy; simultaneously occurring multiple tumor types should be treated individually.
  • [MeSH-major] Carcinoma / etiology. Endometriosis / complications. Ovarian Diseases / complications. Ovarian Neoplasms / etiology. Sarcoma / etiology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Endometrial Neoplasms / complications. Endometrial Neoplasms / drug therapy. Female. Humans. Neoplasms, Multiple Primary


25. Gregory-Bass RC, Olatinwo M, Xu W, Matthews R, Stiles JK, Thomas K, Liu D, Tsang B, Thompson WE: Prohibitin silencing reverses stabilization of mitochondrial integrity and chemoresistance in ovarian cancer cells by increasing their sensitivity to apoptosis. Int J Cancer; 2008 May 1;122(9):1923-30
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  • [Title] Prohibitin silencing reverses stabilization of mitochondrial integrity and chemoresistance in ovarian cancer cells by increasing their sensitivity to apoptosis.
  • Current approaches to the treatment of ovarian cancer are limited because of the development of resistance to chemotherapy.
  • Prohibitin (Phb1) is a possible candidate protein that contributes to development of drug resistance, which could be targeted in neoplastic cells.
  • Our study was designed to determine the role of Phb1 in regulating cellular growth and apoptosis in ovarian cancer cells.
  • Our results showed that Phb1 content is differentially overexpressed in papillary serous ovarian carcinoma and endometrioid ovarian adenocarcinoma when compared to normal ovarian epithelium and was inversely related to Ki67 expression.
  • Immunofluorescence microscopy and Western analyses revealed that Phb1 is primarily associated with the mitochondria in ovarian cancer cells.
  • Over-expression of Phb1 by adenoviral Phb1 infection resulted in an increase in the percentage of ovarian cancer cells accumulating at G0/G1 phase of the cell cycle.
  • Treatment of ovarian cancer cells with staurosporine (STS) induced apoptosis in a time-dependent manner.
  • In contrast, silencing of Phb1 expression by adenoviral small interfering RNA (siRNA) sensitized ovarian cancer cells to STS-induce apoptosis.
  • Taken together, these results suggest that Phb1 induces block at G0/G1 phase of the cell cycle and promotes survival of cancer cells.
  • Furthermore, silencing of the Phb1 gene expression may prove to be a valuable therapeutic approach for chemoresistant ovarian cancer by increasing sensitivity of cancer cells to apoptosis.

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
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  • (PMID = 18183577.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / 1 C06 RR18386; United States / NCRR NIH HHS / RR / G12 RR003034; United States / NCRR NIH HHS / RR / C06 RR018386; United States / NICHD NIH HHS / HD / R01 HD057235; United States / FIC NIH HHS / TW / R21 TW006804-02S1; United States / NCRR NIH HHS / RR / RR03034; United States / NCATS NIH HHS / TR / UL1 TR000454; United States / FIC NIH HHS / TW / R21 TW006804-01; United States / NICHD NIH HHS / HD / U54 HD041749; United States / NICHD NIH HHS / HD / U54 HD041749-01; United States / NICHD NIH HHS / HD / U54 HD41749; United States / FIC NIH HHS / TW / R21 TW006804; United States / FIC NIH HHS / TW / R21 TW006804-02
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Ki-67 Antigen; 0 / RNA, Small Interfering; 0 / Recombinant Proteins; 0 / Repressor Proteins; 0 / prohibitin; EC 3.4.22.- / Caspase 3; H88EPA0A3N / Staurosporine
  • [Other-IDs] NLM/ NIHMS350695; NLM/ PMC3272361
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26. Fujimura M, Katsumata N, Tsuda H, Uchi N, Miyazaki S, Hidaka T, Sakai M, Saito S: HER2 is frequently over-expressed in ovarian clear cell adenocarcinoma: possible novel treatment modality using recombinant monoclonal antibody against HER2, trastuzumab. Jpn J Cancer Res; 2002 Nov;93(11):1250-7
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  • [Title] HER2 is frequently over-expressed in ovarian clear cell adenocarcinoma: possible novel treatment modality using recombinant monoclonal antibody against HER2, trastuzumab.
  • Ovarian clear cell adenocarcinoma (CCA) is generally chemo-resistant.
  • Thus, we investigated the expression level of HER2 in surgically resected CCA and ovarian serous adenocarcinoma, endometrioid adenocarcinoma, and mucinous adenocarcinoma specimens, as well as CCA cell lines, by an immunohistochemical method.
  • HER2 was over-expressed in 42.9% of CCA (P=0.026, vs. ovarian serous adenocarcinoma), 20.8% of ovarian serous adenocarcinoma, 23.1% of ovarian endometrioid adenocarcinoma, and 30.0% of mucinous adenocarcinoma specimens.
  • From these findings, trastuzumab appears to be a candidate as a treatment modality for HER2 over-expressing ovarian CCA.
  • [MeSH-major] Adenocarcinoma, Clear Cell / drug therapy. Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Ovarian Neoplasms / drug therapy. Receptor, ErbB-2 / antagonists & inhibitors
  • [MeSH-minor] Adult. Aged. Animals. Antibodies, Monoclonal, Humanized. Apoptosis / drug effects. Female. Flow Cytometry. Humans. Immunohistochemistry. Mice. Mice, SCID. Middle Aged. Trastuzumab. Tumor Cells, Cultured

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  • (PMID = 12460467.001).
  • [ISSN] 0910-5050
  • [Journal-full-title] Japanese journal of cancer research : Gann
  • [ISO-abbreviation] Jpn. J. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; EC 2.7.10.1 / Receptor, ErbB-2; P188ANX8CK / Trastuzumab
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27. Rees M: Gynaecological oncology perspective on management of the menopause. Eur J Surg Oncol; 2006 Oct;32(8):892-7
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  • Treatment for gynaecological cancer may ablate ovarian function through surgery (oophorectomy), radiotherapy or chemotherapy.
  • This article will describe the use of oestrogen and non-oestrogen-based treatments as well as alternative and complementary therapies in gynaecological cancer survivors.
  • AIMS: To review the use of oestrogen and non-oestrogen-based treatments as well as alternative and complementary therapies in gynaecological cancer survivors in whom ovarian function has been ablated through surgery (oophorectomy), radiotherapy or chemotherapy.
  • RESULTS: Ovarian, cervical, vaginal and vulval cancers are not oestrogen dependent conditions and oestrogen replacement is not contraindicated.
  • However, there is some doubt with regard to endometrioid ovarian cancer and endometrial carcinoma is often listed in data sheets as an absolute contra-indication to hormone replacement therapy.
  • A variety of agents are available for the prevention and treatment of osteoporosis and all except parathyroid hormone and strontium ranelate act mainly by inhibiting bone resorption.
  • There is little scientific evidence that complementary and alternative therapies can help menopausal symptoms or conserve bone mass and there are no safety data in women with gynaecological cancer.
  • CONCLUSIONS: Oestrogen-based therapies are the treatments of choice in young women with a premature menopause since oestrogen deficiency before the age of 40 increases the risk of osteoporosis and cardiovascular disease.
  • [MeSH-minor] Female. Humans. Treatment Outcome

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  • (PMID = 16698224.001).
  • [ISSN] 0748-7983
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 47
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28. Zhou C, Smith JL, Liu J: Role of BRCA1 in cellular resistance to paclitaxel and ionizing radiation in an ovarian cancer cell line carrying a defective BRCA1. Oncogene; 2003 Apr 24;22(16):2396-404
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  • [Title] Role of BRCA1 in cellular resistance to paclitaxel and ionizing radiation in an ovarian cancer cell line carrying a defective BRCA1.
  • BRCA1, the gene responsible for approximately half of all cases of hereditary breast cancer and almost all cases of combined hereditary breast and ovarian cancer, has been implicated in the maintenance of genomic stability through DNA repair.
  • The role of BRCA1 in the development of ovarian cancer is poorly understood, partially owing to the lack of ovarian cancer cell lines with defective BRCA1.
  • The purpose of this study was to further characterize an endometrioid ovarian cancer cell line, SNU-251, which was previously reported to carry a nonsense mutation (from G to A) at amino acid 1815 of BRCA1.
  • In addition, we examined the role of BRCA1 in the cell cycle and in the responses to the chemotherapy drug paclitaxel and ionizing radiation.
  • Loss of the C-terminal 49 amino acids due to this point mutation did not affect the expression of the truncated BRCA1 protein, but caused a loss of transcriptional activation of the endogenous p21(WAF1/CIP1) gene, and could not sustain arrest in the G(2)/M phase of the cell cycle.
  • This sensitivity was reversed by reintroduction of ectopic wild-type BRCA1.
  • Therefore, SNU-251 may be a useful model for studying the molecular mechanism of BRCA1 in the resistance of ovarian cancer to ionizing radiation and chemotherapy treatment and in the development of hereditary human ovarian cancer.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. BRCA1 Protein / metabolism. Ovarian Neoplasms / metabolism. Paclitaxel / pharmacology
  • [MeSH-minor] Cell Line. Drug Resistance, Neoplasm. Female. Humans. In Vitro Techniques. PTEN Phosphohydrolase. Phosphoric Monoester Hydrolases / genetics. Phosphoric Monoester Hydrolases / metabolism. Radiation, Ionizing. Tumor Suppressor Proteins / genetics. Tumor Suppressor Proteins / metabolism

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  • (PMID = 12717416.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / BRCA1 Protein; 0 / Tumor Suppressor Proteins; EC 3.1.3.- / Phosphoric Monoester Hydrolases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; P88XT4IS4D / Paclitaxel
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