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1. Rosen DG, Yang G, Bast RC Jr, Liu J: Use of Ras-transformed human ovarian surface epithelial cells as a model for studying ovarian cancer. Methods Enzymol; 2006;407:660-76
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Use of Ras-transformed human ovarian surface epithelial cells as a model for studying ovarian cancer.
  • Mutations in K-ras or its downstream mediator BRAF have been detected in about two thirds of low-grade serous carcinomas and borderline serous tumors; mutations in K-ras are also often present in benign and invasive mucinous ovarian cancers.
  • Although the oncogenic allele H-ras(V12) is present in only approximately 6% of ovarian cancers, physiologically activated H-ras protein is commonly detected in human ovarian cancer, presumably because of an increase in upstream signals from tyrosine kinase growth factor receptors such as Her-2/neu, despite the lack of a Ras mutation.
  • The mechanisms by which ras oncogenes transform human epithelial cells are not clear.
  • The methods described here are what we use to culture human ovarian surface epithelial cells, to immortalize those cells, and to transform the immortalized cells with oncogenic H-ras or K-ras.
  • These Ras-transformed human ovarian surface epithelial cells form tumors in nude mice and recapitulate many features of human ovarian cancer, thus providing an excellent model system for studying the initiation and progression of human ovarian cancer.
  • [MeSH-major] Cell Transformation, Neoplastic. Oncogene Protein p21(ras) / pharmacology. Ovarian Neoplasms / physiopathology. Ovary / cytology
  • [MeSH-minor] Animals. Antigens, Viral, Tumor / pharmacology. Cells, Cultured. Epithelial Cells / drug effects. Female. Humans. Immunohistochemistry. Mice. Mice, Nude. Simian virus 40 / immunology. Telomerase / pharmacology. Transfection


2. Ota K, Ito K, Akahira J, Sato N, Onogawa T, Moriya T, Unno M, Abe T, Niikura H, Takano T, Yaegashi N: Expression of organic cation transporter SLC22A16 in human epithelial ovarian cancer: a possible role of the adriamycin importer. Int J Gynecol Pathol; 2007 Jul;26(3):334-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of organic cation transporter SLC22A16 in human epithelial ovarian cancer: a possible role of the adriamycin importer.
  • Adriamycin is considered to be an active agent for ovarian cancer.
  • Recently, the benefit of adding adriamycin to the current standard regimen, paclitaxel and platinum, is evaluated to improve the outcome of patients with ovarian cancer.
  • Therefore, we examined the expression of SLC22A16 in ovarian cancers.
  • Twelve ovarian carcinoma cell lines were used for immunoblotting and reverse transcription-polymerase chain reaction to confirm the expression of SLC22A16 mRNA and protein.
  • Five normal ovaries, 12 ovarian adenomas, and 94 ovarian cancer cases were obtained from patients after surgical therapy.
  • The median value of relative SLC22A16 gene expression in cell lines derived from clear-cell adenocarcinoma was significantly higher than that in cell lines from other histologies (P < 0.001).
  • Expression of SLC22A16 protein was also detected in cell lines derived from clear-cell adenocarcinoma.
  • The SLC22A16 immunoreactivity was detected in 15 (16%) of 94 epithelial ovarian cancer, 1 (8.3%) of 12 benign adenomas, but 0 (0%) of 5 normal ovary cases.
  • In ovarian cancer tissues, SLC22A16 immunoreactivity was detected in 2 (5%) of 38 serous adenocarcinoma, 1 (6.7%) of 15 endometrioid adenocarcinoma, 0 (0%) of 14 mucinous adenocarcinoma, and 12 (46.2%) of 26 clear-cell adenocarcinoma (P < 0.0001, clear-cell vs other histologies).
  • In conclusion, SLC22A16 was abundantly expressed in clear-cell adenocarcinoma.
  • Our results suggest that adriamycin-related chemicals that are taken up via SLC22A16 may have the potential to be effective against clear-cell adenocarcinoma.
  • [MeSH-major] Adenocarcinoma, Clear Cell / metabolism. Antibiotics, Antineoplastic / pharmacokinetics. Doxorubicin / pharmacokinetics. Organic Cation Transport Proteins / biosynthesis. Ovarian Neoplasms / metabolism
  • [MeSH-minor] Blotting, Western. Cell Line, Tumor. Female. Humans. Immunohistochemistry. RNA, Neoplasm / chemistry. RNA, Neoplasm / genetics. Retrospective Studies. Reverse Transcriptase Polymerase Chain Reaction


3. McCluggage WG, Sumathi VP, McManus DT: Uterine serous carcinoma and endometrial intraepithelial carcinoma arising in endometrial polyps: report of 5 cases, including 2 associated with tamoxifen therapy. Hum Pathol; 2003 Sep;34(9):939-43
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  • Uterine serous carcinoma (USC) is the prototype of type II endometrial cancer.
  • Endometrial intraepithelial carcinoma (EIC) is the precursor lesion of USC, Rarely, USC and EIC may arise within and be largely confined to otherwise benign endometrial polyps.
  • In 1 case there was a single small focus of extrauterine tumor within an ovarian vascular channel.
  • In 2 cases the invasive tumor within the polyp also contained areas of endometrioid adenocarcinoma, and in 2 cases there was a component of clear cell carcinoma.
  • The cases reported herein show that USC and EIC may rarely arise in benign endometrial polyps and that extrauterine involvement may be present without myometrial infiltration.
  • Because 2 of the patients had been taking tamoxifen, this raises the possibility of an association between tamoxifen and the development of USC and EIC in the endometrial polyps that are characteristic of this medication.
  • [MeSH-major] Antineoplastic Agents, Hormonal / adverse effects. Carcinoma in Situ / pathology. Cystadenocarcinoma, Serous / pathology. Endometrial Neoplasms / pathology. Polyps / pathology. Tamoxifen / adverse effects

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  • (PMID = 14562291.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 094ZI81Y45 / Tamoxifen
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4. Hua K, Feng W, Cao Q, Zhou X, Lu X, Feng Y: Estrogen and progestin regulate metastasis through the PI3K/AKT pathway in human ovarian cancer. Int J Oncol; 2008 Nov;33(5):959-67
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  • [Title] Estrogen and progestin regulate metastasis through the PI3K/AKT pathway in human ovarian cancer.
  • Estrogen and progestin are involved in ovarian carcinogenesis.
  • Change in nm23-H1 expression and the PIK3/AKT pathway are involved in carcinogenesis, development, invasion and metastasis of ovarian cancers.
  • Therefore, it is critical to understand the signaling pathways that regulate hormone-induced cell migration and invasion in ovarian cancer.
  • We investigated nm23-H1, AKT and pAKT expression by using immunohistochemical staining in ovarian clear cell adenocarcinoma, ovarian benign, borderline and malignant serous tumors and analyzed their relationship with prognostic factors.
  • Using ES-2 and SKOV-3 ovarian cancer cell lines, we studied the modulation of estrogen and progestin on cell migration and invasion as well as their effect on AKT, pAKT and nm23-H1 expression.
  • Furthermore, the signaling pathways were examined using pharmacological inhibitors (LY294002 and PD98059) or AKT siRNA combined with estrogen or progestin in the two cell lines.
  • Weak nm23-H1 and high AKT and pAKT expression was observed in ovarian serous adeno-carcinoma and ovarian clear cell adenocarcinoma.
  • Our data demonstrated that the expression of nm23-H1 was negatively correlated with tumor stage and grade and lymph node metastasis, whereas the expression of AKT/pAKT was positively correlated with these clinic factors.
  • Estrogen up-regulated pAKT expression and reduced nm23-H1 expression, which ultimately resulted in increased cell migration and invasion.
  • In contrast, progestin reduced pAKT expression and increased nm23-H1 expression, which inhibited cell migration.
  • Our data suggest that AKT and pAKT are unfavorable prognostic factors for ovarian serous adenocarcinoma and clear cell carcinomas whereas nm23-H1 expression predicates favorable patient prognosis.
  • Estrogen down-regulates nm23-H1 expression and promotes cell migration and invasion by activating the PIK3/AKT pathway.
  • [MeSH-major] Adenocarcinoma / enzymology. Antineoplastic Agents, Hormonal / pharmacology. Cystadenoma, Serous / enzymology. Estrogens / metabolism. Ovarian Neoplasms / enzymology. Phosphatidylinositol 3-Kinases / metabolism. Progestins / pharmacology. Proto-Oncogene Proteins c-akt / metabolism
  • [MeSH-minor] Cell Line, Tumor. Cell Movement. Dose-Response Relationship, Drug. Female. Humans. Medroxyprogesterone Acetate / pharmacology. Middle Aged. NM23 Nucleoside Diphosphate Kinases / metabolism. Neoplasm Metastasis. Neoplasm Staging. Phosphorylation. Prognosis. Protein Kinase Inhibitors / pharmacology. RNA Interference. RNA, Small Interfering / metabolism. Signal Transduction / drug effects. Time Factors

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  • (PMID = 18949358.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Estrogens; 0 / NM23 Nucleoside Diphosphate Kinases; 0 / Progestins; 0 / Protein Kinase Inhibitors; 0 / RNA, Small Interfering; C2QI4IOI2G / Medroxyprogesterone Acetate; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.4.6 / NME1 protein, human
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5. Wang PH, Lee WL, Chao HT, Yuan CC: Disseminated carcinomatosis after laparoscopic surgery for presumably benign ruptured ovarian teratoma. Eur J Obstet Gynecol Reprod Biol; 2000 Mar;89(1):89-91
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  • [Title] Disseminated carcinomatosis after laparoscopic surgery for presumably benign ruptured ovarian teratoma.
  • The authors reported the intraperitoneal carcinomatosis after laparoscopic surgery for presumably benign ruptured ovarian teratoma in a 28-year-old woman.
  • Pathology proved with intraperitoneal carcinomatosis caused by squamous cell carcinoma.
  • All tumor evaluations including tumor markers, a thorough physical examination, imaging studies and evaluations of the nuclear medicine were negative except of intraperitoneal carcinoma, origin to be determined.
  • Although it was not clear that the laparoscopic approach or the disease itself worsened indeed the prognosis because the disease was already disseminated before the laparoscopy, we still emphasized the possible limitation of laparoscopic surgery if diagnosis at original surgery is impaired, of if excision is incomplete and the delay between the laparoscopic procedure and the carcinomatosis.
  • [MeSH-major] Carcinoma, Squamous Cell / etiology. Laparoscopy / adverse effects. Ovarian Neoplasms / surgery. Peritoneal Neoplasms / etiology. Teratoma / surgery
  • [MeSH-minor] Adult. Fatal Outcome. Female. Humans. Neoplasm Seeding. Rupture, Spontaneous

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  • (PMID = 10733031.001).
  • [ISSN] 0301-2115
  • [Journal-full-title] European journal of obstetrics, gynecology, and reproductive biology
  • [ISO-abbreviation] Eur. J. Obstet. Gynecol. Reprod. Biol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] IRELAND
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6. Schilder JM, Thompson AM, DePriest PD, Ueland FR, Cibull ML, Kryscio RJ, Modesitt SC, Lu KH, Geisler JP, Higgins RV, Magtibay PM, Cohn DE, Powell MA, Chu C, Stehman FB, van Nagell J: Outcome of reproductive age women with stage IA or IC invasive epithelial ovarian cancer treated with fertility-sparing therapy. Gynecol Oncol; 2002 Oct;87(1):1-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcome of reproductive age women with stage IA or IC invasive epithelial ovarian cancer treated with fertility-sparing therapy.
  • OBJECTIVES: The purpose of this study was to determine the recurrence rate, survival, and pregnancy outcome in patients with Stage IA and Stage IC invasive epithelial ovarian cancer treated with unilateral adnexectomy.
  • METHODS: A multi-institutional retrospective investigation was undertaken to identify patients with Stage IA and IC epithelial ovarian cancer who were treated with fertility-sparing surgery.
  • All patients with ovarian tumors of borderline malignancy were excluded.
  • Long-term follow-up was obtained through tumor registries and telephone interviews.
  • The time and sites of tumor recurrence, patient survival, and pregnancy outcomes were recorded for every patient.
  • RESULTS: Fifty two patients with Stage I epithelial ovarian cancer treated from 1965 to 2000 at 8 participating institutions were identified.
  • Cell type was distributed as follows: mucinous, 25; serous, 10; endometrioid, 10; clear cell, 5; and mixed, 2.
  • Patients received the following chemotherapeutic agents: cisplatin/taxol or carboplatin/taxol, 11; melphalan, 5; cisplatin and cyclophosphamide, 3; and single-agent cisplatin, 1.
  • Five patients developed tumor recurrence 8-78 months after initial surgery.
  • Nine patients underwent subsequent hysterectomy and contralateral oophorectomy for benign disease.
  • CONCLUSION: The long-term survival of patients with Stage IA and IC epithelial ovarian cancer treated with unilateral adnexectomy is excellent.
  • Fertility-sparing surgery should be considered as a treatment option in women with Stage I epithelial ovarian cancer who desire further childbearing.
  • [MeSH-major] Fertility. Ovarian Neoplasms / surgery
  • [MeSH-minor] Adolescent. Adult. Child. Combined Modality Therapy. Epithelial Cells / pathology. Female. Humans. Neoplasm Recurrence, Local / pathology. Neoplasm Staging. Ovariectomy / methods. Pregnancy. Pregnancy Complications, Neoplastic. Pregnancy Outcome. Retrospective Studies. Survival Rate. Treatment Outcome


7. Popadiuk CM, Xiong J, Wells MG, Andrews PG, Dankwa K, Hirasawa K, Lake BB, Kao KR: Antisense suppression of pygopus2 results in growth arrest of epithelial ovarian cancer. Clin Cancer Res; 2006 Apr 1;12(7 Pt 1):2216-23
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  • [Title] Antisense suppression of pygopus2 results in growth arrest of epithelial ovarian cancer.
  • PURPOSE: The Pygopus proteins are critical elements of the canonical Wnt/beta-catenin transcriptional complex.
  • In epithelial ovarian cancer, constitutively active Wnt signaling is restricted to one (endometrioid) tumor subtype.
  • The purpose of this study was to determine the level of expression and growth requirements of human Pygopus2 (hPygo2) protein in epithelial ovarian cancer.
  • EXPERIMENTAL DESIGN: Expression and subcellular localization of hPygo2 was determined in epithelial ovarian cancer cell lines and tumors using Northern blot, immunoblot, and immunofluorescence.
  • Immunohistochemistry was done on 125 archived patient epithelial ovarian cancer tumors representing all epithelial ovarian cancer subtypes.
  • T-cell factor-dependent transcription levels were determined in epithelial ovarian cancer cells using TOPflash/FOPflash in vivo assays.
  • Phosphorothioated antisense oligonucleotides were transfected into cell lines and growth assayed by cell counting, anchorage-independent colony formation on soft agar, and xenografting into severe combined immunodeficient mice.
  • RESULTS: All six epithelial ovarian cancer cell lines and 82% of the patient samples overexpressed nuclear hPygo2 compared with control cells and benign disease.
  • Depletion of hPygo2 by antisense oligonucleotides in both Wnt-active (TOV-112D) and Wnt-inactive serous (OVCAR-3, SKOV-3) and clear cell (TOV-21G) carcinoma cell lines halted growth, assessed using tissue culture, anchorage-independent, and xenograft assays.
  • CONCLUSIONS: hPygo2 is unexpectedly widely expressed in, and required in the absence of, Wnt signaling for malignant growth of epithelial ovarian cancer, the deadliest gynecologic malignancy.
  • [MeSH-major] Intracellular Signaling Peptides and Proteins / drug effects. Neoplasms, Glandular and Epithelial / drug therapy. Oligodeoxyribonucleotides, Antisense / pharmacology. Ovarian Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Disease Models, Animal. Drug Screening Assays, Antitumor. Female. Gene Expression Regulation, Neoplastic / drug effects. Gene Expression Regulation, Neoplastic / genetics. Humans. In Vitro Techniques. Mice. Neoplasms, Experimental / therapy. Structure-Activity Relationship. Transplantation, Heterologous. Xenograft Model Antitumor Assays

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  • (PMID = 16609037.001).
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Oligodeoxyribonucleotides, Antisense; 0 / PYGO2 protein, human
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8. Suzuki N, Yoshioka N, Ohara T, Yokomichi N, Nako T, Yahagi N, Igarashi S, Kobayashi Y, Yoshimatsu M, Takizawa K, Nakajima Y, Kiguchi K, Ishizuka B: Risk factors for perioperative venous thromboembolism: A retrospective study in Japanese women with gynecologic diseases. Thromb J; 2010;8:17
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  • METHODS: We analyzed 1,232 patients who underwent surgery at the Department of Obstetrics and Gynecology of St. Marianna University School of Medicine between January 2005 and June 2008.
  • Thirty-two patients had cancer and seven patients had benign diseases.
  • Multivariate analysis indicated that ovarian cancer, tumor diameter ≥10 cm, and previous of VTE were independent risk factors for preoperative VTE.
  • Among ovarian cancer patients, multivariate analysis showed that an age ≥50 years, the presence of heart disease, clear cell adenocarcinoma, and tumor diameter ≥20 cm were independent risk factors for preoperative VTE.
  • The factors significantly related to preoperative VTE in patients with benign disease included previous VTE, age ≥55 years, tumor diameter ≥20 cm, and a history of allergic-immunologic disease.

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  • (PMID = 21054901.001).
  • [ISSN] 1477-9560
  • [Journal-full-title] Thrombosis journal
  • [ISO-abbreviation] Thromb J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2989308
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