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1. Wahl H, Daudi S, Kshirsagar M, Griffith K, Tan L, Rhode J, Liu JR: Expression of metabolically targeted biomarkers in endometrial carcinoma. Gynecol Oncol; 2010 Jan;116(1):21-7
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  • [Title] Expression of metabolically targeted biomarkers in endometrial carcinoma.
  • OBJECTIVES: The differential metabolic phenotype observed between malignant and non-transformed cells may constitute a biochemical basis for therapeutic intervention.
  • In this study, we sought to determine if endometrial carcinoma cells express Glut1 and mTOR, and if inhibition of these factors is cytotoxic to endometrial carcinoma cells in vitro.
  • METHODS: Expression of Glut1, pAkt, and pmTOR was assessed in tissue microarrays constructed from 42 type I and 34 type II endometrial tumors by immunohistochemistry, and in a panel of endometrial carcinoma cell lines.
  • Representative endometrial carcinoma cells with wild type or mutant endogenous PTEN were treated with the glucose analog 2-deoxyglucose (2-DG) and rapamycin, an mTOR inhibitor or cisplatin.
  • RESULTS: Glut1, pAkt, and pmTOR were expressed strongly in both types I and II endometrial carcinoma.
  • 2-DG and rapamycin induced apoptotic cell death in type I endometrial carcinoma cells, and profound growth inhibition and cytostasis in type II endometrial carcinoma cells.
  • CONCLUSIONS: Glut1, pAkt, and pmTOR are overexpressed in endometrial carcinomas.
  • Distinct alterations in the phosphatidylinositol 3'-kinase (PI3K) pathway upstream of mTOR, such as pAkt, may identify endometrial carcinoma patients who may benefit from adjuvant treatment with mTOR inhibitors and/or glucose analogs.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Biomarkers, Tumor / antagonists & inhibitors. Endometrial Neoplasms / drug therapy. Endometrial Neoplasms / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Cisplatin / pharmacology. Deoxyglucose / pharmacology. Drug Delivery Systems. Drug Synergism. Female. Glucose Transporter Type 1 / antagonists & inhibitors. Glucose Transporter Type 1 / biosynthesis. Humans. Protein Kinases / biosynthesis. Protein Kinases / metabolism. Proto-Oncogene Proteins c-akt / antagonists & inhibitors. Proto-Oncogene Proteins c-akt / biosynthesis. Signal Transduction / drug effects. Sirolimus / pharmacology. TOR Serine-Threonine Kinases

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  • (PMID = 19878980.001).
  • [ISSN] 1095-6859
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA108456
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glucose Transporter Type 1; 0 / SLC2A1 protein, human; 9G2MP84A8W / Deoxyglucose; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; Q20Q21Q62J / Cisplatin; W36ZG6FT64 / Sirolimus
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2. Ito K, Utsunomiya H, Yaegashi N, Sasano H: Biological roles of estrogen and progesterone in human endometrial carcinoma--new developments in potential endocrine therapy for endometrial cancer. Endocr J; 2007 Dec;54(5):667-79
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  • [Title] Biological roles of estrogen and progesterone in human endometrial carcinoma--new developments in potential endocrine therapy for endometrial cancer.
  • Endometrial carcinoma is one of the most common female pelvic malignancies.
  • It is well known that uterine endometrial cell proliferation is under the control of both estrogen and progesterone.
  • In this review, results of the recent studies on the biosynthesis and action of estrogen and progestin in normal endometrium and its disorders will be summarized and the new aspects of hormonal therapies in the patients with endometrial carcinoma will be discussed including its future prospectives.
  • We reported that the enzymes responsible for intratumoral estrogen metabolism and biosynthesis are markedly different between human breast and endometrial carcinoma, although both of them are considered "estrogen-dependent malignancies".
  • In addition, the biological significance of Progesterone receptor (PR) isoforms is considered to differ between endometrial and breast carcinomas.
  • Clinical data concerning Hormone replacement therapy (HRT) and estrogen-dependent cancer risk also support these findings.
  • These basic and clinical findings help to understand the biology and provide the new knowledge for prevention, diagnosis and treatment of human endomerial carcinoma.
  • Specific endocrine treatment of endometrial carcinoma should be explored in future, although aromatase inhibitors are the most effective endocrine treatments of estrogen-responsive breast carcinoma.
  • Retinoid, metabolities of vitamin A, and synthetic peroxisome proliferator-activated receptor (PPAR) gamma ligands, which have been used for the treatment of insulin resistance in type II diabetes mellitus, may be the important candidates as drugs not only for prevention but also for possible endocrine treatment of endometrial carcinoma.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Carcinoma, Endometrioid / drug therapy. Carcinoma, Endometrioid / etiology. Endometrial Neoplasms / drug therapy. Endometrial Neoplasms / etiology. Estrogens / physiology. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / etiology. Progesterone / physiology
  • [MeSH-minor] Aromatase / metabolism. Aromatase / physiology. Estrogen Replacement Therapy / adverse effects. Female. Humans. Hydroxysteroid Dehydrogenases / metabolism. Models, Biological. Receptors, Estrogen / metabolism. Receptors, Estrogen / physiology. Receptors, Progesterone / metabolism. Receptors, Progesterone / physiology. Risk Factors. Steryl-Sulfatase / metabolism. Steryl-Sulfatase / physiology. Sulfotransferases / metabolism. Sulfotransferases / physiology

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  • (PMID = 17785917.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Estrogens; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 4G7DS2Q64Y / Progesterone; EC 1.1.- / Hydroxysteroid Dehydrogenases; EC 1.1.1.209 / 3(17)-hydroxysteroid dehydrogenase; EC 1.14.14.1 / Aromatase; EC 2.8.2.- / Sulfotransferases; EC 2.8.2.4 / estrone sulfotransferase; EC 3.1.6.2 / Steryl-Sulfatase
  • [Number-of-references] 89
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3. Li L, Heldin NE, Grawé J, Ulmsten U, Fu X: Induction of apoptosis or necrosis in human endometrial carcinoma cells by 2-methoxyestradiol. Anticancer Res; 2004 Nov-Dec;24(6):3983-90
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  • [Title] Induction of apoptosis or necrosis in human endometrial carcinoma cells by 2-methoxyestradiol.
  • BACKGROUND: We investigated the effects of 2methoxyestradiol (2-ME), an endogenous estrogenic metabolite, on human endometrial cancer HEC-1-A and RL-95-2 cell lines.
  • 2-ME had no significant effect on normal human endometrial cells.
  • CONCLUSION: The data suggest that 2-ME has an antitumor effect on human endometrial carcinoma cells (HEC-1-A and RL-95-2) and may contribute as a new therapeutic agent for endometrial cancer patients.
  • [MeSH-major] Apoptosis / drug effects. Endometrial Neoplasms / drug therapy. Estradiol / analogs & derivatives. Estradiol / pharmacology
  • [MeSH-minor] Adult. Cell Cycle / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. DNA-Binding Proteins / biosynthesis. Endometrium / cytology. Endometrium / drug effects. Female. Flow Cytometry. Humans. Intracellular Membranes / drug effects. Intracellular Membranes / physiology. Membrane Potentials / drug effects. Middle Aged. Mitochondria / drug effects. Mitochondria / physiology. Necrosis. Nitric Oxide Synthase / biosynthesis. Nitric Oxide Synthase Type II. STAT1 Transcription Factor. Trans-Activators / biosynthesis

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  • (PMID = 15736443.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / STAT1 Transcription Factor; 0 / STAT1 protein, human; 0 / Trans-Activators; 4TI98Z838E / Estradiol; 6I2QW73SR5 / 2-methoxyestradiol; EC 1.14.13.39 / NOS2 protein, human; EC 1.14.13.39 / Nitric Oxide Synthase; EC 1.14.13.39 / Nitric Oxide Synthase Type II
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4. van Wijk FH, van der Burg ME, Burger CW, Vergote I, van Doorn HC: Management of recurrent endometrioid endometrial carcinoma: an overview. Int J Gynecol Cancer; 2009 Apr;19(3):314-20

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Management of recurrent endometrioid endometrial carcinoma: an overview.
  • In this paper, an overview of the literature on the management of recurrent endometrial cancer is presented, focusing on patients with histopathologic endometrioid type of tumors.
  • The different treatment modalities are described, and a management recommendation scheme is presented.
  • Indications for surgical treatment depend on resectability, site and size of the tumor, and performance status of the patient.
  • Indications for radiotherapy depend on the site of the recurrence and also on the initial therapy received.
  • When considering systemic treatment for patients with recurrent endometrial cancer, it is important to take into account the general health status and condition of the patient as well as which prior therapy the patient has received.
  • The treatments of choice for patients with hormone-sensitive tumors (positive receptor levels, low-grade tumors, and long disease-free interval) are progestagens as first-line treatment and tamoxifen as second-line treatment.
  • Patients with high-grade tumors, negative hormone receptor levels, and short treatment-free interval are best treated with chemotherapy.
  • Paclitaxel, doxorubicin, and cisplatin are the most active combination therapy for these patients but with significant toxicity.
  • In phase II studies, the combination therapy with paclitaxel and carboplatin seems to be as effective but less toxic and can be administered in outpatient clinic.
  • The literature on the management of patients with recurrent endometrial cancer is discussed in detail.
  • [MeSH-major] Carcinoma, Endometrioid / therapy. Endometrial Neoplasms / therapy. Neoplasm Recurrence, Local / therapy

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  • (PMID = 19407552.001).
  • [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] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 90
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5. Singh M, Spoelstra NS, Jean A, Howe E, Torkko KC, Clark HR, Darling DS, Shroyer KR, Horwitz KB, Broaddus RR, Richer JK: ZEB1 expression in type I vs type II endometrial cancers: a marker of aggressive disease. Mod Pathol; 2008 Jul;21(7):912-23
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  • [Title] ZEB1 expression in type I vs type II endometrial cancers: a marker of aggressive disease.
  • Zinc-finger E-box-binding homeobox 1 (ZEB1) is a transcription factor containing two clusters of Kruppel-type zinc-fingers, by which it binds E-box-like sequences on target DNAs.
  • We previously demonstrated that ZEB1 is confined to the stromal compartment in normal endometrium and low-grade endometrial cancers.
  • Here, we quantify ZEB1 protein expression in endometrial samples from 88 patients and confirm that it is expressed at significantly higher levels in the tumor-associated stroma of low-grade endometrioid adenocarcinomas (type I endometrial cancers) compared to hyperplastic or normal endometrium.
  • In addition, as we previously reported, ZEB1 is aberrantly expressed in the epithelial-derived tumor cells of highly aggressive endometrial cancers, such as FIGO grade 3 endometrioid adenocarcinomas, uterine serous carcinomas, and malignant mixed Müllerian tumors (classified as type II endometrial cancers).
  • We now demonstrate, in both human endometrial cancer specimens and cell lines, that when ZEB1 is inappropriately expressed in epithelial-derived tumor cells, E-cadherin expression is repressed, and that this inverse relationship correlates with increased migratory and invasive potential.
  • Conversely, reduction of ZEB1 in a highly migratory and aggressive type II cell line, Hec50co, results in reduced migratory capacity.
  • Thus, ZEB1 may be a biomarker of aggressive endometrial cancers at high risk of recurrence.
  • It may help identify women who would most benefit from chemotherapy.
  • Furthermore, if expression of ZEB1 in type II endometrial cancers could be reversed, it might be exploited as therapy for these highly aggressive tumors.
  • [MeSH-major] Carcinoma, Endometrioid / metabolism. Endometrial Neoplasms / metabolism. Endometrium / metabolism. Homeodomain Proteins / metabolism. Transcription Factors / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Cadherins / metabolism. Cell Line, Tumor. Disease Progression. Endometrial Hyperplasia / metabolism. Endometrial Hyperplasia / pathology. Female. Gene Expression Regulation, Neoplastic. Gene Silencing. Humans. Hysterectomy. Immunohistochemistry. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging. RNA, Messenger / metabolism. Tissue Array Analysis

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  • (PMID = 18487993.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA098258; United States / NCI NIH HHS / CA / CA26869; United States / NCI NIH HHS / CA / P30-CA46934
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cadherins; 0 / Homeodomain Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 0 / ZEB1 protein, human
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6. Jiang S, Dowdy SC, Meng XW, Wang Z, Jones MB, Podratz KC, Jiang SW: Histone deacetylase inhibitors induce apoptosis in both Type I and Type II endometrial cancer cells. Gynecol Oncol; 2007 May;105(2):493-500
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  • [Title] Histone deacetylase inhibitors induce apoptosis in both Type I and Type II endometrial cancer cells.
  • OBJECTIVE: To characterize the molecular pathways involved in apoptosis following administration of histone deacetylase inhibitors to Type I and II endometrial cancer cells.
  • METHODS: Ark2, Ishikawa, and AN3 cell lines representing both Type I and II endometrial cancers were treated with various concentrations of oxamflatin and HDAC inhibitor-1.
  • Cleavage of PARP, caspase-9, and caspase-8 was detected, confirming the activation of apoptotic cascades in endometrial carcinoma cells.
  • This effect was present in both serous and endometrioid cell types.
  • CONCLUSION: Our results suggest that oxamflatin and HDAC inhibitor-1 have potent cytotoxicity in endometrial cancer cells by inducing cell apoptosis.
  • Histone deacetylase inhibitors are promising agents for the treatment of both Type I and II endometrial carcinoma.

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  • (PMID = 17303224.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] ENG
  • [Grant] United States / NICHD NIH HHS / HD / R01 HD041577; United States / NCI NIH HHS / CA / P50 CA098258-05S1; United States / NIDDK NIH HHS / DK / R01 DK041206-15; United States / NCI NIH HHS / CA / P50 CA098258; United States / NIDDK NIH HHS / DK / R01 DK041206-14; United States / NCI NIH HHS / CA / L30 CA116948-02; United States / NICHD NIH HHS / HD / R01 HD41577; United States / NICHD NIH HHS / HD / R01 HD041577-03; United States / NCI NIH HHS / CA / L30 CA116948-01; United States / NICHD NIH HHS / HD / R01 HD041577-02
  • [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 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / oxamflatin
  • [Other-IDs] NLM/ NIHMS350276; NLM/ PMC3273418
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7. Jiang T, Chen N, Zhao F, Wang XJ, Kong B, Zheng W, Zhang DD: High levels of Nrf2 determine chemoresistance in type II endometrial cancer. Cancer Res; 2010 Jul 1;70(13):5486-96
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  • [Title] High levels of Nrf2 determine chemoresistance in type II endometrial cancer.
  • Type II endometrial cancer, which mainly presents as serous and clear cell types, has proved to be the most malignant and recurrent carcinoma among various female genital malignancies.
  • Nrf2 is constitutively upregulated in several types of human cancer tissues and cancer cell lines.
  • Furthermore, inhibition of Nrf2 expression sensitizes cancer cells to chemotherapeutic drugs.
  • In this study, the constitutive level of Nrf2 was compared in different types of human endometrial tumors.
  • It was found that Nrf2 was highly expressed in endometrial serous carcinoma (ESC), whereas complex hyperplasia and endometrial endometrioid carcinoma (EEC) had no or marginal expression of Nrf2.
  • Silencing of Nrf2 rendered SPEC-2 cells more susceptible to chemotherapeutic drugs, whereas it had a limited effect on Ishikawa cells.
  • Inhibition of Nrf2 expression by overexpressing Keap1 sensitized SPEC-2 cells or SPEC-2-derived xenografts to chemotherapeutic treatments using both cell culture and severe combined immunodeficient mouse models.
  • Collectively, we provide a molecular basis for the use of Nrf2 inhibitors to increase the efficacy of chemotherapeutic drugs and to combat chemoresistance, the biggest obstacle in chemotherapy.

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  • [Copyright] Copyright 2010 AACR.
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  • (PMID = 20530669.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA23074; United States / NCI NIH HHS / CA / P30 CA023074; United States / NIEHS NIH HHS / ES / ES015010-04; United States / NIEHS NIH HHS / ES / R01 ES015010-04; United States / NIEHS NIH HHS / ES / ES015010; United States / NIEHS NIH HHS / ES / R01 ES015010
  • [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 / Intracellular Signaling Peptides and Proteins; 0 / KEAP1 protein, human; 0 / NF-E2-Related Factor 2; 0 / NFE2L2 protein, human; 0 / RNA, Messenger; 0 / RNA, Small Interfering; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ NIHMS203767; NLM/ PMC2896449
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8. Sakuragi N, Hareyama H, Todo Y, Yamada H, Yamamoto R, Fujino T, Sagawa T, Fujimoto S: Prognostic significance of serous and clear cell adenocarcinoma in surgically staged endometrial carcinoma. Acta Obstet Gynecol Scand; 2000 Apr;79(4):311-6
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  • [Title] Prognostic significance of serous and clear cell adenocarcinoma in surgically staged endometrial carcinoma.
  • BACKGROUND: The serous adenocarcinoma (SA) and clear cell adenocarcinoma (CCA) of endometrium have been shown to be associated with high relapse rate and poor survival.
  • It is not clear whether prognostic significance of these specific cell types of tumor is independent of retroperitoneal lymph node metastasis and other histopathologic prognostic factors in endometrial carcinoma.
  • METHODS: We examined 240 consecutive patients with clinical stage I to stage III endometrial carcinoma who were treated prospectively with radical surgery and/or platinum-based chemotherapy.
  • RESULTS: SA/CCA were more frequently associated with deep myometrial invasion, high nuclear grade (G3), lymph-vascular space invasion (LVSI), and pelvic lymph node metastasis when compared to endometrioid adenocarcinoma (EMA).
  • Of 216 clinically staged stage I or II disease, seven of 12 cases of SA/CCA had extrauterine disease.
  • A multivariate Cox regression analysis revealed that cell type, grade, LVSI, and paraaortic node metastasis (PANM) were independent prognosticators.
  • CONCLUSIONS: Prognosis of patients with endometrial carcinoma depends on cell type, grade, LVSI, and PANM.
  • [MeSH-major] Adenocarcinoma, Clear Cell / secondary. Cystadenocarcinoma, Serous / secondary. Endometrial Neoplasms / pathology. Lymph Nodes / pathology. Neoplasm Recurrence, Local

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  • (PMID = 10746848.001).
  • [ISSN] 0001-6349
  • [Journal-full-title] Acta obstetricia et gynecologica Scandinavica
  • [ISO-abbreviation] Acta Obstet Gynecol Scand
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] DENMARK
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9. Craighead PS, Sait K, Stuart GC, Arthur K, Nation J, Duggan M, Guo D: Management of aggressive histologic variants of endometrial carcinoma at the Tom Baker Cancer Centre between 1984 and 1994. Gynecol Oncol; 2000 May;77(2):248-53
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  • [Title] Management of aggressive histologic variants of endometrial carcinoma at the Tom Baker Cancer Centre between 1984 and 1994.
  • OBJECTIVE: The aim of this study was to determine the patient characteristics and outcome of patients with aggressive histologic variants (AV) of endometrial carcinoma, including uterine papillary serous carcinoma (UPSC), uterine clear cell carcinoma (UCCC), and mixed type.
  • METHODS AND MATERIALS: All cases with AV histological type of endometrial carcinoma from January 1984 to December 1994 at the Tom Baker Cancer Centre were identified using the Alberta Cancer Registry.
  • Relevant data from the charts of these patients were entered into a study database (Microsoft Excel) and analyzed for presentation, demography, treatment parameters, and outcome of treatment.
  • All pathology was reviewed at the time of diagnosis.
  • RESULTS: A total of 103 patients with AV histological type were identified and analyzed; there were 61, 31, and 11 cases of UPSC, CCC, and mixed tumors, respectively.
  • Sixty-three patients had Stage I, 11 had Stage II, 15 had Stage III, and 14 had Stage IV disease.
  • Forty six percent of all cases underwent surgery alone, 39% underwent treatment which included pelvic RT, and 17% underwent treatment which included chemotherapy.
  • Pelvic recurrence was reduced significantly by radiotherapy in Stages I, II, and III (19% recurrence with no RT vs 7% recurrence with RT, P < 0.005).
  • Chemotherapy improved overall survival, but made little difference in distant relapse rates.
  • CONCLUSIONS: Stage Ia cases treated by surgery alone have a low risk of relapse and need not be offered adjuvant systemic therapy or pelvic radiation.
  • Patients with Ib, Ic, II, and III have significantly lower pelvic failure rates if treated with pelvic radiation, but still have a high distant failure rate.
  • Systemic therapy did not significantly improve distant relapse-free survival, but did extend overall survival.
  • Stage IV patients usually died within 6 months with a few responding to systemic chemotherapy.
  • [MeSH-major] Adenocarcinoma, Clear Cell / therapy. Carcinoma, Papillary / therapy. Endometrial Neoplasms / therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Chemotherapy, Adjuvant. Demography. Female. Humans. Middle Aged. Neoplasm Recurrence, Local. Prognosis. Radiotherapy, Adjuvant. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • [Copyright] Copyright 2000 Academic Press.
  • (PMID = 10785473.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
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10. Aida T, Takebayashi Y, Shimizu T, Okamura C, Higasimoto M, Kanzaki A, Nakayama K, Terada K, Sugiyama T, Miyazaki K, Ito K, Takenoshita S, Yaegashi N: Expression of copper-transporting P-type adenosine triphosphatase (ATP7B) as a prognostic factor in human endometrial carcinoma. Gynecol Oncol; 2005 Apr;97(1):41-5

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of copper-transporting P-type adenosine triphosphatase (ATP7B) as a prognostic factor in human endometrial carcinoma.
  • OBJECTIVE: Copper-transporting P-type adenosine triphosphate (ATP7B) has been reported to be associated with cisplatin resistance in vitro.
  • However, the clinical significance of this transporter has not previously been addressed in endometrial carcinoma.
  • Our goal was to investigate if ATP7B is expressed in endometrial carcinoma and whether its expression correlates with prognosis.
  • METHODS: We performed immunohistochemical analysis of ATP7B using a monoclonal antibody against ATP7B in 51 endometrial endometrioid adenocarcinomas.
  • 27 of 51 patients were treated with cisplatin-based chemotherapy after surgery.
  • ATP7B positivity in the degree of differentiation of G2 and G3 carcinoma was significantly higher than that of G1 carcinoma (P = 0.019).
  • CONCLUSIONS: These findings suggest that overexpression of ATP7B expression in endometrial carcinoma is correlated with unfavorable clinical outcome in patients treated with cisplatin-based chemotherapy.
  • ATP7B expression could be considered as a prognostic factor in patients with endometrial carcinoma.
  • [MeSH-major] Adenocarcinoma / enzymology. Adenosine Triphosphatases / biosynthesis. Biomarkers, Tumor / biosynthesis. Cation Transport Proteins / biosynthesis. Endometrial Neoplasms / enzymology

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  • (PMID = 15790435.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / Cation Transport Proteins; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.3.4 / Wilson disease protein
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11. Schmidt D: [Endometrial carcinomas and precursor lesions--new aspects]. Pathologe; 2009 Jul;30(4):261-7
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  • [Title] [Endometrial carcinomas and precursor lesions--new aspects].
  • Endometrial carcinomas can be separated into two groups which are designated as type I and type II carcinomas today.
  • Only type I carcinomas are associated with hyperestrogenism.
  • The group of type I carcinomas consists of endometrioid carcinoma and its variants, and mucinous carcinoma.
  • The prototypes of type II carcinomas are serous and clear cell carcinoma.
  • Not all carcinomas, however, can be assigned to one of the two groups, because there are hybrid tumors and mixed carcinomas, e.g. endometrioid carcinoma with a serous component.
  • The precursor lesions of the endometrioid carcinoma and the serous carcinoma are well characterized morphologically and by molecular pathology.
  • Atypical hyperplasia is the precursor lesion of endometrioid carcinoma, whereas endometrial intraepithelial carcinoma (EIC) is the precursor lesion of serous carcinoma.
  • No precursor lesion has as yet been identified for clear cell carcinoma.
  • Immunohistochemical markers for endometrial carcinoma are CK7 and vimentin, for serous carcinoma markers are p53 and p16.
  • Correct typing is of essential prognostic necessity in endometrial carcinoma.
  • Of utmost importance is the detection of a serous component, because serous carcinoma leads to early tumor spread with the necessity of radical surgery, chemotherapy and radiotherapy.
  • [MeSH-major] Carcinoma, Endometrioid / pathology. Endometrial Neoplasms / pathology
  • [MeSH-minor] Biomarkers / analysis. Carcinoma / pathology. Female. Humans. Hyperplasia. Menopause. Receptors, Estrogen / analysis. Receptors, Progesterone / analysis. Vimentin / analysis

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  • (PMID = 19495762.001).
  • [ISSN] 1432-1963
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 0 / Vimentin
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12. Bae-Jump VL, Zhou C, Boggess JF, Whang YE, Barroilhet L, Gehrig PA: Rapamycin inhibits cell proliferation in type I and type II endometrial carcinomas: a search for biomarkers of sensitivity to treatment. Gynecol Oncol; 2010 Dec;119(3):579-85
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  • [Title] Rapamycin inhibits cell proliferation in type I and type II endometrial carcinomas: a search for biomarkers of sensitivity to treatment.
  • OBJECTIVES: Our goal was to evaluate the effect of rapamycin, an mTOR inhibitor, in type I and II human endometrial cancer tumor explants.
  • METHODS: Short-term tissue culture with fresh endometrial cancer tumor explants was performed.
  • Cell proliferation was assessed by MTS assay after treatment with rapamycin.
  • Real-time RT-PCR was used to quantify hTERT mRNA expression.
  • RESULTS: Thirteen fresh endometrial cancer tumor explants (nine Type I, four Type II) were placed in short-term culture and treated with rapamycin.
  • Nine of the endometrial cancer tumors responded to rapamycin, with a median IC₅₀ of 11.4 nM.
  • Rapamycin decreased hTERT mRNA expression in all of the endometrial cancer tumors.
  • Telomere length did not correspond with responsiveness to this drug.
  • CONCLUSIONS: Rapamycin demonstrated activity in fresh endometrial tumor explants independent of PTEN and Akt status.
  • Thus, mTOR inhibitors may be a useful targeted therapy for both type I and type II endometrial cancers, but the search remains for a predictive biomarker of sensitivity to this therapy.
  • [MeSH-major] Antibiotics, Antineoplastic / pharmacology. Carcinoma, Endometrioid / drug therapy. Carcinoma, Endometrioid / pathology. Endometrial Neoplasms / drug therapy. Endometrial Neoplasms / pathology. Sirolimus / pharmacology
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Cell Growth Processes / drug effects. Female. Humans. Neoplasm Staging. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. TOR Serine-Threonine Kinases / metabolism. Telomerase / biosynthesis. Telomerase / genetics. Tumor Cells, Cultured

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  • [Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.
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  • (PMID = 20863555.001).
  • [ISSN] 1095-6859
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K23 CA143154; United States / NCRR NIH HHS / RR / KL2 RR025746; United States / NCRR NIH HHS / RR / KL2 RR025746; United States / NCATS NIH HHS / TR / KL2 TR001109
  • [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 / Antibiotics, Antineoplastic; 0 / Biomarkers, Tumor; 0 / RNA, Messenger; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS435459; NLM/ PMC4098865
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13. Ripley D, Tang XM, Ma C, Chegini N: The expression and action of granulocyte macrophage-colony stimulating factor and its interaction with TGF-beta in endometrial carcinoma. Gynecol Oncol; 2001 May;81(2):301-9
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  • [Title] The expression and action of granulocyte macrophage-colony stimulating factor and its interaction with TGF-beta in endometrial carcinoma.
  • Because GM-CSF is administer to cancer patients following chemotherapy, GM-CSF may directly or through interaction with ovarian steroids and other cytokines alter the behavior of endometrial cancer.
  • The aim of this study was to determine the expression of GM-CSF and receptors in endometrial carcinoma and its direct effect and interaction with transforming growth factor beta (TGF-beta) on Ishikawa cells, a human endometrial carcinoma cell line.
  • METHODS: GM-CSF, GM-CSF receptors, TGF-beta1, and TGF-beta type II receptor expression were evaluated using quantitative reverse transcription polymerase chain reaction (Q-RT-PCR).
  • RESULTS: Endometrial carcinomas express significantly higher GM-CSF and GM-CSF alpha and beta receptor mRNA compared with normal postmenopausal endometrium.
  • GM-CSF and TGF-beta1 regulate their own expression and the expression of TGF-beta type II receptor, which were both upregulated by 17beta-estradiol and medroxyprogesterone acetate treatment and reversed following cotreatment with their respective receptor antagonists.
  • CONCLUSION: Endometrial carcinoma expresses an elevated level of GM-CSF and GM-CSF receptors.
  • GM-CSF is not a mitogen for the endometrial cancer cell line; however, either alone or through interaction with TGF-beta1, it regulates its own expression and the expression of TGF-beta1 and TGF-beta type II receptor which inhabits endometrial cancer cells.
  • This interaction may represent a regulatory feedback mechanism that could serve to suppress endometrial carcinoma growth.
  • [MeSH-major] Endometrial Neoplasms / metabolism. Granulocyte-Macrophage Colony-Stimulating Factor / physiology. Receptors, Granulocyte-Macrophage Colony-Stimulating Factor / biosynthesis. Transforming Growth Factor beta / physiology
  • [MeSH-minor] Antineoplastic Agents, Hormonal / pharmacology. Cell Division / drug effects. Drug Interactions. Estradiol / pharmacology. Female. Humans. Medroxyprogesterone Acetate / pharmacology. Protein-Serine-Threonine Kinases. Receptors, Transforming Growth Factor beta / biosynthesis. Transforming Growth Factor beta1. Tumor Cells, Cultured / drug effects

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  • [Copyright] Copyright 2001 Academic Press.
  • (PMID = 11330966.001).
  • [ISSN] 0090-8258
  • [Journal-full-title] Gynecologic oncology
  • [ISO-abbreviation] Gynecol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Granulocyte-Macrophage Colony-Stimulating Factor; 0 / Receptors, Transforming Growth Factor beta; 0 / TGFB1 protein, human; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 4TI98Z838E / Estradiol; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor; C2QI4IOI2G / Medroxyprogesterone Acetate; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor
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14. Deng L, Broaddus RR, McCampbell A, Shipley GL, Loose DS, Stancel GM, Pickar JH, Davies PJ: Identification of a novel estrogen-regulated gene, EIG121, induced by hormone replacement therapy and differentially expressed in type I and type II endometrial cancer. Clin Cancer Res; 2005 Dec 1;11(23):8258-64
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  • [Title] Identification of a novel estrogen-regulated gene, EIG121, induced by hormone replacement therapy and differentially expressed in type I and type II endometrial cancer.
  • Here, we describe the expression pattern of a novel estrogen-induced gene, EIG121, in distinct types of endometrial cancer.
  • EXPERIMENTAL DESIGN: EIG121 was identified by cDNA microarray analysis of endometrial RNA from women receiving either placebo or estrogen replacement therapy.
  • The expression level of EIG121 was then measured by real-time quantitative reverse transcription-PCR in benign, hyperplastic, and malignant endometrial samples.
  • RESULTS: In postmenopausal endometrium, estrogen replacement therapy with Premarin and synthetic estrogen sulfate conjugates induced the expression of EIG121 2- and 3-fold, respectively.
  • In endometrial complex, hyperplasia, and endometrioid adenocarcinoma, neoplastic proliferations associated with estrogen excess, the expression of EIG121 was significantly elevated (on average 3.8-fold in hyperplasias and 21-fold in grade 1 tumors).
  • Although the level of EIG121 mRNA in grade 3 endometrioid carcinoma was still 3.5-fold of that in benign endometrium, EIG121 expression tended to decline with increasing tumor grade and disease stage.
  • Immunohistochemistry showed faint staining of normal endometrial epithelium, but intense staining of endometrioid tumors.
  • In sharp contrast, EIG121 expression was significantly suppressed in both uterine papillary serous carcinoma and uterine malignant mixed mullerian tumor, two tumors not associated with estrogen exposure, to <5% of the level in benign endometrium.
  • CONCLUSIONS: Our results suggest that EIG121 is a good endometrial biomarker associated with a hyperestrogenic state and estrogen-related type I endometrial adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / genetics. Biomarkers, Tumor / genetics. Endometrial Neoplasms / genetics. Estrogen Replacement Therapy. Estrogens / therapeutic use. Gene Expression Regulation, Neoplastic / drug effects. Neoplasm Proteins / genetics
  • [MeSH-minor] Case-Control Studies. Endometrial Hyperplasia / genetics. Endometrial Hyperplasia / pathology. Estrogens, Conjugated (USP) / therapeutic use. Estrone / analogs & derivatives. Estrone / therapeutic use. Expressed Sequence Tags. Female. Gene Expression Profiling. Humans. Immunohistochemistry. Oligonucleotide Array Sequence Analysis. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16322283.001).
  • [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 / 1P50CA098258-01; United States / NICHD NIH HHS / HD / 5T32 HD007324-18
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Estrogens; 0 / Estrogens, Conjugated (USP); 0 / KIAA1324 protein, human; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 2DI9HA706A / Estrone; QTL48N278K / estrone sulfate
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15. Vandenput I, Vanden Bempt I, Leunen K, Neven P, Berteloot P, Moerman P, Vergote I, Amant F: Limited clinical benefit from trastuzumab in recurrent endometrial cancer: two case reports. Gynecol Obstet Invest; 2009;67(1):46-8
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  • [Title] Limited clinical benefit from trastuzumab in recurrent endometrial cancer: two case reports.
  • BACKGROUND: It is hypothesized that the HER-2/neu receptor could be used for targeted therapy in recurrent endometrial cancer.
  • CASES: A patient with type II endometrial cancer (serous), showing strong HER-2/neu overexpression and gene amplification in both primary and recurrent tumor, received single-agent trastuzumab (3x weekly, 8 mg/kg loading, 6 mg/kg maintenance dose).
  • However, progressive disease was also noted after 11 weeks of combined treatment.
  • A second patient, with recurrent type II endometrial cancer (grade III endometrioid), had HER-2/neu gene amplification in the primary tumor.
  • CONCLUSION: Based on lack of response and changes in tumor biology, trastuzumab was of little clinical value in 2 cases of recurrent type II endometrial cancer.
  • This report underscores the importance of reassessment of a recurrent tumor before initiating targeted treatment.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Endometrioid / drug therapy. Endometrial Neoplasms / drug therapy. Neoplasm Recurrence, Local / drug therapy

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  • (PMID = 18843183.001).
  • [ISSN] 1423-002X
  • [Journal-full-title] Gynecologic and obstetric investigation
  • [ISO-abbreviation] Gynecol. Obstet. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Switzerland
  • [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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16. Berstein L, Kovalevskij A, Zimarina T, Maximov S, Gershfeld E, Vasilyev D, Baisheva S, Baymakhasheva A, Thijssen JH: Aromatase and comparative response to its inhibitors in two types of endometrial cancer. J Steroid Biochem Mol Biol; 2005 May;95(1-5):71-4
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  • [Title] Aromatase and comparative response to its inhibitors in two types of endometrial cancer.
  • Aromatase activity (AA) was evaluated totally in 80 tumors collected from primary endometrial cancer (EC) patients.
  • All patients were divided into cases belonging to the types I or II of EC (respectively, 50 and 30 observations).
  • Samples of malignant endometrium from type II demonstrated inclination to the higher AA in comparison with type I samples; the difference reached level of statistical significance in non-smoking patients (p=0.02).
  • Although no positive correlation was revealed between AA in EC tissue and percentage of cells with DNA damage in normal endometrium from the same patients, the rate of DNA damage (percent of comets, comet's tail average length, etc.) was higher in intact endometrium collected from patients with type II of the disease.
  • Of note, though, CYP19 mRNA expression was not revealed in six cases, and all of them belonged to the type I of disease.
  • Finally, in 23 EC patients (15 with type I and 8 with type II of the disease) effects of 2 weeks treatment with letrozole (10 pts) and exemestane (13 pts) were evaluated in neoadjuvant setting.
  • Although diminishing of endometrial M-echo signal and the increases in FSH and LH concentration after treatment were more pronounced in type I patients, decrease in tumor PR content (p=0.04) was more revealing in patients with type II of EC; besides, the decreases in AA in tumor tissue by the end of treatment were noted predominantly in patients with lower body weight (BMI <27.5).
  • Thus, although type II of EC is frequently considered as hormone-independent, increased ability of this type of the tumor to estrogen biosynthesis (at CYP19 gene and protein level) may lead to the reconsideration of such conclusion and warrants further investigation.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Aromatase / metabolism. Aromatase Inhibitors / therapeutic use. Carcinoma, Endometrioid / drug therapy. Carcinoma, Endometrioid / enzymology. Endometrial Neoplasms / drug therapy. Endometrial Neoplasms / enzymology
  • [MeSH-minor] Adult. Aged. Comet Assay. DNA Damage. DNA, Neoplasm / analysis. Female. Humans. Middle Aged. RNA, Messenger / analysis. RNA, Messenger / metabolism. Treatment Outcome

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  • (PMID = 15939586.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Aromatase Inhibitors; 0 / DNA, Neoplasm; 0 / RNA, Messenger; EC 1.14.14.1 / Aromatase
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17. Gadducci A, Tana R, Cosio S, Fanucchi A, Genazzani AR: Molecular target therapies in endometrial cancer: from the basic research to the clinic. Gynecol Endocrinol; 2008 May;24(5):239-49
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  • [Title] Molecular target therapies in endometrial cancer: from the basic research to the clinic.
  • Molecular targeted therapies represent an interesting field of pharmacological research in endometrial cancer.
  • The loss of PTEN (phosphatase and tensin homolog deleted on chromosome 10) function, with consequent activation of the PI3K (phosphatidylinositol-3-kinase)-AKT (serine/threonine-specific protein kinase)-mTOR (mammalian target of rapamycin) signaling pathway, occurs in 32-83% of endometrioid-type endometrial carcinomas, thus suggesting a role for mTOR inhibition in this malignancy.
  • Some analogues of rapamycin (CCI-799, RAD-001, AP-23573) have been developed and tested in different tumors including endometrioid-type endometrial carcinoma.
  • Overexpression of ErbB-2 (epidermal growth factor type II receptor) has been detected in 18-80% of uterine papillary serous carcinomas (UPSCs), thus providing a biological rationale for the use of trastuzumab in these aggressive tumors.
  • CPE-mediated therapy might be a novel treatment modality for UPSC resistant to chemotherapy.
  • A better understanding of the signaling transduction pathways that are dysregulated in endometrioid-type endometrial carcinoma and UPSC will allow the development of novel molecular targeted therapies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Endometrial Neoplasms / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal, Humanized. Carcinoma, Endometrioid / drug therapy. Carcinoma, Endometrioid / metabolism. Cystadenocarcinoma, Papillary / drug therapy. Cystadenocarcinoma, Papillary / metabolism. Drug Delivery Systems / methods. Enterotoxins / pharmacology. Female. Humans. PTEN Phosphohydrolase / metabolism. Protein Kinases / metabolism. Receptor, ErbB-2 / metabolism. Signal Transduction. Sirolimus / analogs & derivatives. Sirolimus / pharmacology. TOR Serine-Threonine Kinases. Trastuzumab

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  • (PMID = 18569027.001).
  • [ISSN] 1473-0766
  • [Journal-full-title] Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology
  • [ISO-abbreviation] Gynecol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Enterotoxins; 0 / enterotoxin, Clostridium; 48Z35KB15K / ridaforolimus; 624KN6GM2T / temsirolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.10.1 / Receptor, ErbB-2; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; P188ANX8CK / Trastuzumab; W36ZG6FT64 / Sirolimus
  • [Number-of-references] 147
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18. Koshiyama M, Fujii H, Kinezaki M, Morita Y, Nanno H, Yoshida M: Immunohistochemical expression of topoisomerase IIalpha (Topo IIalpha) and multidrug resistance-associated protein (MRP), plus chemosensitivity testing, as chemotherapeutic indices of ovarian and endometrial carcinomas. Anticancer Res; 2001 Jul-Aug;21(4B):2925-32
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  • [Title] Immunohistochemical expression of topoisomerase IIalpha (Topo IIalpha) and multidrug resistance-associated protein (MRP), plus chemosensitivity testing, as chemotherapeutic indices of ovarian and endometrial carcinomas.
  • METHODS: We studied the expression of topoisomerase II alpha(Topo II alpha) and multidrug resistance-associated protein (MRP), and then correlated them with the in vitro chemosensitivities of gynecologic tumor cells using immunohistochemistry and a tetrazolium dye (MTT) assay.
  • RESULTS: In the 19 ovarian carcinomas examined, the mean Topo II alpha index (%) and the tumor cell growth inhibition rate (I.R.: %) for doxorubicin and etoposide in the clear cell adenocarcinomas [15.8, 21.4, 32.3] were all lower than in the endometrioid [33.9; p<0.001, 58.3, 61.9; p<0.05, respectively] and serous adenocarcinomas [43.6; p<0.001, 75.0, 79.8; p<0.01, respectively].
  • Comparing these markers with the clinical response to chemotherapy, the overall predictive accuracy of the Topo II alpha index and the MTT assay was 87.5% (14/16) and 81.3% (13/16), respectively.
  • In the 24 endometrial carcinomas examined, the mean Topo II a index and the I.R for doxorubicin and etoposide in the G1 carcinomas [22.2, 26.8, 21.5] were significantly lower than in the G2/G3 carcinomas [38.4, 54.0; p<0.001, 40.5; p<0.05].
  • CONCLUSIONS: The Topo II alpha index and the results of in vitro chemosensitivity testing may be of assistance in selecting the appropriate chemotherapeutic drugs against gynecologic malignancies based on their histological type and differentiation, along with MRP expression.
  • [MeSH-major] Adenocarcinoma, Clear Cell / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Endometrioid / drug therapy. Cystadenocarcinoma, Serous / drug therapy. DNA Topoisomerases, Type II / analysis. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Endometrial Neoplasms / drug therapy. Multidrug Resistance-Associated Proteins / analysis. Neoplasm Proteins / analysis. Ovarian Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Antigens, Neoplasm. Antineoplastic Agents / pharmacology. Cell Differentiation. Cisplatin / administration & dosage. Cisplatin / pharmacology. Cyclophosphamide / administration & dosage. Cyclophosphamide / pharmacology. Cytoplasm / enzymology. DNA-Binding Proteins. Doxorubicin / administration & dosage. Doxorubicin / pharmacology. Etoposide / pharmacology. Female. Humans. Membrane Proteins / analysis. Middle Aged. Predictive Value of Tests. Remission Induction. Treatment Outcome

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  • (PMID = 11712788.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Membrane Proteins; 0 / Multidrug Resistance-Associated Proteins; 0 / Neoplasm Proteins; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha; Q20Q21Q62J / Cisplatin
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19. Ruvalcaba-Limón E, Cantú-de-León D, León-Rodríguez E, Cortés-Esteban P, Serrano-Olvera A, Morales-Vásquez F, Sosa-Sánchez R, Poveda-Velasco A, Crismatt-Zapata A, Santillán-Gómez A, Aguilar-Jiménez C, Alanís-López P, Alfaro-Ramírez P, Alvarez-Avitia MA, Aranda-Flores CE, Arias-Ceballos JH, Arrieta-Rodríguez O, Barragán-Curiel E, Botello-Hernández D, Brom-Valladares R, Cabrera-Galeana PA, Cantón-Romero JC, Capdeville-García D, Cárdenas-Sánchez J, Castorena-Roji G, Cepeda-López FR, Cervantes-Sánchez G, Cetina-Pérez Lde C, Coronel-Martínez JA, Cortés-Cárdenas SA, Cruz-López JC, de la Garza-Salazar JG, Díaz-Romero C, Dueñas-González A, Valle-Solís AE, Escudero-de los Ríos P, Flores-Alvarez E, García-Matus R, Gerson-Cwilich R, González-Enciso A, González-de-León C, Guevara-Torres AG, Herbert-Núñez GS, Hernández-Hernández C, Hernández-Hernández DM, Isla-Ortiz D, Jesús-Sandoval R, Jiménez-Cervantes C, Kuri-Exsome R, López-Obispo JL, Maffuz-Aziz A, Martínez-Barrera LM, Medina-Castro JM, Montalvo-Esquivel G, Mora-Aguilar VH, Morales-Palomares MA, Morán-Mendoza A, Morgan-Villela G, Mota-García A, Muñoz-González DE, Murillo-Cruz DA, Novoa-Vargas A, Ochoa-Carrillo FJ, Oñate-Ocaña LF, Ortega-Rojo A, Palacios-Martínez AG, Palomeque-López A, Pérez-Montiel MD, Quijano-Castro F, Rivera-Rivera S, Rivera-Rubí LM, Robles-Flores JU, Rodríguez-Trejo A, Salas-Gonzáles E, Silva JA, Solorza-Luna G, Souto-del-Bosque R, Tirado-Gómez LL, Torrescano-González S, Torres-Lobatón A, Trejo-Durán E, Villavicencio-Valencia V, Gallardo-Rincón D, Grupo de Investigación en Cáncer de Ovario y Tumores Ginecológicos de México: [The first Mexican consensus of endometrial cancer. Grupo de Investigación en Cáncer de Ovario y Tumores Ginecológicos de México]. Rev Invest Clin; 2010 Nov-Dec;62(6):583, 585-605
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  • [Title] [The first Mexican consensus of endometrial cancer. Grupo de Investigación en Cáncer de Ovario y Tumores Ginecológicos de México].
  • INTRODUCTION: Endometrial cancer (EC) is the second most common gynecologic malignancy worldwide in the peri and postmenopausal period.
  • GICOM collaborative group under the auspice of different institutions have made the following consensus in order to make recommendations for the management of patients with this type of neoplasm.
  • RESULTS: Screening should be performed women at high risk (diabetics, family history of inherited colon cancer, Lynch S. type II).
  • Endometrial thickness in postmenopausal patients is best evaluated by transvaginal US, a thickness greater than or equal to 5 mm must be evaluated.
  • Total abdominal hysterectomy, bilateral salpingo oophorectomy, pelvic and para-aortic lymphadenectomy should be performed except in endometrial histology grades 1 and 2, less than 50% invasion of the myometrium without evidence of disease out of the uterus.
  • Adjuvant treatment after surgery includes radiation therapy to the pelvis, brachytherapy, and chemotherapy.
  • Patients with Stages III and IV should have surgery with intention to achieve optimal cytoreduction because of the impact on survival (51 m vs. 14 m), the treatment of recurrence can be with surgery depending on the pattern of relapse, systemic chemotherapy or hormonal therapy.
  • Multidisciplinary treatment impacts on survival and local control of the disease, including surgery, radiation therapy and chemotherapy, hormonal treatment is reserved to selected cases of recurrence.
  • This is the first attempt of a Mexican Collaborative Group in Gynecology to give recommendations is a special type of neoplasm.
  • [MeSH-major] Carcinoma. Endometrial Neoplasms
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Chemotherapy, Adjuvant. Combined Modality Therapy. Diagnostic Imaging. Estrogen Antagonists / adverse effects. Estrogen Replacement Therapy / adverse effects. Estrogens / adverse effects. Evidence-Based Medicine. Female. Humans. Hysterectomy / methods. Laparoscopy. Lymph Node Excision. Mass Screening. Mexico. Neoplasm Staging / methods. Radiotherapy, Adjuvant. Risk Factors. Salvage Therapy. Tamoxifen / adverse effects

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  • (PMID = 21416918.001).
  • [ISSN] 0034-8376
  • [Journal-full-title] Revista de investigación clínica; organo del Hospital de Enfermedades de la Nutrición
  • [ISO-abbreviation] Rev. Invest. Clin.
  • [Language] spa
  • [Publication-type] Consensus Development Conference; English Abstract; Journal Article; Practice Guideline
  • [Publication-country] Mexico
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Estrogen Antagonists; 0 / Estrogens; 094ZI81Y45 / Tamoxifen
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20. Koshiyama M, Fujii H, Kinezaki M, Yoshida M: Correlation between Topo II alpha expression and chemosensitivity testing for Topo II-targeting drugs in gynaecological carcinomas. Anticancer Res; 2001 Mar-Apr;21(2A):905-10
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  • [Title] Correlation between Topo II alpha expression and chemosensitivity testing for Topo II-targeting drugs in gynaecological carcinomas.
  • BACKGROUND: The purpose of this study was to investigate the correlation between topoisomerase II alpha (Topo II alpha) expression and the chemosensitivity to Topo II-targeting drugs in gynaecological carcinomas.
  • MATERIALS AND METHODS: We analysed the expression of Topo II alpha, and then correlated this with the in vitro chemosensitivities of 43 gynaecological tumors using immunohistochemistry and a tetrazolium dye (MTT) assay.
  • RESULTS: There was a significant correlation between the Topo II alpha index (the number of positive cells per 100 cells: %) and the tumor cell growth inhibition rate in culture (I.R.: %) for doxorubicin and etoposide (r = 0.631, p < 0.001 and r = 0.645, p < 0.001, respectively).
  • The I.Rs for doxorubicin and etoposide in endometrial carcinomas were lower than those in ovarian carcinomas [38.2 +/- 22.8 vs 54.6 +/- 29.8, 37.3 +/- 19.8 vs 59.3 +/- 30.6] (p < 0.05, respectively).
  • Furthermore, the number of high Topo II alpha index (over 30%) tumors in the ovarian carcinoma cases was higher than that in the endometrial carcinoma cases (63.1% vs 45.8%, p < 0.05).
  • CONCLUSIONS: Our data suggest that the Topo II alpha index of a tumor is a reflection of its chemosensitivity to Topo II-targeting drugs.
  • The use of this index may enable prediction of a clinical response to chemotherapy using Topo II-targeting drugs in gynaecological malignancies.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cisplatin / pharmacology. Cyclophosphamide / pharmacology. DNA Topoisomerases, Type II / biosynthesis. Doxorubicin / pharmacology. Endometrial Neoplasms / enzymology. Etoposide / pharmacology. Isoenzymes / biosynthesis. Ovarian Neoplasms / enzymology

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  • (PMID = 11396183.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Isoenzymes; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha; Q20Q21Q62J / Cisplatin
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21. Santin AD, Bellone S, Van Stedum S, Bushen W, Palmieri M, Siegel ER, De Las Casas LE, Roman JJ, Burnett A, Pecorelli S: Amplification of c-erbB2 oncogene: a major prognostic indicator in uterine serous papillary carcinoma. Cancer; 2005 Oct 1;104(7):1391-7
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  • [Title] Amplification of c-erbB2 oncogene: a major prognostic indicator in uterine serous papillary carcinoma.
  • BACKGROUND: Overexpression of the epidermal growth factor type II receptor HER-2/neu has been associated with resistance to chemotherapy and poor survival in several human tumors.
  • In the current study, the authors have determined the frequency and clinical significance of HER-2/neu gene amplification in uterine serous papillary endometrial carcinoma (USPC), a highly aggressive variant of endometrial carcinoma.
  • Patients with USPC harboring tumors with HER-2/neu gene amplification had a significantly shorter survival time from diagnosis to disease-related death when compared with FISH-negative patients (P = 0.0008).
  • Determination of HER-2/neu gene amplification may guide clinical management of patients with USPC and may have important implications for the implementation of novel treatment strategies.


22. Fowble B, Hanlon A, Freedman G, Nicolaou N, Anderson P: Second cancers after conservative surgery and radiation for stages I-II breast cancer: identifying a subset of women at increased risk. Int J Radiat Oncol Biol Phys; 2001 Nov 1;51(3):679-90
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  • [Title] Second cancers after conservative surgery and radiation for stages I-II breast cancer: identifying a subset of women at increased risk.
  • METHODS AND MATERIALS: From 1978 to 1994, 1,253 women with unilateral Stage I-II breast cancer underwent wide excision, axillary dissection, and radiation.
  • Adjuvant therapy consisted of chemotherapy in 19%, tamoxifen in 19%, and both in 8%.
  • Factors analyzed for their association with the cumulative incidence of all second malignancies, contralateral breast cancer, and non-breast cancer malignancy were: age, menopausal status, race, family history, obesity, smoking, tumor size, location, histology, pathologic nodal status, region(s) treated with radiation, and the use and type of adjuvant therapy.
  • RESULTS: One hundred seventy-six women developed a second malignancy (87 contralateral breast cancers at a median interval of 5.8 years, and 98 non-breast cancer malignancies at a median interval of 7.2 years).
  • There was no significant effect of chemotherapy or the regions treated with radiation on contralateral breast cancer or non-breast cancer second malignancy.
  • The most common types of second non-breast cancer malignancies were skin cancers, followed by gynecologic malignancies (endometrial), and gastrointestinal malignancies (colorectal and pancreas).
  • The majority of patients treated with conservative surgery and radiation with or without adjuvant systemic therapy will not develop a second cancer.
  • [MeSH-minor] Adult. Age Factors. Aged. Axilla. Carcinoma, Ductal, Breast / epidemiology. Carcinoma, Ductal, Breast / radiotherapy. Carcinoma, Ductal, Breast / surgery. Carcinoma, Lobular / epidemiology. Carcinoma, Lobular / radiotherapy. Carcinoma, Lobular / surgery. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Lymph Node Excision. Lymphatic Irradiation. Mastectomy, Segmental. Middle Aged. Risk. Risk Factors

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  • (PMID = 11597809.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
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23. Cocco E, Hu Z, Richter CE, Bellone S, Casagrande F, Bellone M, Todeschini P, Krikun G, Silasi DA, Azodi M, Schwartz PE, Rutherford TJ, Buza N, Pecorelli S, Lockwood CJ, Santin AD: hI-con1, a factor VII-IgGFc chimeric protein targeting tissue factor for immunotherapy of uterine serous papillary carcinoma. Br J Cancer; 2010 Sep 7;103(6):812-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] hI-con1, a factor VII-IgGFc chimeric protein targeting tissue factor for immunotherapy of uterine serous papillary carcinoma.
  • BACKGROUND: Uterine serous papillary adenocarcinoma (USPC) is a highly aggressive variant of endometrial cancer.
  • Human immuno-conjugate molecule (hI-con1) is an antibody-like molecule targeted against tissue factor (TF), composed of two human Factor VII (fVII) as the targeting domain, fused to human immunoglobulin (Ig) G1 Fc as an effector domain.
  • We evaluated hI-con1 potential activity against primary chemotherapy-resistant USPC cell lines expressing different levels of TF.
  • Six primary USPC cell lines, half of which overexpress the epidermal growth factor type II (HER2/neu) receptor at 3+ levels, were assessed by flow cytometry and real-time PCR for TF expression.
  • High expression of TF was found in 50% (three out of six) of the USPC cell lines tested by real-time PCR and flow cytometry when compared with normal endometrial cells (NECs; P<0.001).
  • Uterine serous papillary adenocarcinoma cell lines overexpressing TF, regardless of their high or low HER2/neu expression, were highly sensitive to IDCC (mean killing+/-s.d., 65.6+/-3.7%, range 57.5-77.0%, P<0.001), although negligible cytotoxicity against USPC was seen in the absence of hI-con1 or in the presence of Rituximab control antibody.
  • The addition of low doses of IL-2 further increased the cytotoxic effect induced by hI-con1 against chemotherapy-resistant USPC.
  • CONCLUSION: hI-con1 induces strong cytotoxicity against primary chemotherapy-resistant USPC cell lines overexpressing TF.
  • The hI-con1 may represent a novel therapeutic agent for the treatment of patients harbouring advanced, recurrent and/or metastatic USPC refractory to standard treatment modalities.

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  • (PMID = 20700124.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016359; United States / NCI NIH HHS / CA / R01 CA122728; United States / NCI NIH HHS / CA / CA-16359; United States / NCI NIH HHS / CA / R01 CA122728-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Recombinant Fusion Proteins; 9001-25-6 / Factor VII
  • [Other-IDs] NLM/ PMC2966612
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24. Schmidt D: [Changes in the endometrium after tamoxifen therapy]. Pathologe; 2006 Feb;27(1):27-32
Hazardous Substances Data Bank. TAMOXIFEN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Changes in the endometrium after tamoxifen therapy].
  • [Transliterated title] Endometriumveränderungen nach Tamoxifen-Therapie.
  • Depending on the type of tissue, tamoxifen has either an anti-estrogenic or an estrogenic effect on the cells.
  • In the treatment of breast cancer, the anti-estrogenic effect is used.
  • However, at the same time there is a predominant progestin-like and only mild estrogenic effect on the endometrium.
  • However, endometrial hyperplasia or endometrial carcinoma is identified histologically in only a few cases.
  • In the majority of cases, the diagnosis is endometrial atrophy or endometrial polyp.
  • Other findings related to tamoxifen therapy are stromal decidualisation, regressive hyperplasia, and foci of mucinous, clear cell and serous metaplasia.
  • The main reason for the diagnosis of endometrial hyperplasia on ultrasound could be fibrosis and edema along the border between the endometrium and myometrium.
  • Still unsolved is the question of whether endometrial carcinomas developing after tamoxifen therapy belong mostly to type I (endometrioid) or type II (serous, clear cell) carcinomas.
  • Only in rare cases do malignant neoplasms other than carcinomas develop after tamoxifen therapy.
  • These are adenosarcomas, carcinosarcomas and endometrial stromal sarcomas.
  • [MeSH-minor] Atrophy. Endometrial Neoplasms / chemically induced. Endometrial Neoplasms / pathology. Female. Humans. Polyps / chemically induced. Polyps / pathology. Uterus / drug effects. Uterus / pathology

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  • (PMID = 16362260.001).
  • [ISSN] 0172-8113
  • [Journal-full-title] Der Pathologe
  • [ISO-abbreviation] Pathologe
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Estrogen Antagonists; 094ZI81Y45 / Tamoxifen
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25. Tropé C, Kristensen GB, Abeler VM: Clear-cell and papillary serous cancer: treatment options. Best Pract Res Clin Obstet Gynaecol; 2001 Jun;15(3):433-46

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clear-cell and papillary serous cancer: treatment options.
  • Clear-cell carcinoma (CCC) and serous papillary carcinoma of the endometrium (UPSC) are rare subtypes of endometrial carcinoma (10%).
  • The histological diagnosis can be made on the dilation and curettage specimens in both types in a very high percentage of the cases.
  • This is important in the planning of treatment.
  • CCC and UPSC are associated with about 50% of all relapses occurring in endometrial carcinoma, and the 5-year survival rate is, on average, 42% and 27% respectively.
  • Stage Ia patients treated with complete surgical staging alone have a low risk of relapse and need not be offered adjuvant systemic therapy or pelvic radiation.
  • The treatment of patients with CCC and UPSC stage Ib, Ic, II and III should include radical debulking surgery and some form of adjuvant therapy, but it is not clear which type is most effective.
  • Adjuvant pelvic radiotherapy plus intracavitary radiotherapy is usually given in early-stage disease and pelvic radio therapy/or whole abdomen irradiation plus adjuvant systemic chemotherapy (PAC) in advanced disease.
  • Paclitaxel, alone or in combination, is currently being tested in phase II studies.
  • [MeSH-major] Adenocarcinoma, Clear Cell / therapy. Cystadenocarcinoma, Papillary / therapy. Endometrial Neoplasms / therapy
  • [MeSH-minor] Age Factors. Aneuploidy. Combined Modality Therapy. Dilatation and Curettage. Female. Genes, p53. Humans. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Neoplasm Invasiveness / genetics. Neoplasm Staging. Prognosis. Transcriptional Activation. Treatment Outcome

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  • [Copyright] Copyright 2001 Harcourt Publishers Ltd.
  • (PMID = 11476564.001).
  • [ISSN] 1521-6934
  • [Journal-full-title] Best practice & research. Clinical obstetrics & gynaecology
  • [ISO-abbreviation] Best Pract Res Clin Obstet Gynaecol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 61
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26. Emons G, Gründker C, Günthert AR, Westphalen S, Kavanagh J, Verschraegen C: GnRH antagonists in the treatment of gynecological and breast cancers. Endocr Relat Cancer; 2003 Jun;10(2):291-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] GnRH antagonists in the treatment of gynecological and breast cancers.
  • Approximately 80% of human ovarian and endometrial cancers and 50% of breast cancers express GnRH and its receptor as part of an autocrine regulatory system.
  • Recently, a second type of GnRH receptor, specific for GnRH-II, has been identified in ovarian and endometrial cancers, which transmits significantly stronger antiproliferative effects than the GnRH-I receptor.
  • GnRH antagonists have agonistic effects on this type II receptor.
  • Therefore, we performed a phase II clinical trial with the GnRH antagonist, cetrorelix (10 mg/day), in patients with ovarian or mullerian carcinoma refractory to platinum chemotherapy.
  • In this very refractory patient population (median number of prior chemotherapies = 3) these results are quite remarkable when compared with palliative chemotherapy.
  • In addition, cytotoxic GnRH analogs have been developed, where for example doxorubicin was covalently coupled to GnRH analogs.
  • These compounds have superior antitumor effects in cancers expressing GnRH receptors as compared with native doxorubicin and allow for a targeted cytotoxic chemotherapy of gynecologic and breast cancers.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Breast Neoplasms / drug therapy. Genital Neoplasms, Female / drug therapy. Gonadotropin-Releasing Hormone / antagonists & inhibitors

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  • (PMID = 12790790.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, LHRH; 33515-09-2 / Gonadotropin-Releasing Hormone
  • [Number-of-references] 55
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27. Johann S, Mueller MD: [Follow-up after malignant tumours of the uterus (cancer of the uterine corpus / cervical cancer)]. Ther Umsch; 2008 Jun;65(6):341-6
International Agency for Research on Cancer - Screening Group. diagnostics - A practical manual on visual screening for cervical neoplasia .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The endometrial carcinoma with its different histological subtypes counts for most of the malignomas of the uterine body.
  • But the rare category of uterine sarcomas (carcinosarcomas, leiomyosarcomas as well as endometrial stromal sarcomas) also belongs to this group.
  • Cervical cancer presents an own entitity, regarding both histology and therapeutic options.
  • Endometrial cancer is the most common genital malignoma in Northern Europe and North America.
  • Histologically, the endometrial cancer can be subdivided in two groups: type I is hormonal sensitive and well differentiated, type II represents an undifferenciated aggressive tumour with poor prognosis.
  • Due to the main symptom - abnormal vaginal bleeding - endometrial cancer is detected in an early stage in about 75% of all patients.
  • First choice in therapy is stage related surgery.
  • Cervical cancer is mainly a squamous cell carcinoma and oncogenic Human Papilloma Virus (HPV) associated.
  • Surgery is only indicated up to stage IIA, advanced stages should be treated by radio-chemotherapy.
  • Intention is the detection of the curable local relapse.
  • [MeSH-minor] Combined Modality Therapy. Evidence-Based Medicine. Female. Humans. Neoplasm Staging. Positron-Emission Tomography. Prognosis. Tomography, X-Ray Computed


28. Wang J, Zhou F, Dong M, Wu R, Qian Y: Prolonged gonadotropin-releasing hormone agonist therapy reduced expression of nitric oxide synthase in the endometrium of women with endometriosis and infertility. Fertil Steril; 2006 Apr;85(4):1037-44
MedlinePlus Health Information. consumer health - Female Infertility.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prolonged gonadotropin-releasing hormone agonist therapy reduced expression of nitric oxide synthase in the endometrium of women with endometriosis and infertility.
  • OBJECTIVE: To determine whether endometrial expression of endothelial nitric oxide synthase (eNOS) or inducible NOS (iNOS) protein in women with endometriosis-associated infertility is different from that in the fertile controls, whether GnRH agonist (GnRH-a) regulates the endometrial expression of NOS in women with endometriosis-associated infertility, and whether there is a correlation between serum E2 or P levels, and the endometrial expression of eNOS or iNOS.
  • PATIENT(S): Thirty patients with endometriosis-associated infertility and 19 patients with carcinoma in situ of the cervix.
  • INTERVENTION(S): Endometrial biopsy specimens and blood samples.
  • MAIN OUTCOME MEASURE(S): Endometrial eNOS and iNOS protein relative levels and serum concentrations of E2 or P.
  • Eutopic endometrium in women with endometriosis-associated infertility before GnRH-a treatment showed higher levels of eNOS than that of the control group.
  • After 3 months of GnRH-a therapy, eNOS levels in the endometrium were reduced.
  • In addition, a significant positive correlation was found between serum E2 or P concentrations, and the endometrial expression of eNOS.
  • CONCLUSION(S): The GnRH-a treatment attenuated the endometrial expression of eNOS in women with endometriosis-associated infertility.
  • Endogenous ovarian steroids influence endometrial eNOS expression.
  • [MeSH-major] Endometriosis / enzymology. Endometrium / enzymology. Gonadotropin-Releasing Hormone / administration & dosage. Gonadotropin-Releasing Hormone / agonists. Infertility, Female / enzymology. Nitric Oxide Synthase Type II / antagonists & inhibitors. Nitric Oxide Synthase Type III / antagonists & inhibitors
  • [MeSH-minor] Adult. Female. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Enzymologic / physiology. Humans. Menstrual Cycle / drug effects. Menstrual Cycle / metabolism. Prospective Studies

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  • (PMID = 16580392.001).
  • [ISSN] 1556-5653
  • [Journal-full-title] Fertility and sterility
  • [ISO-abbreviation] Fertil. Steril.
  • [Language] eng
  • [Publication-type] Comparative Study; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 33515-09-2 / Gonadotropin-Releasing Hormone; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nitric Oxide Synthase Type III
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29. Wang JH, Zhou FZ, Dong MY, Yuan L: [Influences of gonadotropin releasing hormone agonist treatment on nitric oxide synthase expression in women with endometriosis and infertility]. Zhonghua Fu Chan Ke Za Zhi; 2005 Jun;40(6):383-7
MedlinePlus Health Information. consumer health - Female Infertility.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Influences of gonadotropin releasing hormone agonist treatment on nitric oxide synthase expression in women with endometriosis and infertility].
  • OBJECTIVE: To explore the expression of endothelial and inducible nitric oxide synthase (eNOS and iNOS) in the eutopic endometria of patients with endometriosis and infertility, and to detect the effect of gonadotropin releasing hormone agonist (GnRH-a) therapy on their expressions.
  • METHODS: Immunohistochemistry and Western immunoblot assay were used to screen eNOS and iNOS expression in endometria of patients with stage III to IV endometriosis and infertility without (30 cases, endometriosis group) and with GnRH-a treatment (18 cases, treatment group), and of 19 patients with carcinoma in situ of the cervix (control group).
  • RESULTS: eNOS was localized predominantly to the endometrial glandular epithelium, luminal epithelium, and microvascular endothelium. iNOS staining was light, and it, when present, was predominantly found in glandular epithelium and stromal cells.
  • During the early-, mid-, and late-proliferative phases, and the early-, mid-, and late-secretory phases, endometrial eNOS protein relative levels were 0.30 +/- 0.04, 0.40 +/- 0.03, 0.49 +/- 0.03, 0.43 +/- 0.04, 0.55 +/- 0.04 and 0.48 +/- 0.03 in endometriosis group, 0.22 +/- 0.03, 0.37 +/- 0.03, 0.45 +/- 0.04, 0.35 +/- 0.05, 0.50 +/- 0.03 and 0.41 +/- 0.00 in treatment group, and 0.21 +/- 0.03, 0.33 +/- 0.03, 0.45 +/- 0.04, 0.40 +/- 0.03, 0.47 +/- 0.05 and 0.41 +/- 0.03 in control group, respectively.
  • Compared with endometriosis group, endometrial eNOS levels in treatment group were reduced, but a significant difference was found only in early proliferative phase and early-, mid-secretory phases (P < 0.05).
  • A significant positive correlation was found between serum E(2) or P concentrations and endometrial expression of eNOS (P < 0.01).
  • CONCLUSIONS: The higher endometrial expression of eNOS in patients with stage III to IV endometriosis may be related to the pathogenesis of endometriosis and the associated subfertility.
  • [MeSH-major] Endometriosis / drug therapy. Gene Expression / drug effects. Gonadotropin-Releasing Hormone / agonists. Infertility, Female / drug therapy. Nitric Oxide Synthase Type II / genetics. Nitric Oxide Synthase Type III / genetics

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  • (PMID = 16008888.001).
  • [ISSN] 0529-567X
  • [Journal-full-title] Zhonghua fu chan ke za zhi
  • [ISO-abbreviation] Zhonghua Fu Chan Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 33515-09-2 / Gonadotropin-Releasing Hormone; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nitric Oxide Synthase Type III
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30. Maia HJ, Casoy J: Non-contraceptive health benefits of oral contraceptives. Eur J Contracept Reprod Health Care; 2008 Mar;13(1):17-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The use of combined oral contraceptives (COCs) is associated with a reduced risk of developing endometriosis, myomas, and endometrial and ovarian carcinoma.
  • This is accomplished through inhibition of the endometrial expression of enzymes related to the biosynthesis of prostaglandin and oestrogen, particularly cyclooxygenase type II (Cox-2) and aromatase.
  • The reduction of inflammation in the endometrium may also be the mechanism behind the lower incidence of endometrial carcinoma in COC users.
  • [MeSH-minor] Acne Vulgaris / drug therapy. Aromatase / metabolism. Contraceptives, Oral, Combined / therapeutic use. Cyclooxygenase 2 / metabolism. Endometriosis / prevention & control. Female. Humans. Menorrhagia / drug therapy. Ovarian Neoplasms / prevention & control. Perimenopause. Uterine Neoplasms / prevention & control. Women's Health

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  • (PMID = 17963179.001).
  • [ISSN] 1362-5187
  • [Journal-full-title] The European journal of contraception & reproductive health care : the official journal of the European Society of Contraception
  • [ISO-abbreviation] Eur J Contracept Reprod Health Care
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Contraceptives, Oral, Combined; 0 / Contraceptives, Oral, Hormonal; EC 1.14.14.1 / Aromatase; EC 1.14.99.1 / Cyclooxygenase 2
  • [Number-of-references] 57
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31. Montagnani Marelli M, Moretti RM, Januszkiewicz-Caulier J, Motta M, Limonta P: Gonadotropin-releasing hormone (GnRH) receptors in tumors: a new rationale for the therapeutical application of GnRH analogs in cancer patients? Curr Cancer Drug Targets; 2006 May;6(3):257-69
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Based on this rationale, pituitary GnRH receptors represent the target for the successful utilization of GnRH agonists (that are more stable than the native peptide) for the treatment of hormone-dependent tumors (e.g., prostate, breast, endometrial, ovarian cancers).
  • Interestingly, GnRH receptors have been shown to be expressed also in androgen-independent prostate carcinoma, as well as in tumors that are not classically considered hormone-related (e.g., melanoma), suggesting a clinical utility of the administration of GnRH analogs also in these tumors.
  • More recently, GnRH agonists have been proposed as useful carriers to target cytotoxic drugs or toxins to cancer cells displaying the specific GnRH receptors.
  • A second form of GnRH (designated GnRH-II) has been discovered in most vertebrates, including humans.
  • GnRH-II has been suggested to act through a 'putative' cognate type II GnRH receptor, which is distributed in different tissues, both normal and tumoral.
  • In humans, a full-length functional type II GnRH receptor has not been found.
  • Therefore, its functions as well as its possible utility as a molecular target for a GnRH-II based therapy in oncology still has to be clarified.
  • It will also be discussed whether the presence of these receptors might represent an additional rationale for the clinical utility of GnRH analogs as anticancer drugs.
  • [MeSH-major] Gonadotropin-Releasing Hormone / therapeutic use. Neoplasms / metabolism. Receptors, LHRH / metabolism

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  • (PMID = 16712461.001).
  • [ISSN] 1568-0096
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Receptors, LHRH; 33515-09-2 / Gonadotropin-Releasing Hormone
  • [Number-of-references] 166
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32. Rovirosa A, Ascaso C, Ordi J, Arenas M, Valduvieco I, Lejarcegui JA, Pahisa J, Torne A, Biete A: How to deal with prognostic factors and radiotherapy results in uterine neoplasms with a sarcomatous component? Clin Transl Oncol; 2009 Oct;11(10):681-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • All 76 patients were staged after pathological evaluation of the surgical specimen by FIGO classification with 54 patients being stages I-II and 27 patients stages III-IVA.
  • 5/81 patients received complementary chemotherapy to the surgery and 5 patients received chemotherapy as treatment of local and distant relapse (All the patients were treated with a different chemotherapy schedule).
  • For pathological type the frequency by advanced vs. early stages was 54% vs. 52% for carcinosarcomas, 33.5% vs. 17.5% for leiomyosarcoma, and 30.5% and 12.5% for adenosarcoma and endometrial stromal sarcoma, respectively.
  • Stratification by early (I-II) and advanced stages (III, IV) revealed tumour size >8 cm was the only prognostic factor significantly associated with OS, DFS, LRFS and DMFS on univariate analysis for early stages (HR: OS 2.52, DFS 3.10, LRFS 3.10 and DMFS 2.63).
  • CONCLUSIONS: Uterine tumours with a sarcomatous component have a poor outcome in spite of treatment in comparison to endometrial carcinoma, probably due to the higher frequency of adverse prognostic factors.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Female. Humans. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Rate. Treatment Outcome

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  • (PMID = 19828411.001).
  • [ISSN] 1699-3055
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
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