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Pesquisa : C04.557.470.200.025.045 [Categoria DeCS]
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[PMID]:29325268
[Au] Autor:Li MJ; Li HR; Cheng X; Bi R; Tu XY; Liu F; Chen LH
[Ad] Endereço:Department of Gynecologic Oncology, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
[Ti] Título:[Clinical significance of targeting drug-based molecular biomarkers expression in ovarian clear cell carcinoma].
[So] Source:Zhonghua Fu Chan Ke Za Zhi;52(12):835-843, 2017 Dec 25.
[Is] ISSN:0529-567X
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To assess the expression level of targeting drug-based molecular biomarkers in ovarian clear cell carcinoma (OCCC) tissues and its clinical significance. A total of 63 OCCC patients included 40 primary OCCC and 23 recurrent OCCC for secondary cytoreductive surgery (SCS), who had received primary surgeries at Fudan University Shanghai Cancer Center between January, 2008 and December, 2015 were enrolled, and immunohistochemistry SP method was used to test human epidermal growth factor receptor (EGFR), human epidermal growth factor receptor-2 (HER2), aurora kinase A (AURKA), breast cancer susceptibility gene 1 (BRCA1), BRCA2 and programmed death-ligand 1 (PD-L1)protein expression in paraffin-embedded tissues. The positive rates of EGFR, HER2, AURKA,BRCA1, BRCA2 and PD-L1 in primary and recurrent tumor tissues were respectively 20% (8/40) vs 30% (7/23) , 22% (9/40) vs 35% (8/23) , 38% (15/40) vs 35% (8/23) , 42% (17/40) vs 39% (9/23) , 20% (8/40) vs 22% (5/23) , 25% (10/40) vs 17% (4/23) , and there were no significant differences between primary and recurrent OCCC (all 0.05). χ(2)-test or Fisher exact analysis revealed that HER2 expression in recurrent tumor tissues had a relationship with chemoresistance ( 0.05), while the expression of other biomarkers showed no significant relationship with chemoresistance (all 0.05). Further, Kaplan-Meier survival analysis showed that patients with HER2 and AURKA-positive expression had a significantly shorter progression-free survival time in primary OCCC (4 months vs 10 months, log-rank test, 0.05 for HER2; and 4 months vs 10 months, 0.05 for AURKA); and a shorter overall survival time after SCS in recurrent OCCC (10 months vs 44 months, 0.05 for HER2; and 13 months vs 43 months, 0.05 for AURKA). However, multivariate Cox proportional hazards regression analysis indicated that none of these 6 biomarkers was independent risk factor of progression-free survival time of primary OCCC or overall survival time after SCS for recurrent OCCC ( 0.05). HER2 and AURKA could serve as prognostic factors in ovarian clear cell carcinoma.
[Mh] Termos MeSH primário: Adenocarcinoma de Células Claras/tratamento farmacológico
Adenocarcinoma de Células Claras/metabolismo
Biomarcadores Tumorais/metabolismo
Neoplasias Epiteliais e Glandulares/tratamento farmacológico
Neoplasias Epiteliais e Glandulares/metabolismo
Neoplasias Ovarianas/tratamento farmacológico
Neoplasias Ovarianas/metabolismo
Medicina de Precisão
[Mh] Termos MeSH secundário: Adenocarcinoma de Células Claras/diagnóstico
Adenocarcinoma de Células Claras/mortalidade
Proteína BRCA2
China
Intervalo Livre de Doença
Feminino
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Terapia de Alvo Molecular
Recidiva Local de Neoplasia
Neoplasias Epiteliais e Glandulares/diagnóstico
Neoplasias Epiteliais e Glandulares/mortalidade
Neoplasias Ovarianas/diagnóstico
Neoplasias Ovarianas/mortalidade
Receptor do Fator de Crescimento Epidérmico
Receptor ErbB-2
Análise de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BRCA2 Protein); 0 (BRCA2 protein, human); 0 (Biomarkers, Tumor); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180112
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0529-567x.2017.12.008


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[PMID]:28460432
[Au] Autor:Huang W; Zhou W; Li C; Yang Y; Shang YK; Chen C; Zhang J; Yao R; Wang P; Wen W; Liu HQ; Wang L; Li X; Bian H; Chen ZN
[Ad] Endereço:National Translational Science Center for Molecular Medicine, Department of Cell Biology, Fourth Military Medical University, Xi'an, China.
[Ti] Título:Promoter mutations and cellular distribution of telomerase in non-clear cell and clear cell hepatocellular carcinoma.
[So] Source:Oncotarget;8(16):26288-26297, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Reactivation of telomerase is a critical step in the development of hepatocellular carcinoma (HCC). Here we identified the frequency of mutations in telomerase reverse transcriptase (TERT) promoter was 34% in non-clear cell HCC (NCCHCC, n = 259) and 26.3% in clear cell HCC (CCHCC, n = 57). The mutations were independently associated with poor recurrence-free survival of HCCs. Interestingly immunohistochemical analysis demonstrated a higher positive rate of TERT cytoplasmic localization (95%) than nuclear localization (64%) in HCCs. In NCCHCCs, the mutations correlated with higher TERT nuclear expression and increased telomere-dependent telomerase activity. Higher cytoplasmic expression was found in adjacent tissues compared to tumor tissues, and was associated with tumor well-differentiation and lower level of α-fetoprotein. NCCHCCs with low nuclear as well as high cytoplasmic expression correlated with better prognosis. In CCHCCs, elevated TERT cytoplasmic expression was observed in CCHCCs harboring mutations. Higher TERT cytoplasmic expression was found in tumor tissues compared to adjacent tissues, and was associated with multiple numbers of tumors and poor prognosis of CCHCCs. In conclusion, mutations in TERT promoter disclose the significance of both nuclear and cytoplasmic TERT in HCC. Cytoplasmic TERT should also be considered when determining prognosis and treatment of HCCs.
[Mh] Termos MeSH primário: Adenocarcinoma de Células Claras/genética
Adenocarcinoma de Células Claras/metabolismo
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/metabolismo
Mutação
Regiões Promotoras Genéticas
Telômero/genética
Telômero/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma de Células Claras/mortalidade
Adenocarcinoma de Células Claras/patologia
Adulto
Idoso
Carcinoma Hepatocelular/mortalidade
Carcinoma Hepatocelular/patologia
Feminino
Seguimentos
Seres Humanos
Espaço Intracelular/metabolismo
Neoplasias Hepáticas/genética
Neoplasias Hepáticas/metabolismo
Neoplasias Hepáticas/mortalidade
Neoplasias Hepáticas/patologia
Masculino
Meia-Idade
Gradação de Tumores
Estadiamento de Neoplasias
Transporte Proteico
Recidiva
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15458


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[PMID]:29247567
[Au] Autor:Ueno M; Shiomi T; Mochizuki S; Chijiiwa M; Shimoda M; Kanai Y; Kataoka F; Hirasawa A; Susumu N; Aoki D; Okada Y
[Ad] Endereço:Department of Pathology, Keio University School of Medicine, Tokyo, Japan.
[Ti] Título:ADAM9 is over-expressed in human ovarian clear cell carcinomas and suppresses cisplatin-induced cell death.
[So] Source:Cancer Sci;109(2):471-482, 2018 Feb.
[Is] ISSN:1349-7006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:ADAMs (a disintegrin and metalloproteinases) are involved in various biological events such as cell adhesion, migration and invasion, membrane protein shedding and proteolysis. However, there have been no systematic studies on the expression of ADAMs in human ovarian carcinomas. We therefore examined mRNA expression of all the proteolytic ADAM species including ADAM8, 9, 10, 12, 15, 17, 19, 20, 21, 28, 30, 33 and ADAMDEC1 in human ovarian carcinomas, and found that prototype membrane-anchored ADAM9m, but not secreted isoform ADAM9s, is significantly over-expressed in carcinomas than in control non-neoplastic ovarian tissue. Among the histological subtypes of serous, endometrioid, mucinous and clear cell carcinomas, ADAM9m expression was highest in clear cell carcinomas. Immunohistochemistry showed that all the clear cell carcinoma samples displayed ADAM9m primarily on the carcinoma cell membrane. By immunoblotting, ADAM9m was detected mainly in an active form in the clear cell carcinoma tissues. When two clear cell carcinoma cell lines (RMG-I and TOV21G cells) with ADAM9m expression were treated with cisplatin, viability was significantly reduced and apoptosis increased in ADAM9m knockdown cells compared with mock transfectants. In addition, treatment of the cells with neutralizing anti-ADAM9m antibody significantly decreased viability compared with non-immune IgG, whereas ADAM9m over-expression significantly increased viability compared with mock transfectants. Our data show, to the best of our knowledge, for the first time, that ADAM9m is over-expressed in an activated form in human ovarian clear cell carcinomas, and suggest that ADAM9m plays a key role in cisplatin resistance.
[Mh] Termos MeSH primário: Proteínas ADAM/genética
Adenocarcinoma de Células Claras/genética
Antineoplásicos/farmacologia
Cisplatino/farmacologia
Resistência a Medicamentos Antineoplásicos
Proteínas de Membrana/genética
Neoplasias Ovarianas/genética
[Mh] Termos MeSH secundário: Proteínas ADAM/metabolismo
Adenocarcinoma de Células Claras/metabolismo
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Feminino
Regulação Neoplásica da Expressão Gênica
Técnicas de Silenciamento de Genes
Seres Humanos
Proteínas de Membrana/metabolismo
Neoplasias Ovarianas/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Membrane Proteins); EC 3.4.24.- (ADAM Proteins); EC 3.4.24.- (ADAM9 protein, human); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE
[do] DOI:10.1111/cas.13469


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[PMID]:29374722
[Au] Autor:Kalampokas E; Young H; Bednarek A; Habib M; Parkin DE; Gurumurthy M; Cairns M
[Ad] Endereço:Department of Gynecologic Oncology, Aberdeen Royal Infirmary, Aberdeen, U.K. m.kalampokas@gmail.com.
[Ti] Título:Surgical Outcomes and Morbidity After Radical Surgery for Ovarian Cancer in Aberdeen Royal Infirmary, the Northeast of Scotland Gynaecologic Oncology Centre.
[So] Source:Anticancer Res;38(2):923-928, 2018 02.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Ovarian cancer (OC) has a high mortality rate and usually presents late in advanced stage, which poses challenges to management. Better understanding of the disease biology and application of radical surgery (RS) to achieve no visible residual tumor, alongside with chemotherapy, may lead to longer survival amongst these patients. Our purpose was to examine the demographic characteristics, surgical morbidity and outcomes of patients undergoing RS for OC. MATERIALS AND METHODS: A retrospective cohort study of women undertaking surgery for OC between February 2014 and September 2016 in Aberdeen Royal Infirmary. RESULTS: A total of 121 women had surgery for OC of whom 78 (64.5%) were stage II and above. Of these, 40 (51.3%) women had primary and 38 (48.7%) had interval debulking surgery with 42 (53.8%) having radical surgery. The most common procedures that were performed as part of RS included rectosigmoid resection (n=20, 47.6%), small bowel resection (n=10, 23.8%), splenectomy (n=9, 21.4%). Morbidity outcomes included blood loss >1.5 lt. (n=14, 33.3%), hospitalization >7days (n=31, 73.8%), sepsis (n=8, 19%). There was no short-term mortality. Debulking outcomes were: no macroscopic residual disease (n=36, 85.7%), ≤10 mm disease (n=2, 4.8%), and ≥10 mm disease (n=3, 7.1%). CONCLUSION: Our findings support the practise where RS for OC can be offered to selected patients, with good surgery outcomes and low morbidity rates.
[Mh] Termos MeSH primário: Adenocarcinoma de Células Claras/cirurgia
Adenocarcinoma Mucinoso/cirurgia
Cistadenocarcinoma Seroso/cirurgia
Neoplasias do Endométrio/cirurgia
Neoplasias Ovarianas/cirurgia
[Mh] Termos MeSH secundário: Adenocarcinoma de Células Claras/patologia
Adenocarcinoma Mucinoso/patologia
Idoso
Cistadenocarcinoma Seroso/patologia
Procedimentos Cirúrgicos de Citorredução
Neoplasias do Endométrio/patologia
Feminino
Seguimentos
Seres Humanos
Meia-Idade
Morbidade
Neoplasias Ovarianas/patologia
Estudos Retrospectivos
Escócia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE


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[PMID]:29266433
[Au] Autor:Rekhi B; Deodhar KK; Menon S; Maheshwari A; Bajpai J; Ghosh J; Shylasree ST; Gupta S
[Ad] Endereço:Department of Surgical Pathology, Tata Memorial Hospital, Parel, Mumbai, India.
[Ti] Título:Napsin A and WT 1 are useful immunohistochemical markers for differentiating clear cell carcinoma ovary from high-grade serous carcinoma.
[So] Source:APMIS;126(1):45-55, 2018 Jan.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Clear cell carcinoma (CCC) of the ovary is an uncommon, but an aggressive epithelial ovarian cancer (EOC), which has overlapping histopathologic features with other ovarian tumours. Lately, Napsin A has been identified as its useful diagnostic immunohistochemical (IHC) marker. Fifty-eight prospectively diagnosed ovarian CCCs, 53 high-grade serous carcinomas (HGSCs), 16 endometrioid adenocarcinomas (EMACs), six mixed carcinomas, containing components of CCC and EMAC, seven metastatic mucinous adenocarcinomas and six ovarian yolk sac tumours (YSTs) were tested for Napsin A immunostaining. Fifty ovarian CCCs, 50 HGSCs, seven ovarian EMACs and five mixed carcinomas were tested for WT1 immunostaining. Napsin A was positively expressed in all 58 (100%) CCCs; was focally positive in 1 of 6 YSTs; in 1/16 EMACs and in six cases of mixed carcinomas, while it was negative in all 53 HGSCs and in seven metastatic mucinous adenocarcinomas. Other IHC markers expressed in cases of CCC ovary were CK7 (31/31) (100%), WT1 (0/50), p53 (20/26, 'wild type'), ER (4/31, focal) (12.9%), PAX8 (14/14) (100%), glypican-3 (4/10, focal) (44.4%), p16INK4 (5/5, focal) and CK20 (0/5). Various IHC markers expressed in HGSCs were WT1 (48/50) (96%), p53 (31/31, mostly 'mutation type'), CK7 (9/9) (100%) ER (13/16, variable) (81.2%) and PAX8 (14/14) (100%). IHC markers expressed in EMACs were ER (15/16) (93.7%), CK7 (2/2) (100%) and WT1 (0/7). IHC markers expressed in mixed carcinomas were CK7 (2/2) (100%), WT1 (0/2), focal Napsin A (6/6) and focal ER (5/6). The sensitivity and specificity of Napsin A for the diagnosis of CCC ovary was 100% and 90.9%, respectively. The sensitivity and specificity of WT1 for diagnosis of HGSC ovary was found to be 96% and 100%, respectively. Napsin A and WT1 are highly sensitive and specific IHC markers for diagnosing ovarian CCCs and HGSCs, respectively, and in differentiating these tumours from their mimics. Napsin A is useful in identification of component of CCC in certain EMACs.
[Mh] Termos MeSH primário: Adenocarcinoma de Células Claras/diagnóstico
Ácido Aspártico Endopeptidases/análise
Cistadenocarcinoma Seroso/diagnóstico
Neoplasias Epiteliais e Glandulares/diagnóstico
Neoplasias Ovarianas/diagnóstico
Proteínas WT1/análise
[Mh] Termos MeSH secundário: Adenocarcinoma de Células Claras/patologia
Adulto
Idoso
Biomarcadores Tumorais
Cistadenocarcinoma Seroso/patologia
Diagnóstico Diferencial
Seres Humanos
Imuno-Histoquímica
Meia-Idade
Neoplasias Epiteliais e Glandulares/patologia
Neoplasias Ovarianas/patologia
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (WT1 Proteins); 0 (WT1 protein, human); EC 3.4.23.- (Aspartic Acid Endopeptidases); EC 3.4.23.- (NAPSA protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12784


  6 / 3065 MEDLINE  
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[PMID]:29277787
[Au] Autor:Miyamoto M; Takano M; Aoyama T; Soyama H; Ishibashi H; Kato K; Iwahashi H; Takasaki K; Kuwahara M; Matuura H; Sakamoto T; Yoshikawa T; Furuya K
[Ad] Endereço:Department of Obstetrics and Gynecology, National Defense Medical College Hospital, Tokorozawa, Japan morikazu1118@hotmail.co.jp.
[Ti] Título:Phenoxodiol Increases Cisplatin Sensitivity in Ovarian Clear Cancer Cells Through XIAP Down-regulation and Autophagy Inhibition.
[So] Source:Anticancer Res;38(1):301-306, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: To investigate whether XIAP down-regulation and autophagy inhibition sensitize ovarian clear cell cancer cells to cisplatin. MATERIALS AND METHODS: The ovarian clear cancer cell line KK was used for in vitro analysis. Hydroxychloroquine (HCQ) and phenoxodiol (PXD) or embelin were used as autophagy and XIAP inhibitors, respectively. Non-specific and XIAP-specific siRNAs were transfected using Lipofectamine. Cytotoxicity was assessed by MTT assays. Protein expression was confirmed by western blotting. RESULTS: In KK, down-regulation of XIAP using specific siRNAs together with HCQ treatment enhanced the anti-tumor effect of cisplatin. Although embelin sensitized KK to cisplatin through XIAP down-regulation, it induced autophagy. However, PXD increased cisplatin sensitivity through XIAP down-regulation and autophagy inhibition. Expression of Atg7, Atg12, and Beclin 1 was decreased after PXD treatment. CONCLUSION: PXD increased cisplatin sensitivity through XIAP down-regulation and autophagy inhibition and could be a new candidate for ovarian clear cell carcinoma treatment.
[Mh] Termos MeSH primário: Adenocarcinoma de Células Claras/metabolismo
Antineoplásicos/farmacologia
Cisplatino/farmacologia
Isoflavonas/farmacologia
Neoplasias Ovarianas/metabolismo
Proteínas Inibidoras de Apoptose Ligadas ao Cromossomo X/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma de Células Claras/genética
Autofagia/efeitos dos fármacos
Benzoquinonas/farmacologia
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Regulação para Baixo
Feminino
Seres Humanos
Neoplasias Ovarianas/genética
RNA Interferente Pequeno/genética
Proteínas Inibidoras de Apoptose Ligadas ao Cromossomo X/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Benzoquinones); 0 (Isoflavones); 0 (RNA, Small Interfering); 0 (X-Linked Inhibitor of Apoptosis Protein); 0 (XIAP protein, human); 995FT1W541 (phenoxodiol); Q20Q21Q62J (Cisplatin); SHC6U8F5ER (embelin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:28921520
[Au] Autor:Jung S; Allen N; Arslan AA; Baglietto L; Barricarte A; Brinton LA; Egleston BL; Falk RT; Fortner RT; Helzlsouer KJ; Gao Y; Idahl A; Kaaks R; Krogh V; Merritt MA; Lundin E; Onland-Moret NC; Rinaldi S; Schock H; Shu XO; Sluss PM; Staats PN; Sacerdote C; Travis RC; Tjønneland A; Trichopoulou A; Tworoger SS; Visvanathan K; Weiderpass E; Zeleniuch-Jacquotte A; Dorgan JF
[Ad] Endereço:Department of Epidemiology and Public Health, University of Maryland School of Medicine, Baltimore, MD.
[Ti] Título:Anti-Müllerian hormone and risk of ovarian cancer in nine cohorts.
[So] Source:Int J Cancer;142(2):262-270, 2018 Jan 15.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Animal and experimental data suggest that anti-Müllerian hormone (AMH) serves as a marker of ovarian reserve and inhibits the growth of ovarian tumors. However, few epidemiologic studies have examined the association between AMH and ovarian cancer risk. We conducted a nested case-control study of 302 ovarian cancer cases and 336 matched controls from nine cohorts. Prediagnostic blood samples of premenopausal women were assayed for AMH using a picoAMH enzyme-linked immunosorbent assay. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariable-adjusted conditional logistic regression. AMH concentration was not associated with overall ovarian cancer risk. The multivariable-adjusted OR (95% CI), comparing the highest to the lowest quartile of AMH, was 0.99 (0.59-1.67) (P : 0.91). The association did not differ by age at blood draw or oral contraceptive use (all P : ≥0.26). There also was no evidence for heterogeneity of risk for tumors defined by histologic developmental pathway, stage, and grade, and by age at diagnosis and time between blood draw and diagnosis (all P : ≥0.39). In conclusion, this analysis of mostly late premenopausal women from nine cohorts does not support the hypothesized inverse association between prediagnostic circulating levels of AMH and risk of ovarian cancer.
[Mh] Termos MeSH primário: Adenocarcinoma de Células Claras/etiologia
Adenocarcinoma Mucinoso/etiologia
Biomarcadores/sangue
Cistadenocarcinoma Seroso/etiologia
Neoplasias do Endométrio/etiologia
Neoplasias Ovarianas/etiologia
[Mh] Termos MeSH secundário: Adenocarcinoma de Células Claras/sangue
Adenocarcinoma de Células Claras/epidemiologia
Adenocarcinoma Mucinoso/sangue
Adenocarcinoma Mucinoso/epidemiologia
Adulto
Hormônio Antimülleriano/sangue
Estudos de Casos e Controles
Estudos de Coortes
Cistadenocarcinoma Seroso/sangue
Cistadenocarcinoma Seroso/epidemiologia
Neoplasias do Endométrio/sangue
Neoplasias do Endométrio/epidemiologia
Feminino
Seguimentos
Seres Humanos
Meia-Idade
Gradação de Tumores
Estadiamento de Neoplasias
Neoplasias Ovarianas/sangue
Neoplasias Ovarianas/epidemiologia
Pré-Menopausa
Prognóstico
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 80497-65-0 (Anti-Mullerian Hormone)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.31058


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[PMID]:28929490
[Au] Autor:Gaitskell K; Green J; Pirie K; Barnes I; Hermon C; Reeves GK; Beral V; Million Women Study Collaborators
[Ad] Endereço:Cancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Richard Doll Building, Roosevelt Drive, Oxford, OX3 7LF, United Kingdom.
[Ti] Título:Histological subtypes of ovarian cancer associated with parity and breastfeeding in the prospective Million Women Study.
[So] Source:Int J Cancer;142(2):281-289, 2018 Jan 15.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ovarian cancer risk is known to be reduced amongst women who have had children, but reported associations with breastfeeding are varied. Few studies have had sufficient power to explore reliably these associations by tumour histotype. In a prospective study of 1.1 million UK women, 8719 developed ovarian cancer during follow-up. Cox regression yielded adjusted relative risks (RRs) overall and by tumour histotype amongst women with different childbearing patterns. Nulliparous women had a 24% greater ovarian cancer risk than women with one child, with significant heterogeneity by histotype (p = 0.01). There was no significant increase in serous tumours, a modest increase in mucinous tumours, but a substantial increase in endometrioid (RR = 1.49, 95% CI: 1.18-1.89) and clear-cell tumours (RR = 1.68, 1.29-2.20). Among parous women, each additional birth was associated with an overall 6% reduction in ovarian cancer risk; this association also varied by histotype (p = 0.0006), with the largest reduction in risk for clear-cell tumours (RR per birth = 0.75, 0.65-0.85, p < 0.001) and weak, if any, effect for endometrioid, high-grade serous, or mucinous tumours. We found little association with age at first or last birth. There was about a 10% risk reduction per 12-months breastfeeding (RR = 0.89, 0.84-0.94, p < 0.001), with no significant heterogeneity by histotype, but statistical power was limited. In this large prospective study, ovarian cancer risk associated with parity varied substantially by tumour histotype. Nulliparity was associated with a substantially greater overall risk than expected from the effect of a single birth, especially for clear cell and endometrioid tumours, perhaps suggesting that infertility is associated with these histotypes.
[Mh] Termos MeSH primário: Adenocarcinoma de Células Claras/patologia
Adenocarcinoma Mucinoso/patologia
Aleitamento Materno
Cistadenocarcinoma Seroso/patologia
Neoplasias do Endométrio/patologia
Neoplasias Ovarianas/patologia
Paridade
[Mh] Termos MeSH secundário: Adulto
Feminino
Seguimentos
Seres Humanos
Meia-Idade
Gravidez
Prognóstico
Estudos Prospectivos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171214
[Lr] Data última revisão:
171214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.31063


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[PMID]:27771168
[Au] Autor:Chan JK; Java JJ; Fuh K; Monk BJ; Kapp DS; Herzog T; Bell J; Young R
[Ad] Endereço:Division of Gynecologic Oncology, California Pacific-Palo Alto Medical Foundation Sutter Research Institute, 3838 California Street #410, San Francisco, CA 94115, United States. Electronic address: chanjohn@sutterhealth.org.
[Ti] Título:The association between timing of initiation of adjuvant therapy and the survival of early stage ovarian cancer patients - An analysis of NRG Oncology/Gynecologic Oncology Group trials.
[So] Source:Gynecol Oncol;143(3):490-495, 2016 Dec.
[Is] ISSN:1095-6859
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To determine the association between timing of adjuvant therapy initiation and survival of early stage ovarian cancer patients. METHODS: Data were obtained from women who underwent primary surgical staging followed by adjuvant therapy from two Gynecologic Oncology Group trials (protocols # 95 and 157). Kaplan-Meier estimates and Cox proportional hazards model adjusted for covariates were used for analyses. RESULTS: Of 497 stage I-II epithelial ovarian cancer patients, the median time between surgery and initiation of adjuvant therapy was 23days (25th-75th%: 12-33days). The time interval from surgery to initiation of adjuvant therapy was categorized into three groups: <2weeks, 2-4weeks, and >4weeks. The corresponding 5-year recurrence-free survival rates were 72.8%, 73.9%, and 79.5% (p=0.62). The 5-year overall survival rates were 79.4%, 81.9%, and 82.8%, respectively (p=0.51; p=0.33 - global test). As compared to <2weeks, the hazard ratio for recurrence-free survival was 0.90 (95%CI=0.59-1.37) for 2-4weeks and 0.72 (95%CI=0.46-1.13) for >4weeks. Age, stage, grade, and cytology were important prognostic factors. CONCLUSIONS: Timing of adjuvant therapy initiation was not associated with survival in early stage epithelial ovarian cancer patients.
[Mh] Termos MeSH primário: Adenocarcinoma de Células Claras/tratamento farmacológico
Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Carcinoma Endometrioide/tratamento farmacológico
Quimioterapia Adjuvante/métodos
Procedimentos Cirúrgicos de Citorredução/métodos
Neoplasias Císticas, Mucinosas e Serosas/tratamento farmacológico
Neoplasias Epiteliais e Glandulares/tratamento farmacológico
Neoplasias Ovarianas/tratamento farmacológico
[Mh] Termos MeSH secundário: Adenocarcinoma de Células Claras/patologia
Carboplatina/administração & dosagem
Carcinoma Endometrioide/patologia
Cisplatino/administração & dosagem
Ciclofosfamida/administração & dosagem
Feminino
Seres Humanos
Infusões Intravenosas
Infusões Parenterais
Estimativa de Kaplan-Meier
Meia-Idade
Análise Multivariada
Estadiamento de Neoplasias
Neoplasias Císticas, Mucinosas e Serosas/patologia
Neoplasias Epiteliais e Glandulares/patologia
Neoplasias Ovarianas/patologia
Paclitaxel/administração & dosagem
Prognóstico
Modelos de Riscos Proporcionais
Taxa de Sobrevida
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
8N3DW7272P (Cyclophosphamide); BG3F62OND5 (Carboplatin); P88XT4IS4D (Paclitaxel); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171214
[Lr] Data última revisão:
171214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:29061793
[Au] Autor:Nakatani M; Watari H; Mitamura T; Wang L; Hatanaka Y; Hatanaka KC; Honda K; Nomura T; Nishihara H; Tanaka S; Sakuragi N
[Ad] Endereço:Department of Obstetrics and Gynecology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
[Ti] Título:The Anti-tumor Effect of Cabozantinib on Ovarian Clear Cell Carcinoma and .
[So] Source:Anticancer Res;37(11):6125-6132, 2017 11.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Several reports have shown that the overexpression of the MET proto-oncogene, receptor tyrosine kinase (MET), was more frequently observed in clear cell carcinoma (CCC) than in non-CCC. We evaluated the antitumor activity of cabozantinib, that targets MET. MATERIALS AND METHODS: A gene expression analysis of tumors from human ovarian cancers was carried out by transcriptome sequencing. An in vitro 3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide assay (MTT assay) and in vivo experiments were performed to determine the activity of cabozantinib. RESULTS: The MET levels were higher in tumors with CCC than high-grade serous carcinoma (2.2-fold). Cabozantinib inhibited cell viability and phosphorylation of AKT and MAPK under the treatment of hepatocyte growth factor in RMG-I CCC cells. The tumors removed from mice given cabozantinib of 10 mg/kg weighed 70% less than control on day 15, and the immunohistochemical reactivity of phosphorylated MET was reduced compared with control mice. CONCLUSION: Cabozantinib contributes to tumor reduction, and phosphorylated MET represents an attractive target of CCC.
[Mh] Termos MeSH primário: Adenocarcinoma de Células Claras/patologia
Anilidas/farmacologia
Apoptose/efeitos dos fármacos
Neoplasias Ovarianas/patologia
Piridinas/farmacologia
[Mh] Termos MeSH secundário: Adenocarcinoma de Células Claras/tratamento farmacológico
Adenocarcinoma de Células Claras/metabolismo
Animais
Proliferação Celular/efeitos dos fármacos
Feminino
Seres Humanos
Técnicas In Vitro
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Neoplasias Ovarianas/tratamento farmacológico
Neoplasias Ovarianas/metabolismo
Fosforilação/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-met/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Células Tumorais Cultivadas
Receptor 2 de Fatores de Crescimento do Endotélio Vascular/antagonistas & inibidores
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anilides); 0 (Protein Kinase Inhibitors); 0 (Pyridines); 1C39JW444G (cabozantinib); EC 2.7.10.1 (Proto-Oncogene Proteins c-met); EC 2.7.10.1 (Vascular Endothelial Growth Factor Receptor-2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE



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