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Pesquisa : E05.041.124.892 [Categoria DeCS]
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[PMID]:29392424
[Au] Autor:Shahkarami S; Mehrasa R; Younesian S; Yaghmaie M; Chahardouli B; Vaezi M; Rezaei N; Nikbakht M; Alimoghaddam K; Ghavamzadeh A; Tavakkoly-Bazzaz J; Ghaffari SH
[Ad] Endereço:Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
[Ti] Título:Minimal residual disease (MRD) detection using rearrangement of immunoglobulin/T cell receptor genes in adult patients with acute lymphoblastic leukemia (ALL).
[So] Source:Ann Hematol;97(4):585-595, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:MRD detection with allele-specific oligonucleotide-quantitative polymerase chain reaction (ASO-qPCR) and using clone-specific immunoglobulin/T cell receptor rearrangements is considered as a powerful prognostic factor in acute lymphoblastic leukemia (ALL). In the present study, we evaluated an ASO-qPCR assay for MRD quantification in peripheral blood (PB) samples of adult patients with ALL. DNA was isolated from PB samples of patients with newly diagnosed ALL. They were first investigated by multiplex-PCR assay to identify V/J usage. An ASO-qPCR technique was then applied for 2.5-year monthly MRD quantification for detection of patient-specific Ig/TCR receptor rearrangements as a molecular target. From 98 patients who were diagnosed as ALL, 72 (73.5%) were enrolled in the present study for MRD detection. MRD was successfully quantified in patients with 1-month interval time. MRD level at the end of induction therapy up to day 88 was the only significant prognostic factor. Regarding MRD level, patients were categorized into two groups of low and high-risk. 2.5-year OS in all three time points (days 28, 58 and 88) were significantly lower in high-risk group (P < 0.008). The results of the 2.5-year MRD detection indicate that MRD level at the end of induction up to about 6 months after the first diagnosis was associated with clinical outcome. This study may highlight the usefulness of PB and the definitions of cut-off level for early prediction of relapse and for stratifying ALL patients. Short-interval time points and frequent PB sampling to monitor MRD level is suggested for early clinical relapse prediction and clinical management of the disease.
[Mh] Termos MeSH primário: Rearranjo Gênico do Linfócito T/efeitos dos fármacos
Quimioterapia de Indução
Leucemia-Linfoma Linfoblástico de Células Precursoras/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Alelos
Feminino
Seguimentos
Hospitais Universitários
Seres Humanos
Irã (Geográfico)
Masculino
Reação em Cadeia da Polimerase Multiplex
Proteínas de Neoplasias/química
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/metabolismo
Neoplasia Residual/diagnóstico
Neoplasia Residual/genética
Neoplasia Residual/metabolismo
Neoplasia Residual/patologia
Oligonucleotídeos/química
Oligonucleotídeos/metabolismo
Leucemia-Linfoma Linfoblástico de Células Precursoras/tratamento farmacológico
Leucemia-Linfoma Linfoblástico de Células Precursoras/genética
Leucemia-Linfoma Linfoblástico de Células Precursoras/patologia
Prognóstico
Estudos Prospectivos
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Medição de Risco
Análise de Sobrevida
Carga Tumoral/efeitos dos fármacos
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neoplasm Proteins); 0 (Oligonucleotides)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-018-3230-z


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[PMID]:29305630
[Au] Autor:Ben Lakhal R; Ghedira H; Bellaaj H; Ben Youssef Y; Menif S; Manai Z; Bedoui M; Lakhal A; M'Sadek F; Elloumi M; Khélif A; Ben Romdhane N; Laatiri MA; Ben Othmen T; Meddeb B
[Ad] Endereço:Hematology Department, Aziza Othmana University Hospital, Tunis, Tunisia. raihane.benlakhal@gmail.com.
[Ti] Título:Chronic myeloid leukemia patients in Tunisia: epidemiology and outcome in the imatinib era (a multicentric experience).
[So] Source:Ann Hematol;97(4):597-604, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Data are limited in developing countries regarding the clinicopathologic features and response to therapy of chronic myeloid leukemia (CML) in the era of imatinib (IM). The objective of this study is to report on the clinicoepidemiologic features of CML in Tunisia, to evaluate the long-term outcome of patients in chronic (CP) or accelerated phase (AP) treated with IM 400 mg daily as frontline therapy, and to determine imatinib's efficacy and safety. From October 2002 to December 2014, 410 CML patients were treated with IM in six Tunisian departments of hematology. Response (hematologic, cytogenetic, and molecular responses) and outcome-overall survival (OS), event-free survival (EFS), and progression-free survival (PFS)-were evaluated. The following prognostic factors were analyzed for their impact on the European leukemia net (ELN) response, OS, EFS, and PFS at 5 years: age, sex, leukocyte count, Sokal score, European Treatment and Outcome Study (EUTOS) score, CML phase, time to starting IM, and impact of adverse events. The median age was 45 years (3-85 years). Two hundred ten (51.2%) patients were male. Splenomegaly was present in 322 of the 410 (79%). Additional cytogenetic abnormalities were encountered in 25 (6.3%) patients. At diagnosis, 379 (92.4%) patients were in CP, 31 (7.6%) were in AP. The Sokal risk was low in 87 (22.5%), intermediate in 138 (35.7%), and high in 164 patients (41.9%). The EUTOS risk was low in 217 (74%), and high in 77 (26%) patients. The rates of cumulative complete cytogenetic response (CCyR), major molecular response (MMR), and molecular response 4/5 log (MR4.5) in CP/AP-CML patients were 72, 68.4, and 46.4%, respectively. The median time to reach CCyR, MMR, and MR4.5 was 6 months (3-51), 18 months (3-72), and 24 months (3-100), respectively. According to the ELN criteria, optimal, suboptimal response, and failure were noted in 206 (51.8%), 61 (15.3%), and 125 (31.4%) patients, respectively. Five-year event-free survival (EFS), progression-free survival (PFS), and overall survival (OS) were 81, 90, and 90%, respectively. By multivariate analysis, AP, high EUTOS risk, and baseline WBC ≥ 150G/l remained independent predictive factors of non-optimal response to IM. The adverse events (AE) of IM were moderate and tolerable. With the caveats that the monitoring of the disease was not optimal, response rates were similar to those reported in previous studies. It is clear to us that improvements should be made in treatment of AP-CML and high Sokal risk group of CP-CML. The frontline use of second-generation tyrosine kinase inhibitor (TKI) is expected to improve the results of the first-line treatment of these high-risk Tunisian patients, but cost and accessibility of this therapy remain the problems in developing countries.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Mesilato de Imatinib/uso terapêutico
Leucemia Mieloide de Fase Acelerada/tratamento farmacológico
Leucemia Mieloide de Fase Crônica/tratamento farmacológico
Inibidores de Proteínas Quinases/uso terapêutico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Antineoplásicos/efeitos adversos
Criança
Pré-Escolar
Feminino
Seguimentos
Seres Humanos
Mesilato de Imatinib/efeitos adversos
Leucemia Mieloide de Fase Acelerada/diagnóstico
Leucemia Mieloide de Fase Acelerada/epidemiologia
Leucemia Mieloide de Fase Acelerada/patologia
Leucemia Mieloide de Fase Crônica/diagnóstico
Leucemia Mieloide de Fase Crônica/epidemiologia
Leucemia Mieloide de Fase Crônica/patologia
Masculino
Meia-Idade
Padrões de Prática Médica
Prognóstico
Inibidores de Proteínas Quinases/efeitos adversos
Estudos Retrospectivos
Esplenomegalia/etiologia
Esplenomegalia/patologia
Esplenomegalia/prevenção & controle
Análise de Sobrevida
Carga Tumoral/efeitos dos fármacos
Tunísia/epidemiologia
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Protein Kinase Inhibitors); 8A1O1M485B (Imatinib Mesylate)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3224-2


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[PMID]:28468915
[Au] Autor:Mei Y; Zhao L; Liu Y; Gong H; Song Y; Lei L; Zhu Y; Jin Z; Ma S; Hu B; Sun Q; Liu H
[Ad] Endereço:Institute of Blood and Marrow Transplantation, Department of Hematology, Collaborative Innovation Center of Hematology, the First Affiliated Hospital of Soochow University, Suzhou, P.R. China.
[Ti] Título:Combining DNA Vaccine and AIDA-1 in Attenuated Activates Tumor-Specific CD4 and CD8 T-cell Responses.
[So] Source:Cancer Immunol Res;5(6):503-514, 2017 Jun.
[Is] ISSN:2326-6074
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Stimulation of tumor-specific responses in both CD4 and CD8 T cells has been a challenge for effective tumor vaccines. We designed a vaccine vector containing the AIDA-1 autotransporter and DNA vaccine elements, generating a murine melanoma vaccine that was delivered by the attenuated strain SL7207. Growth of murine subcutaneous melanoma was significantly inhibited by intranasal immunization with the tumor vaccine. The vaccine activated tumor-specific CD4 and CD8 T-cell responses, with increased T-cell proliferation, tumor antigen-specific Th1 cytokine production, increased percentages of tetramer positive cells, and cytotoxicity. CD4 or CD8 T-cell depletion resulted in the loss of antitumor activity of the tumor vaccine, suggesting that the efficacy of the vaccine was dependent on both CD4 and CD8 T cells. Lung metastasis of the tumor was also inhibited by vaccine treatment. Similarly, the percentages of tumor-specific Th1 cytokine production by CD4 and CD8 T cells in the spleen, tumor, and bronchoalveolar lavage were increased after vaccine treatment. Tumor-specific proliferation of CD4 and CD8 T cells was also promoted by the vaccine. Tetramer staining and cytotoxicity assay showed enhanced tumor-specific CD8 T-cell response after vaccine treatment. Therefore, the tumor vaccine could activate both tumor-specific CD4 and CD8 T-cell responses. This vaccine strategy may be widely applicable to the development of oral or nasal vaccines against tumors. .
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Vacinas Anticâncer/administração & dosagem
Neoplasias/imunologia
Salmonella
Vacinas de DNA/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Proteínas de Transporte
Linhagem Celular Tumoral
Feminino
Camundongos Endogâmicos C57BL
Neoplasias/patologia
Neoplasias/terapia
Salmonella/genética
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANKS1B protein, human); 0 (Cancer Vaccines); 0 (Carrier Proteins); 0 (Vaccines, DNA)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1158/2326-6066.CIR-16-0240-T


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[PMID]:29028222
[Au] Autor:Choi HJ; Joo HS; Won HY; Min KW; Kim HY; Son T; Oh YH; Lee JY; Kong G
[Ad] Endereço:Department of Pathology, College of Medicine, Hanyang University, Seoul, Republic of Korea; Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul, Republic of Korea; Institute for Bioengineering and Biopharmaceutical Research (IBBR), Hanyang University,
[Ti] Título:Role of RBP2-Induced ER and IGF1R-ErbB Signaling in Tamoxifen Resistance in Breast Cancer.
[So] Source:J Natl Cancer Inst;110(4), 2018 Apr 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Despite the benefit of endocrine therapy, acquired resistance during or after treatment still remains a major challenge in estrogen receptor (ER)-positive breast cancer. We investigated the potential role of histone demethylase retinoblastoma-binding protein 2 (RBP2) in endocrine therapy resistance of breast cancer. Methods: Survival of breast cancer patients according to RBP2 expression was analyzed in three different breast cancer cohorts including METABRIC (n = 1980) and KM plotter (n = 1764). RBP2-mediated tamoxifen resistance was confirmed by invitro sulforhodamine B (SRB) colorimetric, colony-forming assays, and invivo xenograft models (n = 8 per group). RNA-seq analysis and receptor tyrosine kinase assay were performed to identify the tamoxifen resistance mechanism by RBP2. All statistical tests were two-sided. Results: RBP2 was associated with poor prognosis to tamoxifen therapy in ER-positive breast cancer (P = .04 in HYU cohort, P = .02 in KM plotter, P = .007 in METABRIC, log-rank test). Furthermore, RBP2 expression was elevated in patients with tamoxifen-resistant breast cancer (P = .04, chi-square test). Knockdown of RBP2 conferred tamoxifen sensitivity, whereas overexpression of RBP2 induced tamoxifen resistance invitro and invivo (MCF7 xenograft: tamoxifen-treated control, mean [SD] tumor volume = 70.8 [27.9] mm3, vs tamoxifen-treated RBP2, mean [SD] tumor volume = 387.9 [85.1] mm3, P < .001). Mechanistically, RBP2 cooperated with ER co-activators and corepressors and regulated several tamoxifen resistance-associated genes, including NRIP1, CCND1, and IGFBP4 and IGFBP5. Furthermore, epigenetic silencing of IGFBP4/5 by RBP2-ER-NRIP1-HDAC1 complex led to insulin-like growth factor-1 receptor (IGF1R) activation. RBP2 also increased IGF1R-ErbB crosstalk and subsequent PI3K-AKT activation via demethylase activity-independent ErbB protein stabilization. Combinational treatment with tamoxifen and PI3K inhibitor could overcome RBP2-mediated tamoxifen resistance (RBP2-overexpressing cells: % cell viability [SD], tamoxifen = 89.0 [3.8]%, vs tamoxifen with BKM120 = 41.3 [5.6]%, P < .001). Conclusions: RBP2 activates ER-IGF1R-ErbB signaling cascade in multiple ways to induce tamoxifen resistance, suggesting that RBP2 is a potential therapeutic target for ER-driven cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Carcinoma Ductal de Mama/metabolismo
Resistência a Medicamentos Antineoplásicos
Proteínas de Neoplasias/fisiologia
Receptores Estrogênicos/metabolismo
Proteína 2 de Ligação ao Retinoblastoma/fisiologia
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Análise de Variância
Animais
Antineoplásicos Hormonais/uso terapêutico
Neoplasias da Mama/química
Neoplasias da Mama/tratamento farmacológico
Neoplasias da Mama/patologia
Carcinoma Ductal de Mama/química
Carcinoma Ductal de Mama/tratamento farmacológico
Carcinoma Ductal de Mama/patologia
Proteínas de Transporte/metabolismo
Estudos de Coortes
Colorimetria
Intervalo Livre de Doença
Resistência a Medicamentos Antineoplásicos/genética
Feminino
Xenoenxertos
Seres Humanos
Estimativa de Kaplan-Meier
Células MCF-7
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Proteínas de Neoplasias/metabolismo
Células-Tronco Neoplásicas
Proteínas Nucleares/metabolismo
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Fosfatidilinositol 3-Quinases/metabolismo
Receptor ErbB-2/metabolismo
Receptor IGF Tipo 1/metabolismo
Proteína 2 de Ligação ao Retinoblastoma/metabolismo
Tamoxifeno/uso terapêutico
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Antineoplastic Agents, Hormonal); 0 (Carrier Proteins); 0 (IGFBP5-interacting protein, human); 0 (Neoplasm Proteins); 0 (Nuclear Proteins); 0 (Receptors, Estrogen); 0 (nuclear receptor interacting protein 1); 094ZI81Y45 (Tamoxifen); EC 1.14.11.27 (Retinoblastoma-Binding Protein 2); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.1 (Receptor, ErbB-2); EC 2.7.10.1 (Receptor, IGF Type 1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx207


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[PMID]:28859290
[Au] Autor:Troester MA; Sun X; Allott EH; Geradts J; Cohen SM; Tse CK; Kirk EL; Thorne LB; Mathews M; Li Y; Hu Z; Robinson WR; Hoadley KA; Olopade OI; Reeder-Hayes KE; Earp HS; Olshan AF; Carey LA; Perou CM
[Ad] Endereço:Department of Epidemiology, Lineberger Comprehensive Cancer Center; Department of Pathology and Lab Medicine, Department of Nutrition (EHA), and Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC; Dana Farber Cancer Institute, Harvard University, Boston, MA; Center
[Ti] Título:Racial Differences in PAM50 Subtypes in the Carolina Breast Cancer Study.
[So] Source:J Natl Cancer Inst;110(2), 2018 Feb 01.
[Is] ISSN:1460-2105
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: African American breast cancer patients have lower frequency of hormone receptor-positive (HR+)/human epidermal growth factor receptor 2 (HER2)-negative disease and higher subtype-specific mortality. Racial differences in molecular subtype within clinically defined subgroups are not well understood. Methods: Using data and biospecimens from the population-based Carolina Breast Cancer Study (CBCS) Phase 3 (2008-2013), we classified 980 invasive breast cancers using RNA expression-based PAM50 subtype and recurrence (ROR) score that reflects proliferation and tumor size. Molecular subtypes (Luminal A, Luminal B, HER2-enriched, and Basal-like) and ROR scores (high vs low/medium) were compared by race (blacks vs whites) and age (≤50 years vs > 50 years) using chi-square tests and analysis of variance tests. Results: Black women of all ages had a statistically significantly lower frequency of Luminal A breast cancer (25.4% and 33.6% in blacks vs 42.8% and 52.1% in whites; younger and older, respectively). All other subtype frequencies were higher in black women (case-only odds ratio [OR] = 3.11, 95% confidence interval [CI] = 2.22 to 4.37, for Basal-like; OR = 1.45, 95% CI = 1.02 to 2.06, for Luminal B; OR = 2.04, 95% CI = 1.33 to 3.13, for HER2-enriched). Among clinically HR+/HER2- cases, Luminal A subtype was less common and ROR scores were statistically significantly higher among black women. Conclusions: Multigene assays highlight racial disparities in tumor subtype distribution that persist even in clinically defined subgroups. Differences in tumor biology (eg, HER2-enriched status) may be targetable to reduce disparities among clinically ER+/HER2- cases.
[Mh] Termos MeSH primário: Afroamericanos
Neoplasias da Mama/química
Neoplasias da Mama/etnologia
Grupo com Ancestrais do Continente Europeu
RNA Neoplásico/análise
Receptor ErbB-2/análise
Receptores Estrogênicos/análise
Receptores de Progesterona/análise
[Mh] Termos MeSH secundário: Adulto
Idoso
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Proliferação Celular
Feminino
Seres Humanos
Meia-Idade
Recidiva
Carga Tumoral
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Neoplasm); 0 (Receptors, Estrogen); 0 (Receptors, Progesterone); EC 2.7.10.1 (ERBB2 protein, human); EC 2.7.10.1 (Receptor, ErbB-2)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE
[do] DOI:10.1093/jnci/djx135


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[PMID]:29202956
[Au] Autor:Bray MJ; Edwards TL; Wellons MF; Jones SH; Hartmann KE; Velez Edwards DR
[Ad] Endereço:Vanderbilt Genetics Institute, Vanderbilt University, Nashville, Tennessee.
[Ti] Título:Admixture mapping of uterine fibroid size and number in African American women.
[So] Source:Fertil Steril;108(6):1034-1042.e26, 2017 Dec.
[Is] ISSN:1556-5653
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To evaluate the relationship between genetic ancestry and uterine fibroid characteristics. DESIGN: Cross-sectional study. SETTING: Not applicable. PATIENT(S): A total of 609 African American participants with image- or surgery-confirmed fibroids in a biorepository at Vanderbilt University electronic health record biorepository and the Coronary Artery Risk Development in Young Adults studies were included. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Outcome measures include fibroid number (single vs. multiple), volume of largest fibroid, and largest fibroid dimension of all fibroid measurements. RESULT(S): Global ancestry meta-analyses revealed a significant inverse association between percentage of European ancestry and risk of multiple fibroids (odds ratio: 0.78; 95% confidence interval 0.66, 0.93; P=6.05 × 10 ). Local ancestry meta-analyses revealed five suggestive (P<4.80 × 10 ) admixture mapping peaks in 2q14.3-2q21.1, 3p14.2-3p14.1, 7q32.2-7q33, 10q21.1, 14q24.2-14q24.3, for number of fibroids and one suggestive admixture mapping peak (P<1.97 × 10 ) in 10q24.1-10q24.32 for volume of largest fibroid. Single variant association meta-analyses of the strongest associated region from admixture mapping of fibroid number (10q21.1) revealed a strong association at single nucleotide polymorphism variant rs12219990 (odds ratio: 0.41; 95% confidence interval 0.28, 0.60; P=3.82 × 10 ) that was significant after correction for multiple testing. CONCLUSION(S): Increasing African ancestry is associated with multiple fibroids but not with fibroid size. Local ancestry analyses identified several novel genomic regions not previously associated with fibroid number and increasing volume. Future studies are needed to explore the genetic impact that ancestry plays into the development of fibroid characteristics.
[Mh] Termos MeSH primário: Afroamericanos/genética
Biomarcadores Tumorais/genética
Leiomioma/genética
Leiomioma/patologia
Leiomiomatose/genética
Leiomiomatose/patologia
Carga Tumoral/genética
Neoplasias Uterinas/genética
Neoplasias Uterinas/patologia
[Mh] Termos MeSH secundário: Adulto
Bancos de Espécimes Biológicos
Estudos Transversais
Bases de Dados Factuais
Registros Eletrônicos de Saúde
Feminino
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Hereditariedade
Seres Humanos
Leiomioma/etnologia
Leiomiomatose/etnologia
Modelos Lineares
Modelos Logísticos
Meia-Idade
Razão de Chances
Fenótipo
Polimorfismo de Nucleotídeo Único
Fatores de Risco
Estados Unidos/epidemiologia
Neoplasias Uterinas/etnologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Biomarkers, Tumor)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE


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[PMID]:29480860
[Au] Autor:Zhu H; Zhao Y; Wang X
[Ad] Endereço:Department of Medical Oncology, West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.
[Ti] Título:The radiosensitive effect of apatinib for hepatocellular carcinoma patient with big paraspinal metastasis: A case report.
[So] Source:Medicine (Baltimore);97(2):e9598, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Hepatocellular carcinoma (HCC) is a highly invasive cancer associated with great mortality rates. The prognosis of advanced HCC is very poor. PATIENT CONCERNS: Here, we report a HCC patient with a big paraspinal metastasis with 10 cm in diameter who failed the treatment of sorafenib. DIAGNOSES: Sorafenib refractory HCC with big paraspinal metastasis. INTERVENTIONS: The concurrent treatment of apatinib with stereotactic body radiotherapy (SBRT). OUTCOMES: The paraspinal metastasis with 10 cm in diameter showed nearly complete response. LESSONS: We think that the apatinib may be a good choice for HCC and it may function as a radiosensitizer of HCC. However, it warrants further investigation in the future prospective clinical studies.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/terapia
Neoplasias Hepáticas/terapia
Piridinas/uso terapêutico
Radiossensibilizantes/uso terapêutico
Neoplasias da Coluna Vertebral/secundário
Neoplasias da Coluna Vertebral/terapia
[Mh] Termos MeSH secundário: Adulto
Antineoplásicos/uso terapêutico
Carcinoma Hepatocelular/diagnóstico por imagem
Carcinoma Hepatocelular/patologia
Evolução Fatal
Seres Humanos
Neoplasias Hepáticas/diagnóstico por imagem
Neoplasias Hepáticas/patologia
Masculino
Neoplasias da Coluna Vertebral/diagnóstico por imagem
Carga Tumoral
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Pyridines); 0 (Radiation-Sensitizing Agents); 5S371K6132 (apatinib)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180227
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009598


  8 / 15793 MEDLINE  
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[PMID]:28460476
[Au] Autor:Liu MJ; Liu ZF; Hou YY; Men YM; Zhang YX; Gao LY; Liu H
[Ad] Endereço:Department of Ultrasound, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong, China.
[Ti] Título:Ultrasonographic characteristics of medullary thyroid carcinoma: a comparison with papillary thyroid carcinoma.
[So] Source:Oncotarget;8(16):27520-27528, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study was designed to explore differences in the ultrasonographic characteristics of medullary thyroid carcinoma (MTC) and papillary thyroid carcinoma (PTC). This study included 35 cases of MTC and 96 cases of PTC that were surgically and pathologically confirmed. Preoperative ultrasound images were retrospectively reviewed by two physicians (with 5 years' experience in thyroid ultrasound) under the premise of unknown pathological results. Various ultrasonic features of nodules were assessed objectively. The clinical features of components were determined by other physicians. Age, sex, unilateral or bilateral involvement of thyroid gland, lesion size, margin, shape, echogenicity, calcification, intranodular blood flow, cervical lymph node, and tumor node metastasis (TNM) stage were compared between MTC and PTC groups. Age, sex, involvement of the thyroid gland, margin, and calcification were similar for the MTC and PTC groups. Compared with the PTC group, the lesion size in the MTC group was significantly larger (P < 0.001). A taller-than-wide shape (aspect ratio > 1) was significantly less likely in the MTC group than the PTC group (P < 0.001). A mixed echogenicity was significantly more common in the MTC group than the PTC group (P = 0.003). The MTC group had significantly enhanced intranodular blood flow (P < 0.001). The TNM stage of the MTC group was significantly higher than that of PTC group (P = 0.001). Medullary thyroid carcinomas differ significantly from PTCs in lesion size, shape, echogenicity, and intranodular blood flow.
[Mh] Termos MeSH primário: Carcinoma Neuroendócrino/diagnóstico por imagem
Carcinoma Neuroendócrino/patologia
Carcinoma Papilar/diagnóstico por imagem
Carcinoma Papilar/patologia
Neoplasias da Glândula Tireoide/diagnóstico por imagem
Neoplasias da Glândula Tireoide/patologia
Ultrassonografia
[Mh] Termos MeSH secundário: Adulto
Biomarcadores
Carcinoma Neuroendócrino/sangue
Carcinoma Neuroendócrino/cirurgia
Carcinoma Papilar/sangue
Carcinoma Papilar/cirurgia
Feminino
Seres Humanos
Processamento de Imagem Assistida por Computador
Masculino
Meia-Idade
Estadiamento de Neoplasias
Período Pré-Operatório
Neoplasias da Glândula Tireoide/sangue
Neoplasias da Glândula Tireoide/cirurgia
Carga Tumoral
Ultrassonografia/métodos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers)
[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.15897


  9 / 15793 MEDLINE  
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[PMID]:28460473
[Au] Autor:Dooley J; Lagou V; Garcia-Perez JE; Himmelreich U; Liston A
[Ad] Endereço:VIB Center for Brain and Disease Research, Leuven, Belgium.
[Ti] Título:miR-29a-deficiency does not modify the course of murine pancreatic acinar carcinoma.
[So] Source:Oncotarget;8(16):26911-26917, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The development of cancers involves the complex dysregulation of multiple cellular processes. With key functions in simultaneous regulation of multiple pathways, microRNA (miR) are thought to have important roles in the oncogenic formation process. miR-29a is among the most abundantly expressed miR in the pancreas. Together with altered expression in pancreatic cancer cell lines and biopsies, and known oncogenic functions in leukemia, this expression data has identified miR-29a as a key candidate for miR involvement in pancreatic cancer biology. Here we used miR-29a-deficient mice and the TAg model of pancreatic acinar carcinoma to functionally test the role of miR-29a in vivo. We found no impact of miR-29a loss on the development or growth of pancreatic tumours, nor on the survival of tumour-bearing mice. These results suggest that, despite differential expression, miR-29a is oncogenically neutral in the pancreatic acinar carcinoma context. If these results are extended to other models of pancreatic cancer, they would reduce the attractiveness of miR-29a as a potential therapeutic target in pancreatic cancer.
[Mh] Termos MeSH primário: Deleção de Genes
MicroRNAs/genética
Neoplasias Pancreáticas/genética
Neoplasias Pancreáticas/patologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Transformação Celular Neoplásica
Regulação Neoplásica da Expressão Gênica
Genótipo
Imagem por Ressonância Magnética/métodos
Camundongos
Camundongos Knockout
Neoplasias Pancreáticas/diagnóstico por imagem
Neoplasias Pancreáticas/mortalidade
Prognóstico
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN29 microRNA, mouse); 0 (MicroRNAs)
[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.15850


  10 / 15793 MEDLINE  
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[PMID]:28460470
[Au] Autor:Cheng T; Song Y; Zhang Y; Zhang C; Yin J; Chi Y; Zhou D
[Ad] Endereço:Vaccine Research Center, Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Science, Shanghai 200031, China.
[Ti] Título:A novel oncolytic adenovirus based on simian adenovirus serotype 24.
[So] Source:Oncotarget;8(16):26871-26885, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Among the oncolytic virotherapy, an emerging treatment for tumor, adenoviruses are widely used at present in preclinical and clinical trials. Traditionally, oncolytic adenoviruses were developed based on the human adenovirus serotype 5 (AdHu5). However, AdHu5 has the drawbacks of preexisting anti-AdHu5 immunity in most populations, and extensive sequestration of Adhu5 by the liver through hexon, blood coagulation factor X (FX), and FX receptor interactions. To tackle these problems, we explored a novel oncolytic adenovirus AdC7-SP/E1A-ΔE3 for cancer treatment. AdC7-SP/E1A-ΔE3 was constructed by replacing the E1A promoter with tumor specific promoter survivin promoter and deleting E3 region using direct cloning methods based on simian adenovirus serotype 24 (namely AdC7). We showed that AdC7-SP/E1A-ΔE3 significantly killed tumor cell lines NCI-H508 and Huh7, and inhibited tumor growth in both NCI-H508 and Huh7 xenograft tumor models. Importantly, AdC7-SP/E1A-ΔE3 exhibited the antitumor efficacy via systemic administration. Mechanistically, infected cells were killed by AdC7-SP/E1A-ΔE3 via the p53-independent mitochondrial apoptosis pathway in which phosphorylation of BAD markedly declined and the expresses of Bik significantly went up. Therefore, AdC7-SP/E1A-ΔE3 is a promising candidate for liver and colon tumor treatment.
[Mh] Termos MeSH primário: Adenovirus dos Símios/classificação
Adenovirus dos Símios/genética
Vetores Genéticos/genética
Vírus Oncolíticos/genética
[Mh] Termos MeSH secundário: Proteínas E1A de Adenovirus/genética
Animais
Apoptose/genética
Linhagem Celular Tumoral
Efeito Citopatogênico Viral
Modelos Animais de Doenças
Deleção de Genes
Expressão Gênica
Engenharia Genética
Terapia Genética
Vetores Genéticos/administração & dosagem
Vetores Genéticos/efeitos adversos
Seres Humanos
Proteínas Inibidoras de Apoptose/genética
Camundongos
Mitocôndrias/genética
Terapia Viral Oncolítica
Especificidade de Órgãos/genética
Regiões Promotoras Genéticas
Sorogrupo
Transdução de Sinais
Carga Tumoral
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
Replicação Viral
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adenovirus E1A Proteins); 0 (BIRC5 protein, human); 0 (Inhibitor of Apoptosis Proteins); 0 (Tumor Suppressor Protein p53)
[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.15845



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