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[PMID]:29330228
[Au] Autor:McCormack A; Dekkers OM; Petersenn S; Popovic V; Trouillas J; Raverot G; Burman P; ESE survey collaborators
[Ad] Endereço:St Vincent's Hospital and Garvan Institute of Medical ResearchSydney, Australia.
[Ti] Título:Treatment of aggressive pituitary tumours and carcinomas: results of a European Society of Endocrinology (ESE) survey 2016.
[So] Source:Eur J Endocrinol;178(3):265-276, 2018 03.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To collect outcome data in a large cohort of patients with aggressive pituitary tumours (APT)/carcinomas (PC) and specifically report effects of temozolomide (TMZ) treatment. DESIGN: Electronic survey to ESE members Dec 2015-Nov 2016. RESULTS: Reports on 166 patients (40 PC, 125 APT, 1 unclassified) were obtained. Median age at diagnosis was 43 (range 4-79) years. 69% of the tumours were clinically functioning, and the most frequent immunohistochemical subtype were corticotroph tumours (45%). Ki-67 index did not distinguish APT from PC, median 7% and 10% respectively. TMZ was first-line chemotherapy in 157 patients. At the end of the treatment (median 9 cycles), radiological evaluation showed complete response (CR) in 6%, partial response (PR) in 31%, stable disease (SD) in 33% and progressive disease in 30%. Response was more frequent in patients receiving concomitant radiotherapy and TMZ. CR was seen only in patients with low MGMT expression. Clinically functioning tumours were more likely to respond than non-functioning tumours, independent of MGMT status. Of patients with CR, PR and SD, 25, 40 and 48% respectively progressed after a median of 12-month follow-up. Other oncological drugs given as primary treatment and to TMZ failures resulted in PR in 20%. CONCLUSION: This survey confirms that TMZ is established as first-line chemotherapeutic treatment of APT/PC. Clinically functioning tumours, low MGMT and concurrent radiotherapy were associated with a better response. The limited long-term effect of TMZ and the poor efficacy of other drugs highlight the need to identify additional effective therapies.
[Mh] Termos MeSH primário: Adenoma/terapia
Antineoplásicos Alquilantes/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Carcinoma/terapia
Irradiação Craniana
Dacarbazina/análogos & derivados
Procedimentos Neurocirúrgicos
Neoplasias Hipofisárias/terapia
[Mh] Termos MeSH secundário: Adenoma/metabolismo
Adenoma/patologia
Adolescente
Adulto
Idoso
Bevacizumab/administração & dosagem
Capecitabina/administração & dosagem
Carcinoma/metabolismo
Carcinoma/patologia
Carmustina/administração & dosagem
Criança
Pré-Escolar
Metilases de Modificação do DNA/metabolismo
Enzimas Reparadoras do DNA/metabolismo
Dacarbazina/administração & dosagem
Dacarbazina/uso terapêutico
Endocrinologia
Europa (Continente)
Feminino
Seres Humanos
Antígeno Ki-67/metabolismo
Masculino
Meia-Idade
Invasividade Neoplásica
Neoplasias Hipofisárias/metabolismo
Neoplasias Hipofisárias/patologia
Sociedades Médicas
Inquéritos e Questionários
Talidomida/administração & dosagem
Proteínas Supressoras de Tumor/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 0 (Ki-67 Antigen); 0 (Tumor Suppressor Proteins); 2S9ZZM9Q9V (Bevacizumab); 4Z8R6ORS6L (Thalidomide); 6804DJ8Z9U (Capecitabine); 7GR28W0FJI (Dacarbazine); EC 2.1.1.- (DNA Modification Methylases); EC 2.1.1.63 (MGMT protein, human); EC 6.5.1.- (DNA Repair Enzymes); U68WG3173Y (Carmustine); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180114
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0933


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[PMID]:28453695
[Au] Autor:Suenaga M; Schirripa M; Cao S; Zhang W; Yang D; Murgioni S; Rossini D; Marmorino F; Mennitto A; Ning Y; Okazaki S; Berger MD; Miyamoto Y; Gopez R; Barzi A; Yamaguchi T; Loupakis F; Lenz HJ
[Ad] Endereço:Department of Medical Oncology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, USA.
[Ti] Título:Genetic variants of DNA repair-related genes predict efficacy of TAS-102 in patients with refractory metastatic colorectal cancer.
[So] Source:Ann Oncol;28(5):1015-1022, 2017 05 01.
[Is] ISSN:1569-8041
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background: Tri-phosphorylated trifluridine (FTD) incorporation into DNA is TAS-102's main anti-tumor action. We tested whether genetic polymorphisms in homologous recombination (HR) and cell cycle checkpoint pathway for DNA repair is associated with outcomes in refractory metastatic colorectal cancer (mCRC) patients treated with TAS-102. Patients and methods: We analyzed genomic DNA extracted from 233 samples of three cohorts: an evaluation cohort of 52 patients receiving TAS-102, a validation cohort of 129 patients receiving TAS-102 and a control cohort of 52 patients receiving regorafenib. Single nucleotide polymorphisms of genes involved in HR (ATM, BRCA1, BRCA2, XRCC3, FANCD2, H2AX, RAD51) and cell cycle checkpoint (ATR, CHEK1, CHEK2, CDKN1A, TP53, CHE1, PIN1, PCNA) were analyzed by PCR-based direct sequencing. Results: In univariate analysis for the evaluation cohort, patients with any G allele in ATM rs609429 had longer overall survival (OS) than those with the C/C variant (8.7 vs. 4.4 months, HR 0.37, 95% CI: 0.14-0.99, P = 0.022). Patients carrying any A allele in XRCC3 rs861539 had significantly longer progression-free survival (PFS) (3.8 vs. 2.3 months, HR 0.44, 95% CI: 0.21-0.92, P = 0.024) and OS (15.6 vs. 6.3 months, HR 0.25, 95% CI: 0.08-0.79, P = 0.012) than those with the G/G variant. In multivariable analysis, ATM rs609429 remained significant for OS (P = 0.020). In the validation cohort, patients having ATM rs609429 with any G allele showed longer OS and PFS; the G/A variant in XRCC3 rs861539 showed longer OS, though without statistical significance. Conclusion: Genetic variants in the HR pathway may predict clinical outcome in mCRC patients receiving TAS-102.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Neoplasias Colorretais/genética
Enzimas Reparadoras do DNA/genética
Neoplasias Hepáticas/genética
Trifluridina/uso terapêutico
Uracila/análogos & derivados
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Antineoplásicos/farmacologia
Neoplasias Colorretais/tratamento farmacológico
Neoplasias Colorretais/mortalidade
Neoplasias Colorretais/patologia
Intervalo Livre de Doença
Combinação de Medicamentos
Resistência a Medicamentos Antineoplásicos/genética
Feminino
Estudos de Associação Genética
Seres Humanos
Neoplasias Hepáticas/tratamento farmacológico
Neoplasias Hepáticas/mortalidade
Neoplasias Hepáticas/secundário
Masculino
Meia-Idade
Compostos de Fenilureia/farmacologia
Compostos de Fenilureia/uso terapêutico
Modelos de Riscos Proporcionais
Piridinas/farmacologia
Piridinas/uso terapêutico
Estudos Retrospectivos
Resultado do Tratamento
Trifluridina/farmacologia
Uracila/farmacologia
Uracila/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Drug Combinations); 0 (Phenylurea Compounds); 0 (Pyridines); 0 (TAS 102); 24T2A1DOYB (regorafenib); 56HH86ZVCT (Uracil); EC 6.5.1.- (DNA Repair Enzymes); RMW9V5RW38 (Trifluridine)
[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:170429
[St] Status:MEDLINE
[do] DOI:10.1093/annonc/mdx035


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[PMID]:27776349
[Au] Autor:De Summa S; Guida M; Tommasi S; Strippoli S; Pellegrini C; Fargnoli MC; Pilato B; Natalicchio I; Guida G; Pinto R
[Ad] Endereço:IRCCS Istituto Tumori "Giovanni Paolo II", Molecular Genetics Laboratory, Bari, Italy.
[Ti] Título:Genetic profiling of a rare condition: co-occurrence of albinism and multiple primary melanoma in a Caucasian family.
[So] Source:Oncotarget;8(18):29751-29759, 2017 May 02.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Multiple primary melanoma (MPM) is a rare condition, whose genetic basis has not yet been clarified. Only 8-12% of MPM are due to germline mutations of CDKN2A. However, other genes (POT1, BRCA1/2, MC1R, MGMT) have been demonstrated to be involved in predisposition to this pathology.To our knowledge, this is the first family study based on two siblings with the rare coexistence of MPM and oculocutaneous albinism (OCA), an autosomal recessive disease characterized by the absence or decrease in pigmentation in the skin, hair, and eyes.In this study, we evaluated genes involved in melanoma predisposition (CDKN2A, CDK4, MC1R, MITF, POT1, RB1, MGMT, BRCA1, BRCA2), pathogenesis (BRAF, NRAS, PIK3CA, KIT, PTEN), skin/hair pigmentation (MC1R, MITF) and in immune pathways (CTLA4) to individuate alterations able to explain the rare onset of MPM and OCA in indexes and the transmission in their pedigree.From the analysis of the pedigree, we were able to identify a "protective" haplotype with respect to MPM, including MGMT p.I174V alteration. The second generation offspring is under strict follow up as some of them have a higher risk of developing MPM according to our model.
[Mh] Termos MeSH primário: Albinismo/genética
Estudos de Associação Genética
Predisposição Genética para Doença
Mutação em Linhagem Germinativa
Melanoma/genética
Mutação
Neoplasias Primárias Múltiplas/genética
[Mh] Termos MeSH secundário: Albinismo/diagnóstico
Biomarcadores
Biologia Computacional/métodos
Metilação de DNA
Metilases de Modificação do DNA/química
Metilases de Modificação do DNA/genética
Análise Mutacional de DNA
Enzimas Reparadoras do DNA/química
Enzimas Reparadoras do DNA/genética
Família
Feminino
Genótipo
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Masculino
Melanoma/diagnóstico
Meia-Idade
Modelos Moleculares
Anotação de Sequência Molecular
Neoplasias Primárias Múltiplas/diagnóstico
Linhagem
Filogenia
Conformação Proteica
Irmãos
Proteínas Supressoras de Tumor/química
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Tumor Suppressor Proteins); EC 2.1.1.- (DNA Modification Methylases); EC 2.1.1.63 (MGMT protein, human); EC 6.5.1.- (DNA Repair Enzymes)
[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:161025
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.12777


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[PMID]:29352318
[Au] Autor:William D; Walther M; Schneider B; Linnebacher M; Classen CF
[Ad] Endereço:University Children's and Adolescents' Hospital, University Medicine of Rostock, Rostock, Germany.
[Ti] Título:Temozolomide-induced increase of tumorigenicity can be diminished by targeting of mitochondria in in vitro models of patient individual glioblastoma.
[So] Source:PLoS One;13(1):e0191511, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glioblastoma multiforme (GBM) is a highly heterogeneous and aggressive brain tumor with a dismal prognosis. Development of resistance towards cytostatic drugs like the GBM standard drug temozolomide is a severe problem in GBM treatment. One potential source of GBM relapse could be so called cancer stem like cells (CSCs). These represent an undifferentiated subpopulation of cells with high potential for tumor initiation. Furthermore, it has been shown that differentiated GBM cells can regain CSC properties when exposed to continuous temozolomide treatment in vitro. In this study, treatment of several primary GBM cell lines with clinically relevant doses of temozolomide increased their tumorigenicity as determined by colony formation assays in soft agar. Increased tumorigenicity is a known property of CSCs. Hence, therapy options that specifically target CSCs are under investigation. CSCs appear to be particularly dependent on mitochondria biogenesis which may represent a useful target for CSC elimination. Toxicity towards mitochondria is a known side effect of several antibiotics. Thus, addition of antibiotics like doxycycline may represent a useful tool to inhibit CSCs in GBM. Here, we show that combining temozolomide treatment of primary GBM cells with doxycycline could counteract the increase of tumorigenicity induced by temozolomide treatment.
[Mh] Termos MeSH primário: Antineoplásicos Alquilantes/efeitos adversos
Neoplasias Encefálicas/tratamento farmacológico
Neoplasias Encefálicas/patologia
Dacarbazina/análogos & derivados
Glioblastoma/tratamento farmacológico
Glioblastoma/patologia
[Mh] Termos MeSH secundário: Antibacterianos/administração & dosagem
Antineoplásicos Alquilantes/administração & dosagem
Biomarcadores Tumorais/metabolismo
Neoplasias Encefálicas/metabolismo
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Metilases de Modificação do DNA/genética
Enzimas Reparadoras do DNA/genética
Dacarbazina/administração & dosagem
Dacarbazina/efeitos adversos
Doxiciclina/administração & dosagem
Resistência a Medicamentos Antineoplásicos
Fucosiltransferases/metabolismo
Glioblastoma/metabolismo
Seres Humanos
Antígeno Lewis X/metabolismo
Mitocôndrias/efeitos dos fármacos
Células-Tronco Neoplásicas/efeitos dos fármacos
Células-Tronco Neoplásicas/metabolismo
Células-Tronco Neoplásicas/patologia
Nestina/metabolismo
Ensaio Tumoral de Célula-Tronco
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Antineoplastic Agents, Alkylating); 0 (Biomarkers, Tumor); 0 (Lewis X Antigen); 0 (NES protein, human); 0 (Nestin); 0 (Tumor Suppressor Proteins); 7GR28W0FJI (Dacarbazine); EC 2.1.1.- (DNA Modification Methylases); EC 2.1.1.63 (MGMT protein, human); EC 2.4.1.- (FUT4 protein, human); EC 2.4.1.- (Fucosyltransferases); EC 6.5.1.- (DNA Repair Enzymes); N12000U13O (Doxycycline); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180121
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191511


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[PMID]:29247747
[Au] Autor:Zhao M; Li S; Zhou L; Shen Q; Zhu H; Zhu X
[Ad] Endereço:Department of Obstetrics and Gynecology, the Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
[Ti] Título:Prognostic values of excision repair cross-complementing genes mRNA expression in ovarian cancer patients.
[So] Source:Life Sci;194:34-39, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Excision repair cross-complementing (ERCC) genes, key components of the nucleotide excision repair pathway, are regarded as crucial factors for DNA repair capacity. Previous studies have investigated prognostic values of ERCC genes in a number of malignancies. However, the relationship between ERCC genes and prognosis of ovarian cancer patients remains controversial. Therefore, in the current study, we systematically analyze the prognostic values of ERCC genes in ovarian cancer by the Kaplan-Meier plotter, which includes updated gene expression data and survival information of 1656 ovarian cancer patients. Our results showed that high expression of ERCC1 and ERCC8 mRNA was related to a worse overall survival among ovarian cancer patients, especially in late stage and poor differentiation serous ovarian patients. Increased ERCC4 mRNA expression indicated a better overall survival among serous ovarian cancer patients. The other ERCC genes were uncorrelated with prognosis in ovarian cancer. These results indicate that some ERCC genes have critical prognostic values in ovarian cancer.
[Mh] Termos MeSH primário: Enzimas Reparadoras do DNA/genética
Reparo do DNA
Proteínas de Ligação a DNA/genética
Endonucleases/genética
Neoplasias Ovarianas/genética
RNA Mensageiro/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Estimativa de Kaplan-Meier
Neoplasias Ovarianas/diagnóstico
Neoplasias Ovarianas/patologia
Ovário/metabolismo
Ovário/patologia
Prognóstico
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (ERCC8 protein, human); 0 (RNA, Messenger); 0 (Transcription Factors); 0 (xeroderma pigmentosum group F protein); EC 3.1.- (ERCC1 protein, human); EC 3.1.- (Endonucleases); EC 6.5.1.- (DNA Repair Enzymes)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE


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[PMID]:29277765
[Au] Autor:Yang G; Qiu J; Wang D; Tao Y; Song Y; Wang H; Tang J; Wang X; Sun YU; Yang Z; Hoffman RM
[Ad] Endereço:Hangzhou Third Hospital, Hangzhou, P.R. China.
[Ti] Título:Traditional Chinese Medicine Curcumin Sensitizes Human Colon Cancer to Radiation by Altering the Expression of DNA Repair-related Genes.
[So] Source:Anticancer Res;38(1):131-136, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The aim of the present study was to investigate the radio-sensitizing efficacy of curcumin, a traditional Chinese medicine (TCM) on colon cancer cells in vitro and in vivo. MATERIALS AND METHODS: Human colon cancer HT-29 cells were treated with curcumin (2.5 µM), irradiation (10 Gy) and the combination of irradiation and curcumin. Cell proliferation was assessed using the MTT assay. Apoptotic cells were detected by Annexin V-PE/7-AAD analysis. PCR was performed to determine differential-expression profiling of 95 DNA-repair genes in irradiated cells and cells treated with both irradiation and curcumin. Differentially-expressed genes were confirmed by Western blotting. In vivo radio-sensitizing efficacy of curcumin was assessed in a xenograft mouse model of HT-29 colon cancer. Curcumin was administrated daily by intraperitoneal injection at 20 mg/kg/dose. Mice received irradiation (10 Gy) twice weekly. Apoptosis of the cancer cells following treatment was determined by TUNEL staining. RESULTS: Irradiation induced proliferation inhibition and apoptosis of HT-29 cells in vitro. Concurrent curcumin treatment sensitized the HT-29 tumor to irradiation (p<0.01). DNA repair-related genes CCNH and XRCC5 were upregulated and LIG4 and PNKP downregulated by the combination of curcumin and irradiation compared with irradiation alone (p<0.05). Combined treatment of curcumin and irradiation resulted in a significantly greater tumor-growth inhibition and apoptosis compared to irradiation treatment alone (p<0.01). CONCLUSION: Curcumin sensitizes human colon cancer in vitro and in vivo to radiation. Downregulation of LIG4 and PNKP and upregulation of XRCC5 and CCNH DNA-repair-related genes were involved in the radio-sensitizing efficacy of curcumin in colon cancer.
[Mh] Termos MeSH primário: Neoplasias do Colo/tratamento farmacológico
Neoplasias do Colo/radioterapia
Curcumina/farmacologia
Curcumina/uso terapêutico
Radiossensibilizantes/farmacologia
Radiossensibilizantes/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Apoptose/efeitos da radiação
Proliferação Celular/efeitos dos fármacos
Proliferação Celular/efeitos da radiação
Neoplasias do Colo/metabolismo
Neoplasias do Colo/patologia
Ciclina H/genética
Ciclina H/metabolismo
DNA Ligase Dependente de ATP/genética
DNA Ligase Dependente de ATP/metabolismo
Reparo do DNA/genética
Enzimas Reparadoras do DNA/genética
Enzimas Reparadoras do DNA/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos da radiação
Células HT29
Seres Humanos
Autoantígeno Ku/genética
Autoantígeno Ku/metabolismo
Medicina Tradicional Chinesa
Camundongos Endogâmicos BALB C
Camundongos Nus
Fosfotransferases (Aceptor do Grupo Álcool)/genética
Fosfotransferases (Aceptor do Grupo Álcool)/metabolismo
Carga Tumoral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCNH protein, human); 0 (Cyclin H); 0 (LIG4 protein, human); 0 (Radiation-Sensitizing Agents); EC 2.7.1.- (PNKP protein, human); EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor)); EC 3.6.4.12 (XRCC5 protein, human); EC 4.2.99.- (Ku Autoantigen); EC 6.5.1.- (DNA Repair Enzymes); EC 6.5.1.1 (DNA Ligase ATP); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


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[PMID]:28467681
[Au] Autor:Ma DL; Dong ZZ; Vellaisamy K; Cheung KM; Yang G; Leung CH
[Ad] Endereço:Department of Chemistry, Hong Kong Baptist University, Kowloon Tong, Hong Kong.
[Ti] Título:Luminescent Strategies for Label-Free G-Quadruplex-Based Enzyme Activity Sensing.
[So] Source:Chem Rec;17(11):1135-1145, 2017 11.
[Is] ISSN:1528-0691
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:By catalyzing highly specific and tightly controlled chemical reactions, enzymes are essential to maintaining normal cellular physiology. However, aberrant enzymatic activity can be linked to the pathogenesis of various diseases. Therefore, the unusual activity of particular enzymes can represent testable biomarkers for the diagnosis or screening of certain diseases. In recent years, G-quadruplex-based platforms have attracted wide attention for the monitoring of enzymatic activities. In this Personal Account, we discuss our group's works on the development of G-quadruplex-based sensing system for enzyme activities by using mainly iridium(III) complexes as luminescent label-free probes. These studies showcase the versatility of the G-quadruplex for developing assays for a variety of different enzymes.
[Mh] Termos MeSH primário: Complexos de Coordenação/química
Ensaios Enzimáticos/métodos
Quadruplex G
Irídio/química
Substâncias Luminescentes/química
Medições Luminescentes/métodos
[Mh] Termos MeSH secundário: Animais
Técnicas Biossensoriais/métodos
Enzimas Reparadoras do DNA/análise
Enzimas Reparadoras do DNA/metabolismo
DNA Polimerase Dirigida por DNA/análise
DNA Polimerase Dirigida por DNA/metabolismo
Endonucleases/análise
Endonucleases/metabolismo
Exonucleases/análise
Exonucleases/metabolismo
Seres Humanos
Peptídeo Hidrolases/análise
Peptídeo Hidrolases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Coordination Complexes); 0 (Luminescent Agents); 44448S9773 (Iridium); EC 2.7.7.7 (DNA-Directed DNA Polymerase); EC 3.1.- (Endonucleases); EC 3.1.- (Exonucleases); EC 3.4.- (Peptide Hydrolases); EC 6.5.1.- (DNA Repair Enzymes)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171211
[Lr] Data última revisão:
171211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1002/tcr.201700014


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[PMID]:28834127
[Au] Autor:Kinoshita M; Yamada A; Sawa D; Kamimura S; Miyachi M; Moritake H
[Ad] Endereço:Division of Pediatrics, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.
[Ti] Título:Successful treatment of metastatic alveolar rhabdomyosarcoma with MGMT gene promoter methylation by temozolomide-based combination chemotherapy.
[So] Source:Pediatr Blood Cancer;65(1), 2018 Jan.
[Is] ISSN:1545-5017
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A 3-year-old male presented with a large retroperitoneal mass and multiple metastases. Biopsy results suggested alveolar rhabdomyosarcoma bearing a methylated O6-methylguanine-DNA methyltransferase (MGMT) gene promoter. Serum microRNA-206 levels were elevated and remained high after three cycles of vincristine, dactinomycin, and cyclophosphamide (VAC). Replacement of vincristine, irinotecan, and temozolomide (VIT) for VAC induced a marked tumor reduction and normalization of the miR-206 levels. The patient completed 14 cycles of VIT with local radiotherapy and has been in remission for 31 months. Temozolomide could be effective for tumors with a methylated MGMT gene promoter. Individualized therapy is warranted for such patients.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Quimiorradioterapia
Metilação de DNA
Metilases de Modificação do DNA/metabolismo
Enzimas Reparadoras do DNA/metabolismo
DNA de Neoplasias/metabolismo
Regiões Promotoras Genéticas
Rabdomiossarcoma Alveolar
Proteínas Supressoras de Tumor/metabolismo
[Mh] Termos MeSH secundário: Camptotecina/administração & dosagem
Camptotecina/análogos & derivados
Pré-Escolar
Ciclofosfamida/administração & dosagem
Dacarbazina/administração & dosagem
Dacarbazina/análogos & derivados
Dactinomicina/administração & dosagem
Seres Humanos
Masculino
MicroRNAs/metabolismo
Metástase Neoplásica
RNA Neoplásico/metabolismo
Rabdomiossarcoma Alveolar/metabolismo
Rabdomiossarcoma Alveolar/patologia
Rabdomiossarcoma Alveolar/terapia
Vincristina/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Neoplasm); 0 (MIRN206 microRNA, human); 0 (MicroRNAs); 0 (RNA, Neoplasm); 0 (Tumor Suppressor Proteins); 1CC1JFE158 (Dactinomycin); 5J49Q6B70F (Vincristine); 7673326042 (irinotecan); 7GR28W0FJI (Dacarbazine); 8N3DW7272P (Cyclophosphamide); EC 2.1.1.- (DNA Modification Methylases); EC 2.1.1.63 (MGMT protein, human); EC 6.5.1.- (DNA Repair Enzymes); XT3Z54Z28A (Camptothecin); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1002/pbc.26750


  9 / 4417 MEDLINE  
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[PMID]:29036186
[Au] Autor:Hsu CY; Ho HL; Lin SC; Ho TD; Ho DM
[Ad] Endereço:Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
[Ti] Título:The MGMT promoter single-nucleotide polymorphism rs1625649 had prognostic impact on patients with MGMT methylated glioblastoma.
[So] Source:PLoS One;12(10):e0186430, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Promoter methylation is the most significant mechanism to regulate O6-methylguanine-DNA-methyltransferase (MGMT) expression. Single-nucleotide polymorphisms (SNPs) in the MGMT promoter region may also play a role. The aim of this study was to evaluate the clinical significance of SNPs in the MGMT promoter region of glioblastoma. Genomic DNAs from 118 glioblastomas were collected for polymerase chain reaction (PCR) amplification. Sanger sequencing was used to sequence the MGMT promoter region to detect SNPs. The results were correlated with MGMT status and patient survival. Rs1625649 was the only polymorphic SNP located at the MGMT promoter region in 37.5% of glioblastomas. Homozygous rs1625649 (AA genotype) was correlated with a higher MGMT methylation level and a lower protein expression, but the result was not statistically significant. In patients with MGMT methylated glioblastoma, cases with homozygous rs1625649 (AA genotype) were significantly associated with a lack of MGMT protein expression and a better progression-free survival (PFS) than the cases with wild type rs1625649 (CC genotype) or heterozygous rs1625649 (CA genotype). The survival impact was significant in multivariate analyses. In conclusion, the MGMT promoter homozygous rs1625649 (AA genotype) was found to correlate with a better PFS in patients with MGMT methylated glioblastoma.
[Mh] Termos MeSH primário: Metilação de DNA
Metilases de Modificação do DNA/genética
Enzimas Reparadoras do DNA/genética
Glioblastoma/diagnóstico
Glioblastoma/genética
Polimorfismo de Nucleotídeo Único
Proteínas Supressoras de Tumor/genética
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Masculino
Meia-Idade
Prognóstico
Regiões Promotoras Genéticas/genética
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Tumor Suppressor Proteins); EC 2.1.1.- (DNA Modification Methylases); EC 2.1.1.63 (MGMT protein, human); EC 6.5.1.- (DNA Repair Enzymes)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171017
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186430


  10 / 4417 MEDLINE  
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[PMID]:28977635
[Au] Autor:Kumar V; Fleming T; Terjung S; Gorzelanny C; Gebhardt C; Agrawal R; Mall MA; Ranzinger J; Zeier M; Madhusudhan T; Ranjan S; Isermann B; Liesz A; Deshpande D; Häring HU; Biswas SK; Reynolds PR; Hammes HP; Peperkok R; Angel P; Herzig S; Nawroth PP
[Ad] Endereço:Department of Medicine I and Clinical Chemistry, University Hospital of Heidelberg, INF 410, Heidelberg, Germany.
[Ti] Título:Homeostatic nuclear RAGE-ATM interaction is essential for efficient DNA repair.
[So] Source:Nucleic Acids Res;45(18):10595-10613, 2017 Oct 13.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The integrity of genome is a prerequisite for healthy life. Indeed, defects in DNA repair have been associated with several human diseases, including tissue-fibrosis, neurodegeneration and cancer. Despite decades of extensive research, the spatio-mechanical processes of double-strand break (DSB)-repair, especially the auxiliary factor(s) that can stimulate accurate and timely repair, have remained elusive. Here, we report an ATM-kinase dependent, unforeseen function of the nuclear isoform of the Receptor for Advanced Glycation End-products (nRAGE) in DSB-repair. RAGE is phosphorylated at Serine376 and Serine389 by the ATM kinase and is recruited to the site of DNA-DSBs via an early DNA damage response. nRAGE preferentially co-localized with the MRE11 nuclease subunit of the MRN complex and orchestrates its nucleolytic activity to the ATR kinase signaling. This promotes efficient RPA2S4-S8 and CHK1S345 phosphorylation and thereby prevents cellular senescence, IPF and carcinoma formation. Accordingly, loss of RAGE causatively linked to perpetual DSBs signaling, cellular senescence and fibrosis. Importantly, in a mouse model of idiopathic pulmonary fibrosis (RAGE-/-), reconstitution of RAGE efficiently restored DSB-repair and reversed pathological anomalies. Collectively, this study identifies nRAGE as a master regulator of DSB-repair, the absence of which orchestrates persistent DSB signaling to senescence, tissue-fibrosis and oncogenesis.
[Mh] Termos MeSH primário: Proteínas Mutadas de Ataxia Telangiectasia/metabolismo
Reparo do DNA
Receptor para Produtos Finais de Glicação Avançada/metabolismo
[Mh] Termos MeSH secundário: Animais
Núcleo Celular/enzimologia
Núcleo Celular/metabolismo
Senescência Celular
DNA/metabolismo
Quebras de DNA de Cadeia Dupla
Enzimas Reparadoras do DNA/metabolismo
Proteínas de Ligação a DNA/metabolismo
Homeostase
Pulmão/fisiopatologia
Proteína Homóloga a MRE11
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fibrose Pulmonar/genética
Fibrose Pulmonar/fisiopatologia
Receptor para Produtos Finais de Glicação Avançada/genética
Traumatismo por Reperfusão/genética
Traumatismo por Reperfusão/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ager protein, mouse); 0 (DNA-Binding Proteins); 0 (Mre11a protein, mouse); 0 (Receptor for Advanced Glycation End Products); 9007-49-2 (DNA); EC 2.7.1.- (Atr protein, mouse); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins); EC 3.1.- (MRE11 Homologue Protein); EC 6.5.1.- (DNA Repair Enzymes)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx705



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