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  1 / 2116 MEDLINE  
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[PMID]:28470797
[Au] Autor:O'Kane GM; Ryan É; McVeigh TP; Creavin B; Hyland JM; O'Donoghue DP; Keegan D; Geraghty R; Flannery D; Nolan C; Donovan E; Mehigan BJ; McCormick P; Muldoon C; Farrell M; Shields C; Mulligan N; Kennedy MJ; Green AJ; Winter DC; MacMathuna P; Sheahan K; Gallagher DJ
[Ad] Endereço:St. James's Hospital, Dublin 8, Ireland.
[Ti] Título:Screening for mismatch repair deficiency in colorectal cancer: data from three academic medical centers.
[So] Source:Cancer Med;6(6):1465-1472, 2017 Jun.
[Is] ISSN:2045-7634
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Reflex immunohistochemistry (rIHC) for mismatch repair (MMR) protein expression can be used as a screening tool to detect Lynch Syndrome (LS). Increasingly the mismatch repair-deficient (dMMR) phenotype has therapeutic implications. We investigated the pattern and consequence of testing for dMMR in three Irish Cancer Centres (CCs). CRC databases were analyzed from January 2005-December 2013. CC1 performs IHC upon physician request, CC2 implemented rIHC in November 2008, and CC3 has been performing rIHC since 2004. The number of eligible patients referred to clinical genetic services (CGS), and the number of LS patients per center was determined. 3906 patients were included over a 9-year period. dMMR CRCs were found in 32/153 (21%) of patients at CC1 and 55/536 (10%) at CC2, accounting for 3% and 5% of the CRC population, respectively. At CC3, 182/1737 patients (10%) had dMMR CRCs (P < 0.001). Additional testing for the BRAF V600E mutation, was performed in 49 patients at CC3 prior to CGS referral, of which 29 were positive and considered sporadic CRC. Referrals to CGS were made in 66%, 33%, and 30% of eligible patients at CC1, CC2, and CC3, respectively. LS accounted for CRC in eight patients (0.8%) at CC1, eight patients (0.7%) at CC2, and 20 patients (1.2%) at CC3. Cascade testing of patients with dMMR CRC was not completed in 56%. Universal screening increases the detection of dMMR tumors and LS kindreds. Successful implementation of this approach requires adequate resources for appropriate downstream management of these patients.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Reparo de Erro de Pareamento de DNA
[Mh] Termos MeSH secundário: Centros Médicos Acadêmicos
Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Seres Humanos
Imuno-Histoquímica
Meia-Idade
Mutação
Fenótipo
Proteínas Proto-Oncogênicas B-raf/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[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:10.1002/cam4.1025


  2 / 2116 MEDLINE  
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[PMID]:28453690
[Au] Autor:Auclin E; Zaanan A; Vernerey D; Douard R; Gallois C; Laurent-Puig P; Bonnetain F; Taieb J
[Ad] Endereço:Department of Digestive Oncology, European Georges Pompidou Hospital, Assistance Publique des Hôpitaux de Paris, Paris, France.
[Ti] Título:Subgroups and prognostication in stage III colon cancer: future perspectives for adjuvant therapy.
[So] Source:Ann Oncol;28(5):958-968, 2017 05 01.
[Is] ISSN:1569-8041
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Since the MOSAIC study, oxaliplatin-based adjuvant chemotherapy has been the standard treatment of stage III colon cancer. Combination therapy with fluoropyrimidines and oxaliplatin has improved overall survival (OS) and reduced the risk of recurrence in patients with resected stage III colon cancer. However, only 20% of patients really benefit from adjuvant chemotherapy, exposing 80% of patients to unnecessary toxicity. Recent analyses of large multicenter adjuvant studies have focused on the prognostication of OS and disease-free survival in stage III colon cancer in order to reduce over-treatment and to find more accurate prognostic tools than those used for adjuvant treatment decision-making in stage II disease. Indeed, clinical and pathological prognostic factors, although important, are not sufficient to decide which stage III patients will benefit from adjuvant therapy, and biomarkers will help select patient that need adjuvant treatment. Molecular markers such as microsatellite status and BRAF and KRAS mutations have recently been explored, and molecular signatures have been identified as promising prognostic factor for OS. Furthermore, recent studies have highlighted the prognostic value of immune infiltration. This review focuses on pathologic, immunologic and molecular prognostic markers for stage III colon cancer that could help clinicians tailor adjuvant treatment in a comprehensive transversal approach.
[Mh] Termos MeSH primário: Neoplasias do Colo/diagnóstico
Neoplasias do Colo/tratamento farmacológico
[Mh] Termos MeSH secundário: Quimioterapia Adjuvante
Neoplasias do Colo/genética
Neoplasias do Colo/mortalidade
Ilhas de CpG
Reparo de Erro de Pareamento de DNA
Intervalo Livre de Doença
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Técnicas de Diagnóstico Molecular
Mutação
Estadiamento de Neoplasias
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/annonc/mdx030


  3 / 2116 MEDLINE  
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[PMID]:29390274
[Au] Autor:Yuan LQ; Wang JH; Zhu K; Yang M; Gu WZ; Lai C; Li HM; Shu Q; Chen X
[Ad] Endereço:Departments of Central Laboratory, Pathology, Oncology and Radiology, The Children's Hospital of Zhejiang University School of Medicine.
[Ti] Título:A highly malignant case of neuroblastoma with substantial increase of single-nucleotide variants and normal mismatch repair system: A case report.
[So] Source:Medicine (Baltimore);96(50):e8845, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Neuroblastoma is a common abdominal malignancy in children. The chemoresistant and relapsed cases have poor prognosis. The genetic background and the mechanism of resistance remain unelucidated. Next-generation sequence (NGS) is becoming a popular tool to unravel the genetic background and to guide precision medicine in oncology studies as well as in clinical practice. PATIENT CONCERNS: Here we report a neuroblastoma case of a boy aged 2 years and 8 months when first diagnosed, with multiple metastatic sites found in both lungs. The metastatic tumors were resistant to chemotherapy and the patient suffered from severe bone marrow suppression. NGS of the whole exon revealed somatic mutations including 9666 single-nucleotide variants (SNVs) from 5148 genes, 55 copy number variations (CNVs), and 140 insertion-deletion variations. The high frequency of SNVs makes it distinguished case. However, no mutation of key tumor driver genes with functional significance was identified. No abnormality was found in nucleic acid synthesis enzymes. No amplification of c-Myc and n-Myc was found by fluorescence in situ hybridization (FISH). Both NGS and immunohistochemistry (IHC) analysis indicated that DNA mismatch repair (MMR) system was intact. INTERVENTIONS: After initial diagnosis, the patient received combinational chemotherapy, which includes vindesine, an analogue of adriamycin suggested by NGS data, for 4 months. Radical section of the tumor together with the left kidney and the left adrenal gland was performed 5 months after diagnosis. Postsurgical chemotherapy protocols was similar with the previous. OUTCOMES: The patient died 2 years after initial diagnosis after 8 relapses following combinational chemotherapy. LESSONS: This case of neuroblastoma is with pronounced somatic mutations but unidentified driver gene and therapeutic target. Although NGS is a potentially powerful tool to guide precision medicine, at current stage, its application in the clinic certainly has its limits. The underlying mechanism of the substantially increased SNV number, as well as the malignant behaviors of the tumor, is yet to be revealed.
[Mh] Termos MeSH primário: Abdome
Variações do Número de Cópias de DNA
Reparo de Erro de Pareamento de DNA
Neuroblastoma/genética
Neuroblastoma/patologia
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Pré-Escolar
Evolução Fatal
Seres Humanos
Imuno-Histoquímica
Hibridização in Situ Fluorescente
Masculino
Mutação
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000008845


  4 / 2116 MEDLINE  
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[PMID]:28741532
[Au] Autor:Kloor M; von Knebel Doeberitz M
[Ad] Endereço:Department of Applied Tumor Biology, Institute of Pathology, University Hospital Heidelberg, Clinical Cooperation Unit (CCU 105) of the German Cancer Research Center and Molecular Medicine Partner Unit (MMPU) of the European Molecular Biology Laboratory, Im Neuenheimer Feld 224, 69120 Heidelberg, Germany. Electronic address: matthias.kloor@med.uni-heidelberg.de.
[Ti] Título:The Immune Biology of Microsatellite-Unstable Cancer.
[So] Source:Trends Cancer;2(3):121-133, 2016 Mar.
[Is] ISSN:2405-8025
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Deficient DNA mismatch repair (MMR) boosts the accumulation of frameshift mutations in genes encompassing coding microsatellites (cMS). This results in the translation of proteins with mutation-induced frameshift peptides (neoantigens) rendering microsatellite-unstable (MSI) cancers highly immunogenic. MSI cancers express a defined set of neoantigens resulting from functionally relevant driver mutations, which are shared by most MSI cancers. Patients with MSI cancers and healthy individuals affected by Lynch syndrome, an inherited predisposition for MSI cancers, develop specific immune responses against these neoantigens. In this review, we summarize our current understanding of the immune biology of MSI cancers and outline new concepts and research directions to develop not only therapeutic treatments, but also preventive vaccines based on the MSI cancer genome landscapes.
[Mh] Termos MeSH primário: Instabilidade de Microssatélites
Neoplasias/imunologia
[Mh] Termos MeSH secundário: Antígenos de Neoplasias/imunologia
Vacinas Anticâncer
Neoplasias Colorretais Hereditárias sem Polipose/genética
Reparo de Erro de Pareamento de DNA
Seres Humanos
Neoplasias/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Cancer Vaccines)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


  5 / 2116 MEDLINE  
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[PMID]:27773688
[Au] Autor:Nakae S; Hijikata A; Tsuji T; Yonezawa K; Kouyama KI; Mayanagi K; Ishino S; Ishino Y; Shirai T
[Ad] Endereço:Department of Bioscience, Nagahama Institute of Bio-Science and Technology, Tamura 1266, Nagahama, Shiga 526-0829, Japan.
[Ti] Título:Structure of the EndoMS-DNA Complex as Mismatch Restriction Endonuclease.
[So] Source:Structure;24(11):1960-1971, 2016 11 01.
[Is] ISSN:1878-4186
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Archaeal NucS nuclease was thought to degrade the single-stranded region of branched DNA, which contains flapped and splayed DNA. However, recent findings indicated that EndoMS, the orthologous enzyme of NucS, specifically cleaves double-stranded DNA (dsDNA) containing mismatched bases. In this study, we determined the structure of the EndoMS-DNA complex. The complex structure of the EndoMS dimer with dsDNA unexpectedly revealed that the mismatched bases were flipped out into binding sites, and the overall architecture most resembled that of restriction enzymes. The structure of the apo form was similar to the reported structure of Pyrococcus abyssi NucS, indicating that movement of the C-terminal domain from the resting state was required for activity. In addition, a model of the EndoMS-PCNA-DNA complex was preliminarily verified with electron microscopy. The structures strongly support the idea that EndoMS acts in a mismatch repair pathway.
[Mh] Termos MeSH primário: DNA de Cadeia Simples/metabolismo
Endodesoxirribonucleases/química
Endodesoxirribonucleases/metabolismo
Pyrococcus abyssi/enzimologia
[Mh] Termos MeSH secundário: Proteínas Arqueais/química
Proteínas Arqueais/metabolismo
Sítios de Ligação
Reparo de Erro de Pareamento de DNA
DNA Arqueal/química
DNA Arqueal/metabolismo
DNA de Cadeia Simples/química
Microscopia Eletrônica
Modelos Moleculares
Ligação Proteica
Conformação Proteica
Pyrococcus abyssi/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Archaeal Proteins); 0 (DNA, Archaeal); 0 (DNA, Single-Stranded); EC 3.1.- (Endodeoxyribonucleases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171230
[Lr] Data última revisão:
171230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161103
[St] Status:MEDLINE


  6 / 2116 MEDLINE  
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[PMID]:28471568
[Au] Autor:Fisher Y; Hershkovitz D
[Ad] Endereço:Institute of Pathology, Rambam Health Care Campus, Haifa, Israel.
[Ti] Título:Molecular and Morphometric Tools for Next-Generation Pathology Diagnosis of Colon Carcinoma.
[So] Source:Isr Med Assoc J;18(7):426-432, 2016 Jul.
[Is] ISSN:1565-1088
[Cp] País de publicação:Israel
[La] Idioma:eng
[Mh] Termos MeSH primário: Neoplasias Colorretais/diagnóstico
Microscopia/métodos
Técnicas de Diagnóstico Molecular/métodos
[Mh] Termos MeSH secundário: Neoplasias Colorretais/genética
Neoplasias Colorretais/patologia
Reparo de Erro de Pareamento de DNA/genética
Seres Humanos
Mutação Puntual
Prognóstico
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


  7 / 2116 MEDLINE  
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[PMID]:29069084
[Au] Autor:Dahal BK; Kadyrova LY; Delfino KR; Rogozin IB; Gujar V; Lobachev KS; Kadyrov FA
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Southern Illinois University School of Medicine, Carbondale, IL, United States of America.
[Ti] Título:Involvement of DNA mismatch repair in the maintenance of heterochromatic DNA stability in Saccharomyces cerevisiae.
[So] Source:PLoS Genet;13(10):e1007074, 2017 Oct.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Heterochromatin contains a significant part of nuclear DNA. Little is known about the mechanisms that govern heterochromatic DNA stability. We show here that in the yeast Saccharomyces cerevisiae (i) DNA mismatch repair (MMR) is required for the maintenance of heterochromatic DNA stability, (ii) MutLα (Mlh1-Pms1 heterodimer), MutSα (Msh2-Msh6 heterodimer), MutSß (Msh2-Msh3 heterodimer), and Exo1 are involved in MMR at heterochromatin, (iii) Exo1-independent MMR at heterochromatin frequently leads to the formation of Pol ζ-dependent mutations, (iv) MMR cooperates with the proofreading activity of Pol ε and the histone acetyltransferase Rtt109 in the maintenance of heterochromatic DNA stability, (v) repair of base-base mismatches at heterochromatin is less efficient than repair of base-base mismatches at euchromatin, and (vi) the efficiency of repair of 1-nt insertion/deletion loops at heterochromatin is similar to the efficiency of repair of 1-nt insertion/deletion loops at euchromatin.
[Mh] Termos MeSH primário: Reparo de Erro de Pareamento de DNA
DNA Fúngico/química
Heterocromatina
Proteínas de Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/genética
[Mh] Termos MeSH secundário: Sequência de Bases
Dano ao DNA
DNA Fúngico/genética
Exodesoxirribonucleases/genética
Genes pol
Histona Acetiltransferases/genética
Proteínas MutL/genética
Proteína MutS de Ligação de DNA com Erro de Pareamento/genética
Homologia de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Fungal); 0 (Heterochromatin); 0 (Saccharomyces cerevisiae Proteins); EC 2.3.1.48 (Histone Acetyltransferases); EC 2.3.1.48 (Rtt109 protein, S cerevisiae); EC 3.1.- (Exodeoxyribonucleases); EC 3.1.11.1 (exodeoxyribonuclease I); EC 3.6.1.3 (MutL Proteins); EC 3.6.1.3 (MutS DNA Mismatch-Binding Protein)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171119
[Lr] Data última revisão:
171119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171026
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007074


  8 / 2116 MEDLINE  
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[PMID]:28946809
[Au] Autor:Tangjitgamol S; Kittisiam T; Tanvanich S
[Ad] Endereço:1 Department of Obstetrics and Gynecology, Faculty of Medicine Vajira Hospital, Navamindradhiraj University, Bangkok, Thailand.
[Ti] Título:Prevalence and prognostic role of mismatch repair gene defect in endometrial cancer patients.
[So] Source:Tumour Biol;39(9):1010428317725834, 2017 Sep.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The study was to evaluate the prevalence of mismatch repair gene defect among Thai patients with endometrial cancer and its association with clinico-pathological features and survivals. The formalin fixed paraffin-embedded blocks of EMC tissue from hysterectomy specimens of patients having surgery in our institution between 1 Jan 1995 and 31 December 2016 were assessed for the immunohistochemical expression of 4 mismatch repair proteins (MLH1, PMS, MSH2, MSH 6). Mismatch repair gene defect was determined by a negative expression of at least 1 protein. Among 385 EMC patients included in the study, mean age was 57.3 ± 10.8 years with 62.3% aged ⩽ 60 years. The most frequent mismatch repair gene defect was MSH6 (38.7%), followed by PMS2 (34.3%), MLH1 (33.2%), and MSH2 (16.4%). Overall, 55.1% showed negative expression of at least one protein. We found significantly higher mismatch repair gene defect in patients aged ⩽ 60 years, with early stage disease, and negative lymph node status than the other comparative groups: 59.2% vs 48.3% for age (p = 0.037), 58.2% vs 45.2% (p = 0.027) for stage, and 58.1% vs 44.6% (p = 0.048) for nodal status. The 5-year progression-free survival, overall survival, and endometrial cancer-specific survival of patients with mismatch repair gene defect was higher than those without gene defect. The differences were statistically significant for only progression-free survival and endometrial cancer-specific survival: 87.7% (95% confidence interval = 83.0%-92.4%) vs 81.5% (95% confidence interval = 75.4%-87.6%) (p = 0.049) for progression-free survival and 91.0% (95% confidence interval = 86.9%-95.1%) vs 85.5% (95% confidence interval = 80.0%-91.0%) (p = 0.044) for endometrial cancer-specific survival, respectively. In conclusion, more than half of Thai endometrial cancer patients had mismatch repair gene defect. The patients with mismatch repair gene defect had significantly younger age (⩽ 60 years) and better prognosis in terms of early stage, negative nodal status, and longer survivals.
[Mh] Termos MeSH primário: Reparo de Erro de Pareamento de DNA/genética
Enzimas Reparadoras do DNA/genética
Neoplasias do Endométrio/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Intervalo Livre de Doença
Neoplasias do Endométrio/mortalidade
Feminino
Seres Humanos
Imuno-Histoquímica
Meia-Idade
Prevalência
Prognóstico
Tailândia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 6.5.1.- (DNA Repair Enzymes)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170927
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317725834


  9 / 2116 MEDLINE  
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[PMID]:28934474
[Au] Autor:Liu D; Frederiksen JH; Liberti SE; Lützen A; Keijzers G; Pena-Diaz J; Rasmussen LJ
[Ad] Endereço:Center for Healthy Aging, University of Copenhagen, Denmark.
[Ti] Título:Human DNA polymerase delta double-mutant D316A;E318A interferes with DNA mismatch repair in vitro.
[So] Source:Nucleic Acids Res;45(16):9427-9440, 2017 Sep 19.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:DNA mismatch repair (MMR) is a highly-conserved DNA repair mechanism, whose primary role is to remove DNA replication errors preventing them from manifesting as mutations, thereby increasing the overall genome stability. Defects in MMR are associated with increased cancer risk in humans and other organisms. Here, we characterize the interaction between MMR and a proofreading-deficient allele of the human replicative DNA polymerase delta, PolδD316A;E318A, which has a higher capacity for strand displacement DNA synthesis than wild type Polδ. Human cell lines overexpressing PolδD316A;E318A display a mild mutator phenotype, while nuclear extracts of these cells exhibit reduced MMR activity in vitro, and these defects are complemented by overexpression or addition of exogenous human Exonuclease 1 (EXO1). By contrast, another proofreading-deficient mutant, PolδD515V, which has a weaker strand displacement activity, does not decrease the MMR activity as significantly as PolδD316A;E318A. In addition, PolδD515V does not increase the mutation frequency in MMR-proficient cells. Based on our findings, we propose that the proofreading activity restricts the strand displacement activity of Polδ in MMR. This contributes to maintain the nicks required for EXO1 entry, and in this manner ensures the dominance of the EXO1-dependent MMR pathway.
[Mh] Termos MeSH primário: Reparo de Erro de Pareamento de DNA
DNA Polimerase III/metabolismo
Mutação
[Mh] Termos MeSH secundário: Metilação de DNA/efeitos dos fármacos
DNA Polimerase III/genética
Enzimas Reparadoras do DNA/genética
Enzimas Reparadoras do DNA/metabolismo
Exodesoxirribonucleases/genética
Exodesoxirribonucleases/metabolismo
Células HeLa
Seres Humanos
Metilnitronitrosoguanidina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
12H3O2UGSF (Methylnitronitrosoguanidine); EC 2.7.7.- (DNA Polymerase III); EC 3.1.- (EXO1 protein, human); EC 3.1.- (Exodeoxyribonucleases); EC 6.5.1.- (DNA Repair Enzymes)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx611


  10 / 2116 MEDLINE  
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[PMID]:28927527
[Au] Autor:Liu D; Keijzers G; Rasmussen LJ
[Ad] Endereço:Department of Cellular and Molecular Medicine, Center for Healthy Aging, University of Copenhagen, Copenhagen, Denmark.
[Ti] Título:DNA mismatch repair and its many roles in eukaryotic cells.
[So] Source:Mutat Res;773:174-187, 2017 Jul.
[Is] ISSN:1873-135X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:DNA mismatch repair (MMR) is an important DNA repair pathway that plays critical roles in DNA replication fidelity, mutation avoidance and genome stability, all of which contribute significantly to the viability of cells and organisms. MMR is widely-used as a diagnostic biomarker for human cancers in the clinic, and as a biomarker of cancer susceptibility in animal model systems. Prokaryotic MMR is well-characterized at the molecular and mechanistic level; however, MMR is considerably more complex in eukaryotic cells than in prokaryotic cells, and in recent years, it has become evident that MMR plays novel roles in eukaryotic cells, several of which are not yet well-defined or understood. Many MMR-deficient human cancer cells lack mutations in known human MMR genes, which strongly suggests that essential eukaryotic MMR components/cofactors remain unidentified and uncharacterized. Furthermore, the mechanism by which the eukaryotic MMR machinery discriminates between the parental (template) and the daughter (nascent) DNA strand is incompletely understood and how cells choose between the EXO1-dependent and the EXO1-independent subpathways of MMR is not known. This review summarizes recent literature on eukaryotic MMR, with emphasis on the diverse cellular roles of eukaryotic MMR proteins, the mechanism of strand discrimination and cross-talk/interactions between and co-regulation of MMR and other DNA repair pathways in eukaryotic cells. The main conclusion of the review is that MMR proteins contribute to genome stability through their ability to recognize and promote an appropriate cellular response to aberrant DNA structures, especially when they arise during DNA replication. Although the molecular mechanism of MMR in the eukaryotic cell is still not completely understood, increased used of single-molecule analyses in the future may yield new insight into these unsolved questions.
[Mh] Termos MeSH primário: Reparo de Erro de Pareamento de DNA
Células Eucarióticas/metabolismo
[Mh] Termos MeSH secundário: Animais
Replicação do DNA
Instabilidade Genômica
Seres Humanos
Mutação
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE



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