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[PMID]:29505541
[Au] Autor:Noh HM; Yoo JH; Jeong JY; Park YS
[Ad] Endereço:Department of Family Medicine, Hallym University Sacred Heart Hospital, Hallym University College of Medicine, Anyang.
[Ti] Título:Bone mineral density after treatment for gastric cancer: Endoscopic treatment versus gastrectomy.
[So] Source:Medicine (Baltimore);97(1):e9582, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Changes in bone metabolism among gastric cancer survivors have long been recognized. The aim of our study was to clarify the changes of bone mineral density (BMD) among gastric cancer survivors who underwent endoscopic resection or gastrectomy. Forty-nine patients diagnosed with tumor, node, and metastasis (TNM) stage 1 gastric cancer with pathologic confirmation, who underwent BMD measurement just before the procedure, and had no prior osteoporosis treatment, were studied. BMD was measured with dual energy x-ray absorptiometry before and after treatment. Laboratory tests were performed using fresh serum, and serum levels of alkaline phosphatase, albumin, calcium, and phosphorus were measured. We used a nested case-control design to compare groups. Of the 49 patients, 34 underwent gastrectomy and 15 underwent endoscopic treatment. There were no differences in baseline clinical characteristics, including BMD, and biochemical data between groups. The mean and median follow-up intervals for BMD measurement were 32.6 months (standard deviation, 16.5) and 31.0 months (interquartile range: 21.5, 41.0), respectively. The follow-up BMDs of the femoral neck and total hip were lower in the gastrectomy group (P = .010 and .011, respectively). The percentage changes in BMD for the lumbar spine, femoral neck, and total hip were -3.30%, -1.52%, and 0.40%, respectively, in the endoscopic treatment group, and -7.17%, -6.30%, and -3.49%, respectively, in the gastrectomy group. Bone loss of the lumbar spine and femoral neck were greater in the gastrectomy group (P = .028 and .022, respectively). BMD is lower after gastrectomy than after endoscopic treatment among early stage gastric cancer survivors.
[Mh] Termos MeSH primário: Adenocarcinoma/cirurgia
Densidade Óssea
Gastrectomia
Gastroscopia
Neoplasias Gástricas/cirurgia
[Mh] Termos MeSH secundário: Adenocarcinoma/metabolismo
Adulto
Idoso
Osso e Ossos/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
Estudos Retrospectivos
Neoplasias Gástricas/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180306
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009582


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[PMID]:29441968
[Au] Autor:Li X; Liang J; Liu YX; Wang Y; Yang XH; Luan BH; Zhang GL; Du J; Wu XH
[Ti] Título:miR-149 reverses cisplatin resistance of gastric cancer SGC7901/DDP cells by targeting FoxM1.
[So] Source:Pharmazie;71(11):640-643, 2016 11 02.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Drug resistance remains a major unresolved obstacle for gastric cancer (GC) treatment. Recently, increasing studies have showen that microRNAs (miRNAs) are involved in cancer chemotherapeutic resistance and can potentially be applied to reverse drug resistance in cancers. The relationship between miRNA-149 expression and cisplatin (DDP) resistance in GC cells is still unknown. Here, we detected miR-149 expression by using RT-PCR and found that expression of miR-149 was downregulated in SGC7901/DDP cells compared with SGC7901cells, indicating a role of miR-149 in determining cisplatin-resistance of GC cells. Then, SGC7901/DDP cells were tansfected with miR-149 mimics, MTT assay was performed to determine SGC7901/DDP cell viability, and showed that overexpression of miR-149 inhibited the cell viability after cisplatin treatment, suggesting that up-regulation of miR-149 enhanced SGC7901/DDP cell sensitivity to cisplatin. Furthermore, we confirmed that Forkhead box M1 (FoxM1) is a direct target of miR-149 in SGC7901/DDP cells by using luciferase reporter assay. Besides, we also demonstrated that miR-149 enhances SGC7901/DDP cell sensitivity to cisplatin by downregulating FoxM1 expression. In summary, our data provide new insights that miR-149 plays an important role in determining sensitivity of cisplatin-resistant GC cells by targeting FoxM1 and suggest that miR-149 could be a potential target for reversing drug resistance in GC.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Cisplatino/farmacologia
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Proteína Forkhead Box M1/efeitos dos fármacos
MicroRNAs/farmacologia
Neoplasias Gástricas/tratamento farmacológico
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas/genética
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Marcação de Genes
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Antineoplastic Agents); 0 (FOXM1 protein, human); 0 (Forkhead Box Protein M1); 0 (MIRN149 microRNA, human); 0 (MicroRNAs); Q20Q21Q62J (Cisplatin)
[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:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6696


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[PMID]:29442033
[Au] Autor:Xia M; Wei J; Tong K
[Ti] Título:MiR-224 promotes proliferation and migration of gastric cancer cells through targeting PAK4.
[So] Source:Pharmazie;71(8):460-464, 2016 Aug 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Although recent studies have shown the important role and overexpression of miR-224 in several tumors, its function in gastric cancer has not yet been defined. In the present study, we tried to confirm the result of microRNAs microarray and further investigated the functions of miR-224 in gastric cancer, and tried to find new downstream targets of miR-224. In this study, the level of miR-224 was measured in gastric cancer cells with the normal human gastric epithelial cell. The effects of miR-224 of on proliferation, migration, and target protein expression were evaluated by CCK8 assay, colony assay, transwell migration assay, western blotting. In addition, luciferase reporter plasmid was constructed to demonstrate the direct target of miR-224. Overexpression of miR-224 was detected in the gastric cancer cells, especially in SCG-7901. Exogenous miR-224 expression promoted the proliferation and migration of gastric cells and abrogating expression of miR-224 suppressed proliferation, and migration of SCG-7901 cells in vitro. Luciferase assays revealed that miR-224 directly targeted the 3'UTR of p21-activated kinase 4 (PAK4). The present study provides an experimental foundation for miR-224 as a potential tumor suppressor that may decrease PAK4 expression to inhibit gastric cancer cells and that in the future, targeting of this miRNA may provide a novel strategy for the diagnosis and treatment of patients with this lethal disease.
[Mh] Termos MeSH primário: Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
MicroRNAs/uso terapêutico
Neoplasias Gástricas/patologia
Quinases Ativadas por p21/efeitos dos fármacos
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Células Epiteliais/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica
Genes Reporter/genética
Seres Humanos
MicroRNAs/genética
MicroRNAs/farmacologia
Plasmídeos/genética
Regulação para Cima
Cicatrização/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN224 microRNA, human); 0 (MicroRNAs); EC 2.7.1.11 (PAK4 protein, human); EC 2.7.11.1 (p21-Activated Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6580


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[PMID]:28453696
[Au] Autor:Böger C; Krüger S; Behrens HM; Bock S; Haag J; Kalthoff H; Röcken C
[Ad] Endereço:Department of Pathology, Christian-Albrechts-University, Kiel, Germany
[Ti] Título:Epstein-Barr virus-associated gastric cancer reveals intratumoral heterogeneity of PIK3CA mutations.
[So] Source:Ann Oncol;28(5):1005-1014, 2017 05 01.
[Is] ISSN:1569-8041
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Background: Recent whole-genome sequencing identified four molecular subtypes of gastric cancer (GC), of which the subgroup of Epstein-Barr virus-associated GC (EBVaGC) showed a significant enrichment of PIK3CA mutations. We here aimed to validate independently the enrichment of PIK3CA mutations in EBVaGC of a Central European GC cohort, to correlate EBV status with clinico-pathological patient characteristics and to test for a major issue of GC, intratumoral heterogeneity. Patients and methods: In a first step, 484 GCs were screened for EBV and PIK3CA hot spot mutations of exon 9/20 using EBER in situ hybridization and pyrosequencing, respectively. Secondly, an extended sequencing of PIK3CA also utilizing next generation sequencing was carried out in all EBVaGCs and 96 corresponding lymph node metastases. Results: Twenty-two GCs were EBER-positive, all being of latency type I. Intratumoral heterogeneity of EBER-positivity was found in 18% of EBVaGCs. Twenty-three GCs held PIK3CA mutations in hot spot regions of exon 9 or 20, being significantly more common in EBVaGCs (P < 0.001). Subsequent extended sequencing of PIK3CA of EBVaGCs showed that 14% harvested three to five different PIK3CA genotypes (including wildtype) in the same primary tumor, albeit in histologically and spatially distinct tumor areas, and that intratumoral heterogeneity of PIK3CA was also present in the corresponding lymph node metastases. Conclusions: Our findings unravel issues of tumor heterogeneity and illustrate that the assessment of the EBV status in tissue biopsies might carry the risk of sampling errors, which may significantly hamper adequate molecular tumor classification in a more clinical setting. Moreover, this is the first report of intratumoral heterogeneity of PIK3CA mutations in GC, and our findings lead to the conclusion that PIK3CA mutant and -wildtype tumor subclones are skilled to metastasize independently to different regional lymph nodes.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Classe I de Fosfatidilinositol 3-Quinases/genética
Infecções por Vírus Epstein-Barr/genética
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/mortalidade
Adenocarcinoma/secundário
Adenocarcinoma/virologia
Idoso
Infecções por Vírus Epstein-Barr/mortalidade
Infecções por Vírus Epstein-Barr/patologia
Infecções por Vírus Epstein-Barr/virologia
Feminino
Frequência do Gene
Estudos de Associação Genética
Heterogeneidade Genética
Predisposição Genética para Doença
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Estimativa de Kaplan-Meier
Metástase Linfática
Masculino
Técnicas de Diagnóstico Molecular
Mutação
Neoplasias Gástricas/mortalidade
Neoplasias Gástricas/patologia
Neoplasias Gástricas/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.1.137 (Class I Phosphatidylinositol 3-Kinases); EC 2.7.1.137 (PIK3CA protein, human)
[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:170429
[St] Status:MEDLINE
[do] DOI:10.1093/annonc/mdx047


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[PMID]:29397592
[Au] Autor:National Clinical Research Center for Digestive Disease of China; Chinese Society of Digestive Endoscopy; Chinese Association of Endoscopologist, Gastroenterologist & Hepatologist
[Ti] Título:[Clinical guidelines for perioperative management of gastric endoscopic submucosal dissection].
[So] Source:Zhonghua Nei Ke Za Zhi;57(2):84-96, 2018 Feb 01.
[Is] ISSN:0578-1426
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Gastric cancer has become one of the important public health issues endangering people's health in China. Currently, endoscopic submucosal dissection (ESD) has been used as the curative procedure of early gastric cancer without lymph node metastasis. Endoscopic resection has several advantages, including less invasiveness, permitting en bloc, histologically completed resection, accurate pathological diagnosis, lower recurrent rate and rapid recovery. The perioperative period of ESD is the time of a patient's endoscopic operative procedure; more specifically, it includes ward admission, indication, contraindication, preoperative preparation, endoscopic operation, postoperative complications, recovery and the disposal of specimen. The aim of this guideline is to assist endoscopists in providing standardized operation to patients, as well as managing perioperative complications.
[Mh] Termos MeSH primário: Ressecção Endoscópica de Mucosa
Mucosa Gástrica/cirurgia
Guias de Prática Clínica como Assunto
Neoplasias Gástricas/diagnóstico
Neoplasias Gástricas/cirurgia
[Mh] Termos MeSH secundário: China
Detecção Precoce de Câncer
Endoscopia
Seres Humanos
Metástase Linfática
Complicações Pós-Operatórias
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180206
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0578-1426.2018.02.002


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[PMID]:29378685
[Au] Autor:Khin MO; Bromham N; Harrison M; Eadon H; Guideline Committee
[Ad] Endereço:National Guideline Alliance, Royal College of Obstetricians and Gynaecologists, London NW1 4RG, UK.
[Ti] Título:Assessment and management of oesophago-gastric cancer: summary of NICE guidance.
[So] Source:BMJ;360:k213, 2018 01 29.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Neoplasias Esofágicas/diagnóstico
Neoplasias Esofágicas/terapia
Guias de Prática Clínica como Assunto
Neoplasias Gástricas/diagnóstico
Neoplasias Gástricas/terapia
[Mh] Termos MeSH secundário: Gerenciamento Clínico
Seres Humanos
Avaliação de Sintomas/normas
Reino Unido
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.k213


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[PMID]:29305865
[Au] Autor:Yin K; Dang S; Cui L; Fan X; Xie R; Qu J; Shang M; Chen J
[Ad] Endereço:Department of General Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu, China.
[Ti] Título:Netrin-1 promotes metastasis of gastric cancer by regulating YAP activity.
[So] Source:Biochem Biophys Res Commun;496(1):76-82, 2018 01 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Yes-associated protein (YAP) is a major downstream molecular of the Hippo pathway, which plays important role in cancer development. Netrin-1 conveys oncogenic activity in many types of malignant tumors. However, the downstream signaling of netrin-1 mediating its oncogenic effects in gastric cancer (GC) is not well defined. Here, we aim to investigate the role of netrin-1 in metastasis potential of GC by regulating YAP. In this study, we showed that netrin-1 inhibition significantly decreased migration and invasion abilities of GC cells, while netrin-1 overexpression effectively reversed this effect. We also demonstrated that netrin-1 upregulated YAP expression via its transmembrane receptor neogenin. Furthermore, our in vitro and in vivo results showed that the effect of netrin-1 on GC cells migration and invasion abilities was regulated by YAP. Collectively, our results defined netrin-1 as a positive regulator of malignant tumor metastasis in GC by activating the YAP signaling, with potential implications for new approaches to GC therapy.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Regulação Neoplásica da Expressão Gênica
Netrina-1/metabolismo
Fosfoproteínas/metabolismo
Neoplasias Gástricas/metabolismo
Neoplasias Gástricas/patologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Invasividade Neoplásica
Metástase Neoplásica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (NTN1 protein, human); 0 (Phosphoproteins); 0 (YAP1 (Yes-associated) protein, human); 158651-98-0 (Netrin-1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE


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[PMID]:28460635
[Au] Autor:Chen I; Mathews-Greiner L; Li D; Abisoye-Ogunniyan A; Ray S; Bian Y; Shukla V; Zhang X; Guha R; Thomas C; Gryder B; Zacharia A; Beane JD; Ravichandran S; Ferrer M; Rudloff U
[Ad] Endereço:Thoracic and Gastrointestinal Oncology Branch, National Cancer Institute, National Institutes for Health, CCR 4 West/4-3740, 10 Center Drive, Bethesda, MD, 20892-0001, USA.
[Ti] Título:Transcriptomic profiling and quantitative high-throughput (qHTS) drug screening of CDH1 deficient hereditary diffuse gastric cancer (HDGC) cells identify treatment leads for familial gastric cancer.
[So] Source:J Transl Med;15(1):92, 2017 May 01.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Patients with hereditary diffuse gastric cancer (HDGC), a cancer predisposition syndrome associated with germline mutations of the CDH1 (E-cadherin) gene, have few effective treatment options. Despite marked differences in natural history, histopathology, and genetic profile to patients afflicted by sporadic gastric cancer, patients with HDGC receive, in large, identical systemic regimens. The lack of a robust preclinical in vitro system suitable for effective drug screening has been one of the obstacles to date which has hampered therapeutic advances in this rare disease. METHODS: In order to identify therapeutic leads selective for the HDGC subtype of gastric cancer, we compared gene expression profiles and drug phenotype derived from an oncology library of 1912 compounds between gastric cancer cells established from a patient with metastatic HDGC harboring a c.1380delA CDH1 germline variant and sporadic gastric cancer cells. RESULTS: Unsupervised hierarchical cluster analysis shows select gene expression alterations in c.1380delA CDH1 SB.mhdgc-1 cells compared to a panel of sporadic gastric cancer cell lines with enrichment of ERK1-ERK2 (extracellular signal regulated kinase) and IP3 (inositol trisphosphate)/DAG (diacylglycerol) signaling as the top networks in c.1380delA SB.mhdgc-1 cells. Intracellular phosphatidylinositol intermediaries were increased upon direct measure in c.1380delA CDH1 SB.mhdgc-1 cells. Differential high-throughput drug screening of c.1380delA CDH1 SB.mhdgc-1 versus sporadic gastric cancer cells identified several compound classes with enriched activity in c.1380 CDH1 SB.mhdgc-1 cells including mTOR (Mammalian Target Of Rapamycin), MEK (Mitogen-Activated Protein Kinase), c-Src kinase, FAK (Focal Adhesion Kinase), PKC (Protein Kinase C), or TOPO2 (Topoisomerase II) inhibitors. Upon additional drug response testing, dual PI3K (Phosphatidylinositol 3-Kinase)/mTOR and topoisomerase 2A inhibitors displayed up to >100-fold increased activity in hereditary c.1380delA CDH1 gastric cancer cells inducing apoptosis most effectively in cells with deficient CDH1 function. CONCLUSION: Integrated pharmacological and transcriptomic profiling of hereditary diffuse gastric cancer cells with a loss-of-function c.1380delA CDH1 mutation implies various pharmacological vulnerabilities selective to CDH1-deficient familial gastric cancer cells and suggests novel treatment leads for future preclinical and clinical treatment studies of familial gastric cancer.
[Mh] Termos MeSH primário: Caderinas/deficiência
Avaliação Pré-Clínica de Medicamentos
Perfilação da Expressão Gênica
Ensaios de Triagem em Larga Escala
Neoplasias Gástricas/tratamento farmacológico
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Adulto
Caderinas/genética
Linhagem Celular Tumoral
Diglicerídeos/metabolismo
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica
Predisposição Genética para Doença
Mutação em Linhagem Germinativa/genética
Seres Humanos
Fosfatos de Inositol/metabolismo
Masculino
Linhagem
Reprodutibilidade dos Testes
Neoplasias Gástricas/patologia
Regulação para Cima/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDH1 protein, human); 0 (Cadherins); 0 (Diglycerides); 0 (Inositol Phosphates); 0 (inositol 3,4,5-trisphosphate); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[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:10.1186/s12967-017-1197-5


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[PMID]:28460479
[Au] Autor:Xie S; Zhang H; Wang X; Ge Q; Hu J
[Ad] Endereço:Department of Gastroenterology, Huaihe Hospital of Henan University, Kaifeng, Henan, 475000, China.
[Ti] Título:The relative efficacy and safety of targeted agents used in combination with chemotherapy in treating patients with untreated advanced gastric cancer: a network meta-analysis.
[So] Source:Oncotarget;8(16):26959-26968, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gastric cancer is one of the leading mortal causes. Targeted therapy is a new type of cancer treatment, which precisely identifies and attacks cancer cells and significantly reduces side effects. In this network meta-analysis, we focused on the efficacy and safety of 12 targeted agents on gastric cancer among a total of 8,405 patients from 24 trials. Hazard ratio (HR) with 95% credible interval (CrI) were calculated for primary outcomes, including overall survival (OS) and progression-free survival (PFS), while odds ratio (OR) with 95% CrI were calculated for secondary outcomes. Surface under the cumulative ranking curve (SUCRA) were calculated to illustrate the rank probability of various agents for different outcomes. Compared with other analyzed treatments, ramucirumab is outstanding in survival outcomes. However, higher risk of hematological events should be noted during its application. Lapatinib is also efficacious in progression reduction, while it is always combined with severe gastrointestinal events. Trastuzumab is proposed for its high efficacy in improving survival rate and safety, which is proper for most patients. In conclusion, trastuzumab was recommended as the optimal targeted agent combined with chemotherapy for gastric cancer patients.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Terapia de Alvo Molecular
Neoplasias Gástricas/tratamento farmacológico
Neoplasias Gástricas/patologia
[Mh] Termos MeSH secundário: Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Seres Humanos
Metástase Neoplásica
Estadiamento de Neoplasias
Metanálise em Rede
Razão de Chances
Modelos de Riscos Proporcionais
Neoplasias Gástricas/mortalidade
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[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.15923


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[PMID]:28460431
[Au] Autor:Du J; Wu X; Tong X; Wang X; Wei J; Yang Y; Chang Z; Mao Y; Shao YW; Liu B
[Ad] Endereço:The Comprehensive Cancer Centre of Drum Tower Hospital, Medical School of Nanjing University, Clinical Cancer Institute of Nanjing University, Nanjing, Jiangsu, 210008, China.
[Ti] Título:Circulating tumor DNA profiling by next generation sequencing reveals heterogeneity of crizotinib resistance mechanisms in a gastric cancer patient with MET amplification.
[So] Source:Oncotarget;8(16):26281-26287, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Crizotinib has been used to counter MET gene amplification in a number of different human malignancies. Transient response to crizotinib in MET-amplified gastric cancer has been reported, but the mechanisms of resistance are not well studied. Here, we reported a stage IV gastric cancer patient with high levels of MET amplification. The implementation of crizotinib treatment led to significant symptomatic improvement in the first 2 months, but was followed by rapid disease progression. Periodic mutation profiling of patient's circulating tumor DNA (ctDNA) by next generation sequencing (NGS) revealed a number of genetic alterations including re-occurrence of MET amplification, multiple secondary MET mutations, a dramatic increase of FGFR2 gene relative copy number as well as mutations in other downstream and bypassing elements, which may collectively related to the patient's cancer progression. Our results illustrate the complex and heterogeneous molecular mechanisms for crizotinib resistance in this patient, and demonstrate the great potential of ctDNA profiling for treatment decision-making and prognosis in clinical practice.
[Mh] Termos MeSH primário: DNA Tumoral Circulante
Resistência a Medicamentos Antineoplásicos/genética
Amplificação de Genes
Proteínas Proto-Oncogênicas c-met/genética
Pirazóis/farmacologia
Piridinas/farmacologia
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Adulto
Linhagem Celular Tumoral
Feminino
Perfilação da Expressão Gênica
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Modelos Biológicos
Modelos Moleculares
Mutação
Estadiamento de Neoplasias
Tomografia Computadorizada com Tomografia por Emissão de Pósitrons
Conformação Proteica
Inibidores de Proteínas Quinases/farmacologia
Inibidores de Proteínas Quinases/uso terapêutico
Proteínas Proto-Oncogênicas c-met/química
Pirazóis/uso terapêutico
Piridinas/uso terapêutico
Neoplasias Gástricas/diagnóstico
Neoplasias Gástricas/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Circulating Tumor DNA); 0 (Protein Kinase Inhibitors); 0 (Pyrazoles); 0 (Pyridines); 53AH36668S (crizotinib); EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
[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.15457



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