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[PMID]:28455969
[Au] Autor:Wang MH; Zhou XM; Zhang MY; Shi L; Xiao RW; Zeng LS; Yang XZ; Zheng XFS; Wang HY; Mai SJ
[Ad] Endereço:State Key Laboratory of Oncology in South China, Guangzhou, 510060, China.
[Ti] Título:BMP2 promotes proliferation and invasion of nasopharyngeal carcinoma cells via mTORC1 pathway.
[So] Source:Aging (Albany NY);9(4):1326-1340, 2017 Apr.
[Is] ISSN:1945-4589
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone morphogenetic protein-2 (BMP2) is a secreted protein that highly expressed in a variety of cancers and contributes to cell proliferation, migration, invasiveness, mobility, metastasis and EMT. However, its clinical significance and biological function in nasopharyngeal carcinoma (NPC) remain unknown up to now. Up-regulation of BMP2 was first observed in NPC cell lines by a genome-wide transcriptome analysis in our previous study. In this study, BMP2 mRNA was detected by qRT-PCR and data showed that it was upregulated in NPC compared with non-cancerous nasopharynx samples. Immunohistochemistry (IHC) analysis in NPC specimens revealed that high BMP2 expression was significantly associated with clinical stage, distant metastasis and shorter survival of NPC patients. Moreover, overexpression of BMP2 in NPC cells promoted cell proliferation, migration, invasiveness and epithelial-mesenchymal transition (EMT). Mechanistically, BMP2 overexpression increase phosphorylated protein level of mTOR, S6K and 4EBP1. Correspondingly, mTORC1 inhibitor rapamycin blocked the effect of BMP2 on NPC cell proliferation and invasion. In conclusion, our results suggest that BMP2 overexpression in NPC enhances proliferation, invasion and EMT of tumor cells through the mTORC1 signaling pathway.
[Mh] Termos MeSH primário: Proteína Morfogenética Óssea 2/farmacologia
Proliferação Celular/efeitos dos fármacos
Alvo Mecanístico do Complexo 1 de Rapamicina/efeitos dos fármacos
Neoplasias Nasofaríngeas/patologia
Invasividade Neoplásica/patologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica
Estudo de Associação Genômica Ampla
Seres Humanos
Alvo Mecanístico do Complexo 1 de Rapamicina/genética
Neoplasias Nasofaríngeas/genética
Metástase Neoplásica
RNA Mensageiro/biossíntese
RNA Mensageiro/genética
Receptores da Colecistocinina/biossíntese
Transdução de Sinais/efeitos dos fármacos
Transcriptoma/genética
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Protein 2); 0 (RNA, Messenger); 0 (Receptors, Cholecystokinin); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.18632/aging.101230


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[PMID]:28592602
[Au] Autor:Desai AJ; Dong M; Langlais BT; Dueck AC; Miller LJ
[Ad] Endereço:Department of Molecular Pharmacology and Experimental Therapeutics and.
[Ti] Título:Cholecystokinin responsiveness varies across the population dependent on metabolic phenotype.
[So] Source:Am J Clin Nutr;106(2):447-456, 2017 Aug.
[Is] ISSN:1938-3207
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cholecystokinin (CCK) is an important satiety factor, acting at type 1 receptors (CCK1Rs) on vagal afferent neurons; however, CCK agonists have failed clinical trials for obesity. We postulated that CCK1R function might be defective in such patients due to abnormal membrane composition, such as that observed in cholesterol gallstone disease. Due to the challenges in directly studying CCK1Rs relevant to appetite control, our goal was to develop and apply a method to determine the impact of a patient's own cellular environment on CCK stimulus-activity coupling and to determine whether CCK sensitivity correlated with the metabolic phenotype of a high-risk population. Wild-type CCK1Rs were expressed on leukocytes from 112 Hispanic patients by using adenoviral transduction and 24-h culture, with quantitation of cholesterol composition and intracellular calcium responses to CCK. Results were correlated with clinical, biochemical, and morphometric characteristics. Broad ranges of cellular cholesterol and CCK responsiveness were observed, with elevated cholesterol correlated with reduced CCK sensitivity. This was prominent with increasing degrees of obesity and the presence of diabetes, particularly when poorly controlled. No single standard clinical metric correlated directly with CCK responsiveness. Reduced CCK sensitivity best correlated with elevated serum triglycerides in normal-weight participants and with low HDL concentrations and elevated glycated hemoglobin in obese and diabetic patients. CCK responsiveness varies widely across the population, with reduced signaling in patients with obesity and diabetes. This could explain the failure of CCK agonists in previous clinical trials and supports the rationale to develop corrective modulators to reverse this defective servomechanism for appetite control. This trial was registered at www.clinicaltrials.gov as NCT03121755.
[Mh] Termos MeSH primário: Regulação do Apetite/efeitos dos fármacos
Glicemia/metabolismo
Colecistocinina/metabolismo
Diabetes Mellitus/metabolismo
Lipídeos/sangue
Obesidade/metabolismo
Receptores da Colecistocinina/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Fármacos Antiobesidade/farmacologia
Colecistocinina/agonistas
HDL-Colesterol/sangue
Diabetes Mellitus/sangue
Diabetes Mellitus/tratamento farmacológico
Feminino
Hemoglobinas/metabolismo
Seres Humanos
Hipoglicemiantes/farmacologia
Masculino
Meia-Idade
Obesidade/sangue
Obesidade/tratamento farmacológico
Fenótipo
Valores de Referência
Saciação/fisiologia
Transdução de Sinais
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Obesity Agents); 0 (Blood Glucose); 0 (Cholesterol, HDL); 0 (Hemoglobins); 0 (Hypoglycemic Agents); 0 (Lipids); 0 (Receptors, Cholecystokinin); 0 (Triglycerides); 9011-97-6 (Cholecystokinin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.3945/ajcn.117.156943


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[PMID]:28186337
[Au] Autor:Wang HH; Liu M; Li X; Portincasa P; Wang DQ
[Ad] Endereço:Division of Gastroenterology and Hepatology, Department of Internal Medicine, Saint Louis University School of Medicine, St. Louis, MO, USA.
[Ti] Título:Impaired intestinal cholecystokinin secretion, a fascinating but overlooked link between coeliac disease and cholesterol gallstone disease.
[So] Source:Eur J Clin Invest;47(4):328-333, 2017 Apr.
[Is] ISSN:1365-2362
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Coeliac disease is a chronic, small intestinal, immune-mediated enteropathy caused by a permanent intolerance to dietary gluten in genetically predisposed individuals. Clinical studies have found that intestinal cholecystokinin secretion and gallbladder emptying in response to a fatty meal are impaired before coeliac patients start the gluten-free diet (GFD). DESIGN: However, it was never really appreciated whether coeliac disease is associated with gallstones because there were very few studies investigating the mechanism underlying the impact of coeliac disease on the pathogenesis of gallstones. RESULTS: We summarize recent progress on the relationship between coeliac disease and gallstones and propose that coeliac disease is an important risk factor for gallstone formation because defective intestinal cholecystokinin secretion markedly increases susceptibility to cholesterol gallstones via a mechanism involving dysmotility of both the gallbladder and the small intestine. Because GFD can significantly improve the coeliac enteropathy, early diagnosis and therapy in coeliac patients is crucial for preventing the long-term impact of cholecystokinin deficiency on the biliary and intestinal consequences. When gluten is reintroduced, clinical and histologic relapse often occurs in coeliac patients. Moreover, some of the coeliac patients do not respond well to GFD. CONCLUSIONS: It is imperative to routinely examine by ultrasonography whether gallbladder motility function is preserved in coeliac patients and monitor whether biliary sludge (a precursor of gallstones) appears in the gallbladder, regardless of whether they are under the GFD programme. To prevent gallstones in coeliac patients, it is urgently needed to investigate the prevalence and pathogenesis of gallstones in these patients.
[Mh] Termos MeSH primário: Doença Celíaca/complicações
Colecistocinina/secreção
Cálculos Biliares/etiologia
[Mh] Termos MeSH secundário: Animais
Doença Celíaca/metabolismo
Modelos Animais de Doenças
Previsões
Esvaziamento da Vesícula Biliar/fisiologia
Cálculos Biliares/metabolismo
Seres Humanos
Intestino Delgado/secreção
Camundongos Knockout
Receptores da Colecistocinina/agonistas
Receptores da Colecistocinina/metabolismo
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Cholecystokinin); 9011-97-6 (Cholecystokinin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170211
[St] Status:MEDLINE
[do] DOI:10.1111/eci.12734


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[PMID]:27931080
[Au] Autor:Carbone F; Oliveira PJ; Bonaventura A; Montecucco F
[Ad] Endereço:Department of Internal Medicine, First Clinic of Internal Medicine, University of Genoa, Genoa, Italy.
[Ti] Título:The pathophysiological role of cholecystokinin-1 receptor in mouse cholelithogenesis.
[So] Source:Eur J Clin Invest;47(2):195-196, 2017 02.
[Is] ISSN:1365-2362
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Colecistocinina
Receptores da Colecistocinina
[Mh] Termos MeSH secundário: Animais
Camundongos
Receptor de Colecistocinina A
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (Receptor, Cholecystokinin A); 0 (Receptors, Cholecystokinin); 9011-97-6 (Cholecystokinin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161209
[St] Status:MEDLINE
[do] DOI:10.1111/eci.12713


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[PMID]:27885812
[Au] Autor:Oehlers SH; Flores MV; Hall CJ; Wang L; Ko DC; Crosier KE; Crosier PS
[Ad] Endereço:Department of Molecular Medicine and Pathology, School of Medical Sciences, University of Auckland, New Zealand.
[Ti] Título:A whole animal chemical screen approach to identify modifiers of intestinal neutrophilic inflammation.
[So] Source:FEBS J;284(3):402-413, 2017 Feb.
[Is] ISSN:1742-4658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:By performing two high-content small molecule screens on dextran sodium sulfate- and trinitrobenzene sulfonic acid-induced zebrafish enterocolitis models of inflammatory bowel disease, we have identified novel anti-inflammatory drugs from the John Hopkins Clinical Compound Library that suppress neutrophilic inflammation. Live imaging of neutrophil distribution was used to assess the level of acute inflammation and concurrently screen for off-target drug effects. Supporting the validity of our screening strategy, most of the anti-inflammatory drug hits were known antibiotics or anti-inflammatory agents. Novel hits included cholecystokinin (CCK) and dopamine receptor agonists. Using a pharmacological approach, we show that while CCK and dopamine receptor agonists alleviate enterocolitis-associated inflammation, receptor antagonists exacerbate inflammation in zebrafish. This work highlights the utility of small molecule screening in zebrafish enterocolitis models as a tool to identify novel bioactive molecules capable of modulating acute inflammation.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Colite Ulcerativa/tratamento farmacológico
Doença de Crohn/tratamento farmacológico
Disbiose/tratamento farmacológico
Ensaios de Triagem em Larga Escala
Fatores Imunológicos/farmacologia
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Colite Ulcerativa/induzido quimicamente
Colite Ulcerativa/imunologia
Colite Ulcerativa/patologia
Doença de Crohn/induzido quimicamente
Doença de Crohn/imunologia
Doença de Crohn/patologia
Sulfato de Dextrana
Modelos Animais de Doenças
Agonistas de Dopamina/farmacologia
Disbiose/induzido quimicamente
Disbiose/imunologia
Disbiose/patologia
Embrião não Mamífero
Expressão Gênica
Seres Humanos
Intestinos/efeitos dos fármacos
Intestinos/imunologia
Intestinos/patologia
Neutrófilos/efeitos dos fármacos
Neutrófilos/imunologia
Neutrófilos/patologia
Receptores da Colecistocinina/agonistas
Receptores da Colecistocinina/genética
Receptores da Colecistocinina/imunologia
Receptores Dopaminérgicos/genética
Receptores Dopaminérgicos/imunologia
Bibliotecas de Moléculas Pequenas/farmacologia
Ácido Trinitrobenzenossulfônico
Peixe-Zebra
[Pt] Tipo de publicação:EDITORIAL
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Dopamine Agonists); 0 (Immunologic Factors); 0 (Receptors, Cholecystokinin); 0 (Receptors, Dopamine); 0 (Small Molecule Libraries); 8T3HQG2ZC4 (Trinitrobenzenesulfonic Acid); 9042-14-2 (Dextran Sulfate)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161126
[St] Status:MEDLINE
[do] DOI:10.1111/febs.13976


  6 / 2971 MEDLINE  
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[PMID]:27546513
[Au] Autor:Li Y; Jiang HN; Cui ZJ
[Ad] Endereço:Institute of Cell Biology, Beijing Normal University, Beijing 100875.
[Ti] Título:[Photodynamic modulation of cellular functions].
[So] Source:Sheng Li Xue Bao;68(4):534-46, 2016 Aug 25.
[Is] ISSN:0371-0874
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Photodynamic action, due to the rather limited lifetime (1 µs) and effective reactive distance of singlet oxygen (< 10 nm), could subcellular-specifically regulate different cellular functions. Photodynamic action could activate permanently cholecystokinin (CCK) 1 receptors, and sensitize or desensitize other G protein-coupled receptors. The emergence in recent years of genetically- encoded protein photosensitisers has enabled more precisely-targeted photodynamic modulation of subcellular organelles and functional proteins. Protein photosensitisers (such as KillerRed, miniSOG or SOPP) expressed on the plasma membrane, mitochondria, lysosomes or endoplasmic reticulum can modulate photodynamically subcellular functions and fine-tune protein activity by targeted photooxidation. With the newly emerged active illumination technique, simultaneous photodynamic action localized at multiple sites is now possible, and the contribution of subcellular regions to the whole cell or individual cells to a cell cluster could be quantitated. Photodynamic action with protein photosensitiser will be a powerful tool for nano-manipulation in cell physiology research.
[Mh] Termos MeSH primário: Luz
[Mh] Termos MeSH secundário: Retículo Endoplasmático
Mitocôndrias
Fármacos Fotossensibilizantes
Receptores da Colecistocinina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Photosensitizing Agents); 0 (Receptors, Cholecystokinin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160823
[St] Status:MEDLINE


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[PMID]:27430985
[Au] Autor:Cho EH; Lim JC; Lee SY; Jung SH
[Ad] Endereço:RI Research Division, Research Reactor Utilization Department, Korea Atomic Energy Research Institute (KAERI), Daejeon 305-353, Republic of Korea. Electronic address: choeh36@kaeri.re.kr.
[Ti] Título:An assessment tumor targeting ability of (177)Lu labeled cyclic CCK analogue peptide by binding with cholecystokinin receptor.
[So] Source:J Pharmacol Sci;131(3):209-14, 2016 Jul.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The cholecystokinin (CCK) receptor is known as a receptor that is overexpressed in many human tumors. The present study was designed to investigate the targeting ability of cyclic CCK analogue in AR42J pancreatic cells. The CCK analogues, DOTA-K(glucose)-Gly-Trp-Nle-Asp-Phe (DOTA-glucose-CCK) and DOTA-Nle-cyclo(Glu-Trp-Nle-Asp-Phe-Lys-NH2) (DOTA-[Nle]-cCCK), were synthesized and radiolabeled with (177)Lu, and competitive binding was evaluated. The binding appearance of synthesized peptide with AR42J cells was evaluated by confocal microscopy. And bio-distribution was performed in AR42J xenografted mice. Synthesized peptides were prepared by a solid phase synthesis method, and their purity was over 98%. DOTA is the chelating agent for (177)Lu-labeling, in which the peptides were radiolabeled with (177)Lu by a high radiolabeling yield. A competitive displacement of (125)I-CCK8 on the AR42J cells revealed that the 50% inhibitory concentration value (IC50) was 12.3 nM of DOTA-glucose-CCK and 1.7 nM of DOTA-[Nle]-cCCK. Radio-labeled peptides were accumulated in AR42J tumor in vivo, and %ID/g of the tumor was 0.4 and 0.9 at 2 h p.i. It was concluded that (177)Lu-DOTA-[Nle]-cCCK has higher binding affinity than (177)Lu-DOTA-glucose-CCK and can be a potential candidate as a targeting modality for a CCK receptor over-expressing tumors.
[Mh] Termos MeSH primário: Colecistocinina/metabolismo
Lutécio/metabolismo
Neoplasias/metabolismo
Peptídeos Cíclicos/metabolismo
Radioisótopos/metabolismo
Receptores da Colecistocinina/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Xenoenxertos
Seres Humanos
Masculino
Camundongos Endogâmicos BALB C
Camundongos Nus
Neoplasias Pancreáticas/patologia
Ligação Proteica
Ensaio Radioligante
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peptides, Cyclic); 0 (Radioisotopes); 0 (Receptors, Cholecystokinin); 5H0DOZ21UJ (Lutetium); 9011-97-6 (Cholecystokinin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170417
[Lr] Data última revisão:
170417
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160720
[St] Status:MEDLINE


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[PMID]:27306028
[Au] Autor:Rehfeld JF
[Ad] Endereço:Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, DK-2100 Copenhagen, Denmark.
[Ti] Título:Cholecystokinin expression in tumors: biogenetic and diagnostic implications.
[So] Source:Future Oncol;12(18):2135-47, 2016 Sep.
[Is] ISSN:1744-8301
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cholecystokinin (CCK) is a classic gut hormone. CCK is also a complex system of peptides expressed in several molecular forms in enteroendocrine I cells, in cerebral and peripheral neurons, in cardiac myocytes and spermatozoa. CCK gene expression has now been found at protein or peptide level in different neuroendocrine tumors; cerebral gliomas and astrocytomas and specific pediatric tumors. Tumor hypersecretion of CCK was recently reported in a patient with a metastatic islet cell tumor and hypercholecystokininemia resulting in a novel tumor syndrome, the cholecystokininoma syndrome. This review presents an overview of the cell-specific biogenesis of CCK peptides, and a description of the CCK expression in tumors and of the cholecystokininoma syndrome. Finally, assays for the diagnosis of CCK-producing tumors are reviewed.
[Mh] Termos MeSH primário: Colecistocinina/genética
Regulação Neoplásica da Expressão Gênica
Neoplasias/genética
[Mh] Termos MeSH secundário: Biomarcadores Tumorais
Proliferação Celular
Colecistocinina/química
Colecistocinina/metabolismo
Seres Humanos
Família Multigênica
Neoplasias/diagnóstico
Prognóstico
Ligação Proteica
Processamento de Proteína Pós-Traducional
Transporte Proteico
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores da Colecistocinina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (RNA, Messenger); 0 (Receptors, Cholecystokinin); 9011-97-6 (Cholecystokinin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160617
[St] Status:MEDLINE
[do] DOI:10.2217/fon-2015-0053


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[PMID]:27072272
[Au] Autor:Rai R; Kim JJ; Tewari M; Shukla HS
[Ad] Endereço:School of Biotechnology, Yeungnam University, Gyeongsan, Gyeongbuk 712-749, Korea; Department of Surgical Oncology, Banaras Hindu University, Varanasi, Uttar Pradesh, India, .
[Ti] Título:Heterogeneous expression of cholecystokinin and gastrin receptor in stomach and pancreatic cancer: An immunohistochemical study.
[So] Source:J Cancer Res Ther;12(1):411-6, 2016 Jan-Mar.
[Is] ISSN:1998-4138
[Cp] País de publicação:India
[La] Idioma:eng
[Ab] Resumo:AIM: Cholecystokinin (CCK) and gastrin (Gs) are a well known trophic factor for the gastrointestinal tract and their trophic effects are shown mainly toward pancreas and stomach, respectively. Though, the exact characterization of CCK and Gs receptors subtype (cholecystokinin type A receptor [CCKAR] and cholecystokinin type B receptor/gastrin receptor [CCKBR/GR]) in stomach cancer (SC) and pancreatic cancer (PC) is still controversial and necessities further validation. SUBJECTS AND METHODS: CCKAR and CCKBR/GR expression was analyzed by immunohistochemistry in 55 SC, 25 benign gastric diseases (BGDs), 38 PC (including periampullary carcinoma), and 10 normal pancreatic tissue. The results were statistically correlated with the patient's clinical history to observe the prognostic significance if any. RESULT: CCKAR expression was detected in 18.2% of SC, 20% of BGD, 65.8% of PC, and 30.0% of normal pancreas tissue samples. The CCKBR/GR expression was detected in 58.2% of SC, 48.0% of BGD, 18.4% of PC, and 60.0% of normal pancreas tissue samples. CCKBR/GR expression was significantly high in well and moderately differentiated SC samples as compared to poorly differentiated samples. CONCLUSION: Our study showed significantly higher expression of CCKAR and down regulation of CCKBR in PC as compared to control while CCKBR/GR was detected in majority of SC samples. Thus, our study suggests that CCK and Gs receptors may have diagnostic and therapeutic implications. However, study need to be validated in significantly bigger sample size and need to be replicated in different cohorts.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/biossíntese
Neoplasias Pancreáticas/genética
Receptor de Colecistocinina B/biossíntese
Receptores da Colecistocinina/biossíntese
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores Tumorais/genética
Colecistocinina/genética
Feminino
Gastrinas/genética
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
Meia-Idade
Pâncreas/patologia
Neoplasias Pancreáticas/patologia
Receptor de Colecistocinina B/genética
Receptores da Colecistocinina/genética
Estômago/patologia
Neoplasias Gástricas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Gastrins); 0 (Receptor, Cholecystokinin B); 0 (Receptors, Cholecystokinin); 9011-97-6 (Cholecystokinin)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160414
[St] Status:MEDLINE
[do] DOI:10.4103/0973-1482.168970


  10 / 2971 MEDLINE  
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[PMID]:26929735
[Au] Autor:Smith JP; Fonkoua LK; Moody TW
[Ad] Endereço:1. Department of Medicine, Georgetown University, Washington, DC, USA.
[Ti] Título:The Role of Gastrin and CCK Receptors in Pancreatic Cancer and other Malignancies.
[So] Source:Int J Biol Sci;12(3):283-91, 2016.
[Is] ISSN:1449-2288
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:The gastrointestinal (GI) peptide gastrin is an important regulator of the release of gastric acid from the stomach parietal cells and it also plays an important role in growth of the gastrointestinal tract. It has become apparent that gastrin and its related peptide cholecystokinin (CCK) are also significantly involved with growth of GI cancers as well as other malignancies through activation of the cholecystokinin-B (CCK-B) receptor. Of interest, gastrin is expressed in the embryologic pancreas but not in the adult pancreas; however, gastrin becomes re-expressed in pancreatic cancer where it stimulates growth of this malignancy by an autocrine mechanism. Strategies to down-regulate gastrin or interfere with its interface with the CCK receptor with selective antibodies or receptor antagonists hold promise for the treatment of pancreatic cancer and other gastrin--responsive tumors.
[Mh] Termos MeSH primário: Gastrinas/metabolismo
Neoplasias Pancreáticas/metabolismo
Receptores da Colecistocinina/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Gastrins); 0 (Receptors, Cholecystokinin)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160302
[St] Status:MEDLINE
[do] DOI:10.7150/ijbs.14952



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