Database : MEDLINE
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[PMID]: 29501692
[Au] Autor:Liang C; Zhang B; Ge H; Xu Y; Li G; Wu J
[Ad] Address:Department of General Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
[Ti] Title:Long non-coding RNA CRNDE as a potential prognostic biomarker in solid tumors: A meta-analysis.
[So] Source:Clin Chim Acta;481:99-107, 2018 Mar 01.
[Is] ISSN:1873-3492
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND AND AIM: Long non-coding RNA colorectal neoplasia differentially expressed (CRNDE) has been demonstrated to be highly expressed in many malignant tumors; however, the role of CRNDE in cancer remains undetermined because of limitations in sample size. We conducted a meta-analysis to assess the role of CRNDE in cancer. METHODS: PubMed, Medline, Cochrane Library, Web of Science, EMBASE database, Ovid, Chinese CNKI, and Chinese WanFang database were systematically searched. The relation between CRNDE and the clinicopathological characteristics and prognosis of patients with cancer was determined using pooled odds ratios (ORs) and hazard ratios (HRs) with 95% confidence interval (CI). RESULTS: Thirteen studies with 1570 patients were included. The pooled results indicated that high CRNDE expression was related to lymph node metastasis (YES vs. NO: OR = 3.50, 95% CI = [1.05, 8.09]) and TNM stage (I + II vs. III + IV: OR = 0.26, 95% CI = [0.18, 0.37]) but not to gender, tumor size, and differentiation. High CRNDE expression indicated poor overall survival (OS) (HR = 2.06, 95% CI = [1.66, 2.47]). CRNDE could be an independent predictive factor for OS (HR = 1.62, 95% CI = [1.15, 2.08]) in patients with cancer. CONCLUSION: Therefore, high CRNDE expression was associated with advanced clinicopathological characteristics, and CRNDE could be used as a reliable prognostic biomarker in human cancer. However, more high-quality studies with a large sample size are needed to support this meta-analysis.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 282160 MEDLINE  
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[PMID]: 29211796
[Au] Autor:Saison-Ridinger M; DelGiorno KE; Zhang T; Kraus A; French R; Jaquish D; Tsui C; Erikson G; Spike BT; Shokhirev MN; Liddle C; Yu RT; Downes M; Evans RM; Saghatelian A; Lowy AM; Wahl GM
[Ad] Address:Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California, United States of America.
[Ti] Title:Reprogramming pancreatic stellate cells via p53 activation: A putative target for pancreatic cancer therapy.
[So] Source:PLoS One;12(12):e0189051, 2017.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pancreatic ductal adenocarcinoma (PDAC) is characterized by an extremely dense fibrotic stroma, which contributes to tumor growth, metastasis, and drug resistance. During tumorigenesis, quiescent pancreatic stellate cells (PSCs) are activated and become major contributors to fibrosis, by increasing growth factor signaling and extracellular matrix deposition. The p53 tumor suppressor is known to restrict tumor initiation and progression through cell autonomous mechanisms including apoptosis, cell cycle arrest, and senescence. There is growing evidence that stromal p53 also exerts anti-tumor activity by paracrine mechanisms, though a role for stromal p53 in PDAC has not yet been described. Here, we demonstrate that activation of stromal p53 exerts anti-tumor effects in PDAC. We show that primary cancer-associated PSCs (caPSCs) isolated from human PDAC express wild-type p53, which can be activated by the Mdm2 antagonist Nutlin-3a. Our work reveals that p53 acts as a major regulator of PSC activation and as a modulator of PDAC fibrosis. In vitro, p53 activation by Nutlin-3a induces profound transcriptional changes, which reprogram activated PSCs to quiescence. Using immunofluorescence and lipidomics, we have also found that p53 activation induces lipid droplet accumulation in both normal and tumor-associated fibroblasts, revealing a previously undescribed role for p53 in lipid storage. In vivo, treatment of tumor-bearing mice with the clinical form of Nutlin-3a induces stromal p53 activation, reverses caPSCs activation, and decreases fibrosis. All together our work uncovers new functions for stromal p53 in PDAC.
[Mh] MeSH terms primary: Carcinoma, Pancreatic Ductal/therapy
Cellular Reprogramming
Genes, p53
Pancreatic Neoplasms/therapy
Pancreatic Stellate Cells/metabolism
[Mh] MeSH terms secundary: Animals
Carcinoma, Pancreatic Ductal/metabolism
Carcinoma, Pancreatic Ductal/pathology
Cholesterol Esters/metabolism
Humans
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Pancreatic Neoplasms/metabolism
Pancreatic Neoplasms/pathology
Transcription, Genetic
Triglycerides/metabolism
Tumor Cells, Cultured
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Cholesterol Esters); 0 (Triglycerides)
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[Js] Journal subset:IM
[Da] Date of entry for processing:171207
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189051

  3 / 282160 MEDLINE  
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[PMID]: 29523416
[Au] Autor:Rouyer M; Franois E; Cunha AS; Monnereau A; Noize P; Robinson P; Droz-Perroteau C; Le Monies de Sagazan A; Jov J; Lassalle R; Moore N; Fourrier-Rglat A; Smith D; EREBUS Study Group
[Ad] Address:Bordeaux PharmacoEpi, INSERM CIC1401, Universit de Bordeaux, CHU de Bordeaux, Bordeaux, France.
[Ti] Title:Effectiveness of Cetuximab as First-Line Therapy for Patients With Wild-Type KRAS and Unresectable Metastatic Colorectal Cancer in Real-Life Practice: Results of the EREBUS Cohort.
[So] Source:Clin Colorectal Cancer;, 2018 Jan 31.
[Is] ISSN:1938-0674
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Few real-life data are available on cetuximab benefit. The EREBUS cohort was performed to assess metastases resection rate, use, safety, and survival outcomes in wild-type KRAS (Kirsten rat sarcoma viral oncogene) patients with initially unresectable metastatic colorectal cancer (mCRC) treated by cetuximab in real practice. PATIENTS AND METHODS: The study cohort comprised patients initiating cetuximab between January 2009 and December 2010 in 65 French centers, with initially unresectable mCRC and wild-type KRAS. Kaplan-Meier analysis estimated 24-month probability of metastases resection and progression-free survival, and 36-month overall survival (OS). Cox proportional hazards models investigated factors associated with survival outcomes. RESULTS: Among the 389 patients included, median age was 64 years, 67.4% were male, 77.9% had Eastern Cooperative Oncology Group performance status≤ 1, and hepatic metastases were most frequent at baseline (n= 146 exclusively, n= 149 not exclusively, n= 94 nonliver only). Median duration of cetuximab use was 4.8 months. Metastases resection was performed in 106 patients (27.2%) (n= 60 liver exclusively, n= 33 not exclusively, n= 13 nonliver only). The 24-month probability (95% confidence interval) of metastases resection occurrence was 33.6% (28.5-39.3). Median progression-free survival was 9.2 (8.5-9.8) months for the total cohort and 13.0 (11.6-15.1) for those resected; median OS was 23.0 (20.6-26.3) months for the total cohort and was not reached after 36 months for those who were resected. The strongest factor associated with higher OS was metastases resection with complete remission (hazard ratio, 0.41; 95% confidence interval, 0.19-0.88). CONCLUSION: This cohort study highlights in French real-life practice the benefit of cetuximab in first-line mCRC therapy, notably in case of metastases resection with complete remission.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 282160 MEDLINE  
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[PMID]: 29505541
[Au] Autor:Noh HM; Yoo JH; Jeong JY; Park YS
[Ad] Address:Department of Family Medicine, Hallym University Sacred Heart Hospital, Hallym University College of Medicine, Anyang.
[Ti] Title: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] Country of publication:United States
[La] Language:eng
[Ab] Abstract: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] MeSH terms primary: Adenocarcinoma/surgery
Bone Density
Gastrectomy
Gastroscopy
Stomach Neoplasms/surgery
[Mh] MeSH terms secundary: Adenocarcinoma/metabolism
Adult
Aged
Bone and Bones/metabolism
Female
Humans
Male
Middle Aged
Retrospective Studies
Stomach Neoplasms/metabolism
[Pt] Publication type:COMPARATIVE STUDY; JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180306
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009582

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[PMID]: 29505523
[Au] Autor:Kang X; Zeng Y; Liang J; Li J; Ren D; Chai L; Sun Z; Yu S; Wu X; Han W; Wang W
[Ad] Address:Department of Dermatology.
[Ti] Title:Aberrations and clinical significance of BRAF in malignant melanoma: A series of 60 cases in Chinese Uyghur.
[So] Source:Medicine (Baltimore);97(1):e9509, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Malignant melanoma (MM) is a highly malignant melanocytic tumor, it occurs mostly in the skin, the mucous membrane close to the skin, but also in the tunicae rhagoides and the pia mater. The Uyghur is the largest ethnic group living in the Xinjiang Uyghur Autonomous Region of China, accounting for 46% of the total population of 20 million. Large-scale studies on MMs in Asian countries are limited. This study aimed to investigate BRAF mRNA expression and mutations in Chinese Uyghur patients with MMs and to identify the clinical features associated with these parameters.Formalin-fixed, paraffin wax-embedded tumor sections from 60 MMs were analyzed for BRAF expression using reverse transcription polymerase chain reaction (RT-PCR). Exons 11 and 15 of BRAF were analyzed for the presence of mutations using PCR and DNA sequencing. Sixty MMs were followed by mobile phone for survival analysis.BRAF mRNA expression was higher in MMs than in pigmented moles and normal skin tissues. Fourteen of 60 MMs had BRAF mutations. The frequency of BRAF mutations was significantly higher in patients younger than 60 years (10/28, 4/32, P = .02). A significant difference was observed in the frequency of BRAF mutations among specimens of mucosal, acral, chronic sun-induced damage (CSD), and non-CSD MMs (2/10, 3/19, 8/25, 1/6, P = .002). No significant association was found among BRAF mutations, sex, ulceration, or lymph node metastasis. MMs lymph node metastasis (hazard ratio 2.54 [95% confidence interval 1.062 - 6.066], P = .01) affected survival.This study indicated that BRAF mutations and expression might serve as independent adverse prognostic factors in melanoma.
[Mh] MeSH terms primary: Melanoma/genetics
Proto-Oncogene Proteins B-raf/genetics
Skin Neoplasms/genetics
[Mh] MeSH terms secundary: Aged
Asian Continental Ancestry Group/genetics
China/epidemiology
Female
Humans
Male
Melanoma/metabolism
Melanoma/mortality
Middle Aged
Mutation
Proto-Oncogene Proteins B-raf/metabolism
Skin Neoplasms/metabolism
Skin Neoplasms/mortality
Survival Analysis
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180306
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009509

  6 / 282160 MEDLINE  
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[PMID]: 29431540
[Au] Autor:Hong JH
[Ad] Address:a Department of Urology , Dankook University College of Medicine , Cheonan , Republic of Korea.
[Ti] Title:Pharmacokinetic/pharmacodynamic drug evaluation of enzalutamide for treating prostate cancer.
[So] Source:Expert Opin Drug Metab Toxicol;14(3):361-369, 2018 Mar.
[Is] ISSN:1744-7607
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Enzalutamide is the first approved second-generation androgen receptor (AR) antagonist in the treatment of metastatic castration-resistant prostate cancer (mCRPC) with or without docetaxel-based chemotherapy. Over the past 5years, a number of attempts were made to determine the efficacy of enzalutamide in the different clinical settings. Areas covered: A literature search was performed at the PubMed, Embase, and Web of Science database to collect the most relevant and impactful studies, including basic science investigations, clinical trials, and reviews. This article focuses on the pharmacology, efficacy, tolerability, and future perspective of enzalutamide. Expert opinion: The treatment paradigm of CRPC has been dramatically challenged of late. Enzalutamide are in wide use because of its favorable efficacy and safety, but primary or acquired resistance to the drug will eventually develop. Further studies are thus necessary to identify appropriate patients who can achieve apparent benefits from enzalutamide alone or in combination with other drugs.
[Mh] MeSH terms primary: Androgen Receptor Antagonists/administration & dosage
Phenylthiohydantoin/analogs & derivatives
Prostatic Neoplasms, Castration-Resistant/drug therapy
[Mh] MeSH terms secundary: Androgen Receptor Antagonists/pharmacokinetics
Androgen Receptor Antagonists/pharmacology
Animals
Antineoplastic Combined Chemotherapy Protocols/administration & dosage
Antineoplastic Combined Chemotherapy Protocols/pharmacokinetics
Antineoplastic Combined Chemotherapy Protocols/pharmacology
Drug Resistance, Neoplasm
Humans
Male
Neoplasm Metastasis
Phenylthiohydantoin/administration & dosage
Phenylthiohydantoin/pharmacokinetics
Phenylthiohydantoin/pharmacology
Prostatic Neoplasms, Castration-Resistant/pathology
Taxoids/administration & dosage
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Androgen Receptor Antagonists); 0 (MDV 3100); 0 (Taxoids); 15H5577CQD (docetaxel); 2010-15-3 (Phenylthiohydantoin)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180213
[St] Status:MEDLINE
[do] DOI:10.1080/17425255.2018.1440288

  7 / 282160 MEDLINE  
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[PMID]: 29421442
[Au] Autor:Wu S; Mao L; Li Y; Yin Y; Yuan W; Chen Y; Ren W; Lu X; Li Y; Chen L; Chen B; Xu W; Tian T; Lu Y; Jiang L; Zhuang X; Chu M; Wu J
[Ad] Address:Jiangsu Provincial Key Laboratory of Geriatrics, Department of Geriatrics, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
[Ti] Title:RAGE may act as a tumour suppressor to regulate lung cancer development.
[So] Source:Gene;651:86-93, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Although the correlation of the RAGE rs2070600 polymorphism and cancer risk has been confirmed, detailed studies with functional and experimental evaluations are lacking. In this study, we first aimed to examine whether this polymorphism is associated with cancer risk based on the latest published data, and consistent with previous meta-analyses, a significant association between the rs2070600 polymorphism and cancer risk was observed (A versus G: OR = 1.25; 95% CI = 1.12-1.40). In additional stratified analyses based on cancer type, rs2070600 was significantly associated with an increased risk of lung cancer (A versus G: OR = 1.20; 95% CI = 1.09-1.33). Moreover, TCGA database showed that the expression level of RAGE was significantly lower in lung cancer tumour tissues than in adjacent non-tumour tissues, which was validated in the GEO database. Additionally, eQTL analysis indicated that the rs2070600 polymorphism may modify the expression level of RAGE in lung squamous cell carcinoma tissues (P = 0.09). Finally, we performed functional experiments in lung cancer cells and preliminarily demonstrated that RAGE may act as a tumour suppressor in lung cancer development. These findings provide evidence that the variant A allele of rs2070600 may decrease the expression of the tumour suppressor gene RAGE, thereby increasing lung cancer risk.
[Mh] MeSH terms primary: Genes, Tumor Suppressor
Lung Neoplasms/genetics
Polymorphism, Single Nucleotide
Receptor for Advanced Glycation End Products/genetics
[Mh] MeSH terms secundary: Cell Line
Cell Line, Tumor
Gene Expression
Genetic Predisposition to Disease
Humans
Lung Neoplasms/pathology
Phenotype
Quantitative Trait Loci
[Pt] Publication type:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Name of substance:0 (Receptor for Advanced Glycation End Products)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180209
[St] Status:MEDLINE

  8 / 282160 MEDLINE  
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[PMID]: 29408272
[Au] Autor:Saif I; Kasmi Y; Allali K; Ennaji MM
[Ad] Address:Team of Virology, Oncology and Medical Biotechnologies, Laboratory of Virology, Microbiology, Quality and Biotechnologies/ETB, Faculty of Science sand Technologies-Mohammedia, Hassan II University of Casablanca, Morocco.
[Ti] Title:Prediction of DNA methylation in the promoter of gene suppressor tumor.
[So] Source:Gene;651:166-173, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The epigenetics methylation of cytosine is the most common epigenetic form in DNA sequences. It is highly concentrated in the promoter regions of the genes, leading to an inactivation of tumor suppressors regardless of their initial function. In this work, we aim to identify the highly methylated regions; the cytosine-phosphate-guanine (CpG) island located on the promoters and/or the first exon gene known for their key roles in the cell cycle, hence the need to study gene-gene interactions. The Frommer and hidden Markov model algorithms are used as computational methods to identify CpG islands with specificity and sensitivity up to 76% and 80%, respectively. The results obtained show, on the one hand, that the genes studied are suspected of developing hypermethylation in the promoter region of the gene involved in the case of a cancer. We then showed that the relative richness in CG results from a high level of methylation. On the other hand, we observe that the gene-gene interaction exhibits co-expression between the chosen genes. This let us to conclude that the hidden Markov model algorithm predicts more specific and valuable information about the hypermethylation in gene as a preventive and diagnostics tools for the personalized medicine; as that the tumor-suppresser-genes have relative co-expression and complementary relations which the hypermethylation affect in the samples studied in our work.
[Mh] MeSH terms primary: Computational Biology/methods
CpG Islands
DNA Methylation
Genes, Tumor Suppressor
Promoter Regions, Genetic
[Mh] MeSH terms secundary: Algorithms
DNA, Neoplasm
Datasets as Topic
Epistasis, Genetic
Humans
Markov Chains
Models, Genetic
Neoplasms/genetics
[Pt] Publication type:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Name of substance:0 (DNA, Neoplasm)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180207
[St] Status:MEDLINE

  9 / 282160 MEDLINE  
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[PMID]: 29394261
[Au] Autor:Patel N; Garikapati KR; Makani VKK; Nair AD; Vangara N; Bhadra U; Pal Bhadra M
[Ad] Address:Centre for Chemical Biology, CSIR-Indian Institute of Chemical Technology, Tarnaka, Hyderabad, Telangana State, India.
[Ti] Title:Regulating BMI1 expression via miRNAs promote Mesenchymal to Epithelial Transition (MET) and sensitizes breast cancer cell to chemotherapeutic drug.
[So] Source:PLoS One;13(2):e0190245, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Polycomb group (PcG) proteinB lymphoma Mo-MLV insertion region 1 homolog (BMI1) is a transcriptional repressor that plays an important role in human carcinogenesis. MicroRNAs (miRNAs) are endogenous small non-coding RNAsthat implicate a negative regulation on gene expression. Deregulation of the expression of miRNAs has been implicated in tumorigenesis. Here, we have shown that knock-down ofBMI1increases theexpression of tumor-suppressivemiRNAs. Elevated levels of expression of miR-200a, miR-200b, miR-15a, miR-429, miR-203were observed upon knock-down of BMI1. Up-regulation of these miRNAsleads to down-regulation ofPRC1 group of proteins i.e. BMI1, RING1A, RING1B and Ub-H2A. Interestingly, overexpression of miR-200a, miR-200b and miR-15aalso produced decreased BMI1 and Ub-H2A protein expression in the CD44+ Cancer Stem Cellpopulation of MDAMB-231cells. Also,elevating the levels of BMI1 regulated miRNAspromoted Mesenchymal to Epithelial transition by regulating the expression of N-Cadherin, Vimentin, -Catenin, Zeb, Snail thereby resulting in decreased invasion, migration and proliferation. Here, we also report that miR-200a, miR-200b, miR-203 accretes the sensitivity of MDAMB-231 cells to the histone deacetylase inhibitor (HDACi) SAHA and miR-15a sensitized breast cancer cells to the chemotherapeutic drug cisplatin leading to apoptosis. These findings suggest that modulatingspecific miRNAs may serve as a therapeutic approach for the treatment of breast cancer.
[Mh] MeSH terms primary: Breast Neoplasms/pathology
Epithelial-Mesenchymal Transition/genetics
Gene Expression Regulation, Neoplastic/genetics
Polycomb Repressive Complex 1/genetics
[Mh] MeSH terms secundary: 3' Untranslated Regions
Drug Resistance, Neoplasm
Female
Humans
Neoplasm Invasiveness
Neoplasm Metastasis
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (3' Untranslated Regions); 0 (BMI1 protein, human); EC 2.3.2.27 (Polycomb Repressive Complex 1)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180203
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190245

  10 / 282160 MEDLINE  
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[PMID]: 29366405
[Au] Autor:Walaszczyk A; Pietrowska M; Wojakowska A; Abramowicz A; Chmura A; Maslyk B; Rodziewicz P; Polanska J; Behrendt K; Nowicka E; Tarnawski R; Widlak P
[Ti] Title:Therapy-Related Changes in the Serum Proteome Patterns of Early Stage Breast Cancer Patients with Different Outcomes.
[So] Source:Protein Pept Lett;24(1):37-45, 2017.
[Is] ISSN:1875-5305
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Adjuvant chemo- and/or radiotherapy is applied in a majority of patients treated for early stage breast cancer, although only a small percentage of these individuals are at high risk of metastasis or recurrence. Hence, knowledge of the biomarkers associated with the risk of disease progression might facilitate the planning of an optimal therapy and protect many patients from the toxicity of unnecessary treatment. In this study, we characterized the serum proteome of patients diagnosed with early-stage breast cancer, exhibiting either no evidence of disease five years after the end of therapy or suffering from metastasis, relapse or a second cancer during the corresponding follow-up. Samples collected before treatment and one year after the end of therapy, when no clinical symptoms of a treatment failure was evidenced, were analyzed using two classical proteomics approaches: LC-MS/MS and 2D-PAGE. A total of 42 proteins with relative quantities that were significantly different between pre- and post-treatment samples were identified in either group of patients; however, the observed changes were more frequent in the treatment-failure group. Among the posttreatment samples, 30 proteins were upregulated, and 10 proteins were downregulated, while 11 proteins were upregulated, and eight proteins were downregulated in the control group. Moreover, several proteins exhibited different patterns of changes in both groups of patients. For example, haptoglobin expression increased in the treatment-failure group but decreased in the control group (this pattern of changes was confirmed using an immunoassay). Notably, proteins affected in posttreatment samples in either group of patients could be associated with different molecular and cellular functions, including angiogenesis, blood coagulation and wound healing in the treatment-failure group and cell adhesion and cell death in the control group.
[Mh] MeSH terms primary: Blood Proteins/analysis
Breast Neoplasms/blood
Breast Neoplasms/therapy
[Mh] MeSH terms secundary: Aged
Biomarkers, Tumor/analysis
Biomarkers, Tumor/blood
Electrophoresis, Gel, Two-Dimensional
Female
Haptoglobins/analysis
Humans
Middle Aged
Proteome/analysis
Proteomics
Tandem Mass Spectrometry
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Biomarkers, Tumor); 0 (Blood Proteins); 0 (Haptoglobins); 0 (Proteome)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180126
[St] Status:MEDLINE
[do] DOI:10.2174/0929866523666161128154412


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