Database : MEDLINE
Search on : Lung and Neoplasms [Words]
References found : 231883 [refine]
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[PMID]: 29449199
[Au] Autor:Jessup DL; Glover Iv M; Daye D; Banzi L; Jones P; Choy G; Shepard JO; Flores EJ
[Ad] Address:Department of Radiology, Massachusetts General Hospital, Boston, MA, United States.
[Ti] Title:Implementation of Digital Awareness Strategies to Engage Patients and Providers in a Lung Cancer Screening Program: Retrospective Study.
[So] Source:J Med Internet Res;20(2):e52, 2018 Feb 15.
[Is] ISSN:1438-8871
[Cp] Country of publication:Canada
[La] Language:eng
[Ab] Abstract:BACKGROUND: Lung cancer is the leading cause of cancer-related deaths in the United States. Despite mandated insurance coverage for eligible patients, lung cancer screening rates remain low. Digital platforms, including social media, provide a potentially valuable tool to enhance health promotion and patient engagement related to lung cancer screening (LCS). OBJECTIVE: The aim was to assess the effectiveness of LCS digital awareness campaigns on utilization of low-dose computed tomography (LDCT) and visits to institutional online educational content. METHODS: A pay-per-click campaign utilizing Google and Facebook targeted adults aged 55 years and older and caregivers aged 18 years and older (eg, spouses, adult children) with LCS content during a 20-week intervention period from May to September 2016. A concurrent pay-per-click campaign using LinkedIn and Twitter targeted health care providers with LCS content. Geographic target radius was within 60 miles of an academic medical center. Social media data included aggregate demographics and click-through rates (CTRs). Primary outcome measures were visits to institutional Web pages and scheduled LDCT exams. Study period was 20 weeks before, during, and after the digital awareness campaigns. RESULTS: Weekly visits to the institutional LCS Web pages were significantly higher during the digital awareness campaigns compared to the 20-week period prior to implementation (mean 823.9, SD 905.8 vs mean 51, SD 22.3, P=.001). The patient digital awareness campaign surpassed industry standard CTRs on Google (5.85%, 1108/18,955 vs 1.8%) and Facebook (2.59%, 47,750/1,846,070 vs 0.8%). The provider digital awareness campaign surpassed industry standard CTR on LinkedIn (1.1%, 630/57,079 vs 0.3%) but not Twitter (0.19%, 1139/587,133 vs 0.25%). Mean scheduled LDCT exam volumes per week before, during, and after the digital awareness campaigns were 17.4 (SD 7.5), 20.4 (SD 5.4), and 26.2 (SD 6.4), respectively, with the difference between the mean number of scheduled exams after the digital awareness campaigns and the number of exams scheduled before and after the digital awareness campaigns being statistically significant (P<.001). CONCLUSIONS: Implementation of the LCS digital awareness campaigns was associated with increased visits to institutional educational Web pages and scheduled LDCT exams. Digital platforms are an important tool to enhance health promotion activities and engagement with patients and providers.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.2196/jmir.8932

  2 / 231883 MEDLINE  
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[PMID]: 29309307
[Au] Autor:Antonescu CR; Agaram NP; Sung YS; Zhang L; Swanson D; Dickson BC
[Ad] Address:Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY.
[Ti] Title:A Distinct Malignant Epithelioid Neoplasm With GLI1 Gene Rearrangements, Frequent S100 Protein Expression, and Metastatic Potential: Expanding the Spectrum of Pathologic Entities With ACTB/MALAT1/PTCH1-GLI1 Fusions.
[So] Source:Am J Surg Pathol;42(4):553-560, 2018 Apr.
[Is] ISSN:1532-0979
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:ACTB-GLI1 fusions have been reported as the pathognomonic genetic abnormality defining an unusual subset of actin-positive, perivascular myoid tumors, known as "pericytoma with the t(7;12) translocation." In addition, GLI1 oncogenic activation through a related MALAT1-GLI1 gene fusion has been recently reported in 2 unrelated gastric tumors, namely plexiform fibromyxoma and gastroblastoma. Triggered by unexpected targeted RNA-sequencing results detecting GLI1-related fusions in a group of malignant neoplasms with round to epithelioid morphology, and frequently strong S100 protein immunoreactivity, we investigated their clinicopathologic features in relation to other known pathologic entities sharing similar genetics. On the basis of a combined approach of targeted RNA sequencing and fluorescence in situ hybridization screening, we identified 6 cases with GLI1 gene fusions, including 4 fused to ACTB, 1 with MALAT1 and 1 with PTCH1 gene. Patients had a mean age of 36 years at diagnosis (range, 16 to 79 y) and slight female predilection all except 1 tumor originated in the soft tissue. Microscopically, the tumors had a monomorphic epithelioid phenotype arranged in a distinctive nested or cord-like architecture, separated by thin septae and delicate capillary network. All except 2 cases were strongly positive for S100 protein, whereas being negative for SOX10, SMA, and EMA. Only 1 tumor showed focal cytokeratin positivity in rare cells. Although the tumors showed some resemblance to pericytic/glomus tumors or myoepithelial tumors, the immunoprofile was not supportive of either lineage. Moreover, in contrast to the benign course of so-called pericytoma with t(7;12), 3 patients in this series developed metastatic disease to either lymph nodes or lung. In fact the only patient with lung metastases showed a novel PTCH1-GLI1 gene fusion. It remains to be determined whether these tumors represent a clinically and immunohistologically distinct subset of pericytoma, or an altogether novel soft tissue sarcoma. Our findings open new opportunities for targeted therapy, as tumors with GLI1 oncogenic activation, and subsequent PTCH1 overexpression, might be sensitive to sonic hedgehog pathway inhibitors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1097/PAS.0000000000001010

  3 / 231883 MEDLINE  
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[PMID]: 29505522
[Au] Autor:Zhang BJ; Tian HT; Li HO; Meng J
[Ad] Address:Department of Anesthesia, Jining No. 1 People's Hospital, Jining City, Shandong Province, China.
[Ti] Title:The effects of one-lung ventilation mode on lung function in elderly patients undergoing esophageal cancer surgery.
[So] Source:Medicine (Baltimore);97(1):e9500, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The objective of the present study was to explore the effects of different one-lung ventilation (OLV) modes on lung function in elderly patients undergoing esophageal cancer surgery. A total of 180 consecutive elderly patients (ASA Grades I-II, with OLV indications) undergoing elective surgery were recruited in the study. Patients were randomly divided into 4 groups (n = 45). In Group A, patients received low tidal volume (VT < 8 mL/kg) + pressure controlled ventilation (PCV), low tidal volume (VT < 8 mL/kg) + volume-controlled ventilation (VCV) in Group B, high tidal volume (VT ≥ 8 mL/kg) + PCV in Group C and high tidal volume (VT ≥ 8 mL/kg) + VCV in Group D. Two-lung ventilation involved routine tidal volume (8-10 mL/kg) at a frequency of 12 to 18 times/min, and VCV mode. Clinical efficacy among 4 groups was compared. The partial pressure of end-tidal carbon dioxide (PetCO2) did not significantly differ among 4 groups (all P > .05), and the oxygenation index and SO2 in Group A were significantly higher than in the other groups (P < .05). The PetCO2, peak airway pressure (Ppeak), platform airway pressure (Pplat), and mean airway pressure (Pmean) in Group A were significantly lower than those in the other groups (all P < .05). However, airway resistance (Raw) among 4 groups did not significantly differ (all P > .05). The incidence of pulmonary infection, anastomotic fistula, ventilator-induced lung injury, lung dysfunction, difficulty weaning from mechanical ventilation, and multiple organ dysfunction in Groups A and B were lower than that in Groups C and D (all P < .05). The expression levels of IL-6, tumor necrosis factor-α, and C-reactive protein in lavage fluid in Group A were significantly lower than those in the other groups (all P < .05). OLV with low tidal volume (VT < 8 mL/kg) + PCV (5 cmH2O PEEP) improved lung function and mitigated inflammatory responses in elderly patients undergoing esophageal cancer surgery.
[Mh] MeSH terms primary: Esophageal Neoplasms/surgery
One-Lung Ventilation/methods
[Mh] MeSH terms secundary: Aged
Bronchoalveolar Lavage Fluid/chemistry
C-Reactive Protein/analysis
Female
Humans
Interleukin-6/analysis
Male
Middle Aged
Respiratory Function Tests
Tumor Necrosis Factor-alpha/analysis
[Pt] Publication type:JOURNAL ARTICLE; OBSERVATIONAL STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Name of substance:0 (IL6 protein, human); 0 (Interleukin-6); 0 (Tumor Necrosis Factor-alpha); 9007-41-4 (C-Reactive Protein)
[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.0000000000009500

  4 / 231883 MEDLINE  
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[PMID]: 29505510
[Au] Autor:Chen XR; Dong JN; Zhang F; Yao TL
[Ad] Address:Department of Ultrasound, The Second Affiliated Hospital of Mudanjiang Medical University.
[Ti] Title:Efficacy and safety of image-guidance radiotherapy by helical tomotherapy in patients with lung cancer.
[So] Source:Medicine (Baltimore);97(1):e9243, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:This study aimed to explore the efficacy and toxicity of image-guided stereotactic body radiotherapy (IGSBR) by helical tomotherapy in patients with lung cancer among Chinese Han population.A total of 21 patients with stage I lung cancer were included. They received a total of 60 Gy factions IGSBR. The outcomes included complete response (CR), partial response (PR), stable disease (SD), progress disease (PD), overall response rate (ORR), and overall survival (OS). In addition, toxicities were also recorded in this study.Three-year CR, PR, SD, PD, ORR, and OS were 47.6%, 38.1%, 9.5%, 4.8%, 85.7%, and 48.0 months, respectively. Additionally, mild toxicities were found in this study.This study demonstrated that IGSBR is efficacious for patients with stage I lung cancer with mild toxicities among Chinese Han population.
[Mh] MeSH terms primary: Carcinoma/radiotherapy
Lung Neoplasms/radiotherapy
[Mh] MeSH terms secundary: Adult
Aged
Aged, 80 and over
Asian Continental Ancestry Group
Carcinoma, Non-Small-Cell Lung/radiotherapy
Female
Humans
Male
Middle Aged
Radiotherapy, Image-Guided
Radiotherapy, Intensity-Modulated
Retrospective Studies
[Pt] Publication type:JOURNAL ARTICLE
[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.0000000000009243

  5 / 231883 MEDLINE  
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[PMID]: 29505507
[Au] Autor:Wang CG; Zeng DX; Huang JA; Jiang JH
[Ad] Address:Department of Respiratory and Critical Care, First Affiliated Hospital of Soochow University, Suzhou, P.R. China.
[Ti] Title:Effective assessment of low times MET amplification in pleural effusion after epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) acquired resistance: Cases report.
[So] Source:Medicine (Baltimore);97(1):e9021, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: The mechanism of the first-generation epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) acquired resistance included T790M mutation, cellular-mesenchymal to epithelial transition factor (MET) or EGFR amplification, PIK3CA mutation, and transformation to small cell lung cancer. MET amplification accounted for only about 5% of the resistance cases. PATIENTS CONCERNS: Few report detected MET amplification in pleural effusion. Here, we reported 2 lung adenocarcinoma cases with MET amplification in pleural effusion rapidly responded to crizotinib after EGFR-TKIs acquired resistance. DIAGNOSES: Biopsy via bronchoscopy, next-generation sequencing (NGS) in pleural effusion. INTERVENTIONS: EGFR-TKIs (Icotinib), MET inhibitor crizotinib. OUTCOMES: After a progression-free survival of 9 months and 23months, respectively, both cases progressed accompanying with pleural effusion. Results of NGS in pleural effusion showed MET amplification (2-3 times) in both cases. The 2 patients were treated with a MET inhibitor crizotinib and rapidly responded. CONCLUSION: MET amplification in pleural effusion could predict a perfect response to crizotinib after EGFR-TKIs acquired resistance, even only a low times gene amplification.
[Mh] MeSH terms primary: Adenocarcinoma/genetics
Drug Resistance, Neoplasm/genetics
Lung Neoplasms/genetics
Pleural Effusion, Malignant/metabolism
Proto-Oncogene Proteins c-met/genetics
[Mh] MeSH terms secundary: Adenocarcinoma/drug therapy
Aged
Female
Gene Amplification
Humans
Lung Neoplasms/drug therapy
Male
Middle Aged
Protein Kinase Inhibitors/therapeutic use
Proto-Oncogene Proteins c-met/metabolism
Pyrazoles/therapeutic use
Pyridines/therapeutic use
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:0 (Protein Kinase Inhibitors); 0 (Pyrazoles); 0 (Pyridines); 53AH36668S (crizotinib); EC 2.7.10.1 (MET protein, human); EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
[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.0000000000009021

  6 / 231883 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

  7 / 231883 MEDLINE  
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[PMID]: 29376605
[Au] Autor:Govorov AV; Vasilyev AO; Shiryaev AA; Sukhikh SO; Sidorenkov AV; Pushkarev AV; Tsiganov DI; Pushkar DY
[Ad] Address:Department of Urology, A.I. Evdokimov Moscow State University of Medicine and Dentistry, Moscow, Russia.
[Ti] Title:[Current methods of early diagnosis of prostate cancer].
[So] Source:Urologiia;(6):101-106, 2017 Dec.
[Is] ISSN:1728-2985
[Cp] Country of publication:Russia (Federation)
[La] Language:rus
[Ab] Abstract:Prostate cancer is the most common cancer among men, except for lung cancer. Therefore, it is imperative to identify diagnostic methods for early detection of prostate cancer to determine patients from healthy populations, which helps guide a timely treatment at an initial stage of the disease. The article provides an in-depth review of the most current diagnostic biomarkers of prostate cancer, their role in clinical practice as a means of the early detection and screening for prostate cancer.
[Mh] MeSH terms primary: Clinical Laboratory Techniques/methods
Prostatic Neoplasms/diagnosis
[Mh] MeSH terms secundary: Clinical Laboratory Techniques/trends
Humans
Male
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180130
[St] Status:MEDLINE

  8 / 231883 MEDLINE  
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[PMID]: 29364966
[Au] Autor:Maleki Vareki S; Salim KY; Danter WR; Koropatnick J
[Ad] Address:Cancer Research Laboratory Program, Lawson Health Research Institute, London, Ontario, Canada.
[Ti] Title:Novel anti-cancer drug COTI-2 synergizes with therapeutic agents and does not induce resistance or exhibit cross-resistance in human cancer cell lines.
[So] Source:PLoS One;13(1):e0191766, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Emerging drug-resistance and drug-associated toxicities are two major factors limiting successful cancer therapy. Combinations of chemotherapeutic drugs have been used in the clinic to improve patient outcome. However, cancer cells can acquire resistance to drugs, alone or in combination. Resistant tumors can also exhibit cross-resistance to other chemotherapeutic agents, resulting in sub-optimal treatment and/or treatment failure. Therefore, developing novel oncology drugs that induce no or little acquired resistance and with a favorable safety profile is essential. We show here that combining COTI-2, a novel clinical stage agent, with multiple chemotherapeutic and targeted agents enhances the activity of these drugs in vitro and in vivo. Importantly, no overt toxicity was observed in the combination treatment groups in vivo. Furthermore, unlike the tested chemotherapeutic drugs, cancer cells did not develop resistance to COTI-2. Finally, some chemo-resistant tumor cell lines only showed mild cross-resistance to COTI-2 while most remained sensitive to it.
[Mh] MeSH terms primary: Aminoquinolines/therapeutic use
Antineoplastic Combined Chemotherapy Protocols/therapeutic use
Thiosemicarbazones/therapeutic use
[Mh] MeSH terms secundary: Animals
Carcinoma, Non-Small-Cell Lung/pathology
Cell Line, Tumor
Cisplatin/administration & dosage
Deoxycytidine/administration & dosage
Deoxycytidine/analogs & derivatives
Drug Resistance, Neoplasm
Lung Neoplasms/pathology
Mice
Paclitaxel/administration & dosage
Vinblastine/administration & dosage
Vinblastine/analogs & derivatives
Xenograft Model Antitumor Assays
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Aminoquinolines); 0 (COTI-2 compound); 0 (Thiosemicarbazones); 0W860991D6 (Deoxycytidine); 5V9KLZ54CY (Vinblastine); B76N6SBZ8R (gemcitabine); P88XT4IS4D (Paclitaxel); Q20Q21Q62J (Cisplatin); Q6C979R91Y (vinorelbine)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191766

  9 / 231883 MEDLINE  
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[PMID]: 29339155
[Au] Autor:Kuwabara J; Umakoshi A; Abe N; Sumida Y; Ohsumi S; Usa E; Taguchi K; Choudhury ME; Yano H; Matsumoto S; Kunieda T; Takahashi H; Yorozuya T; Watanabe Y; Tanaka J
[Ad] Address:Department of Gastrointestinal Surgery and Surgical Oncology, Graduate School of Medicine, Ehime University, Toon, Ehime, Japan.
[Ti] Title:Truncated CD200 stimulates tumor immunity leading to fewer lung metastases in a novel Wistar rat metastasis model.
[So] Source:Biochem Biophys Res Commun;496(2):542-548, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:CD200 mediates immunosuppression in immune cells that express its receptor, CD200R. There are two CD200 variants; truncated CD200 that lacks the part of N-terminal sequence necessary for CD200R binding (CD200S) and full-length CD200 (CD200L). We established a novel lung metastasis model by subcutaneously transplanting C6 glioma cells into the backs of neonatal Wistar rats. All transplanted rats developed large back tumors, nearly 90% of which bore lung metastases. To compare the effects of CD200S and CD200L on tumor immunity, CD200L (C6-L)- or CD200S (C6-S)-expressing C6 cells were similarly transplanted. The results showed that 100% of rats with C6-L tumors developed lung metastases, while metastases were found in only 44% of rats with C6-S tumors (n = 25). Tumors disappeared in approximately 20% of the C6-S-bearing rats, and these animals evaded death 180 d after transplantation, while all C6-L tumor-bearing rats died after 45 d. Next generation sequencing revealed that C6-S tumors expressed chemokines and granzyme B at much higher levels than C6-L tumors. Flow cytometry revealed that C6-S tumors contained more dead cells and more CD45 cells, including natural killer cells and CD8 lymphocytes. In particular, multiple subsets of dendritic cells expressing CD11c, MHC class II, CD8, and/or CD103 were more abundant in C6-S than in C6-L tumors. These results suggested that CD200S induced the accumulation of multiple dendritic cell subsets that activated cytotoxic T lymphocytes, leading to the elimination of metastasizing tumor cells.
[Mh] MeSH terms primary: Antigens, CD/immunology
Glioma/immunology
Glioma/pathology
Lung Neoplasms/immunology
Lung Neoplasms/secondary
[Mh] MeSH terms secundary: Animals
Antigens, CD/genetics
Dendritic Cells/immunology
Dendritic Cells/pathology
Gene Expression Regulation, Neoplastic
Glioma/genetics
Immune Tolerance
Immunity, Cellular
Lung/immunology
Lung/pathology
Lung Neoplasms/genetics
Lung Neoplasms/pathology
Mutation
Rats, Wistar
T-Lymphocytes, Cytotoxic/immunology
T-Lymphocytes, Cytotoxic/pathology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Antigens, CD); 0 (antigens, CD200)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180118
[St] Status:MEDLINE

  10 / 231883 MEDLINE  
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[PMID]: 29337059
[Au] Autor:Lin L; Li M; Lin L; Xu X; Jiang G; Wu L
[Ad] Address:Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai 200433, China; Tongji University School of Medicine, Shanghai 200092, China.
[Ti] Title:FPPS mediates TGF-1-induced non-small cell lung cancer cell invasion and the EMT process via the RhoA/Rock1 pathway.
[So] Source:Biochem Biophys Res Commun;496(2):536-541, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Farnesyl pyrophosphate synthase (FPPS), a key enzyme in the mevalonate pathway, was recently shown to play a role in cancer progression. However, its role in non-small cell lung cancer (NSCLC) metastasis and the underlying mechanism remain unclear. In this study, FPPS expression was significantly correlated with TNM stage, and metastasis. Inhibition or knockdown of FPPS blocked TGF-1-induced cell invasion and epithelial-to-mesenchymal transition (EMT) process. FPPS expression of FPPS was induced by TGF-1 and FPPS promoted cell invasion and EMT via the RhoA/Rock1 pathway. In conclusion, FPPS mediates TGF-1-induced lung cancer cell invasion and EMT via the RhoA/Rock1 pathway. These findings suggest new treatment strategies to reduce mortality associated with metastasis in patients with NSCLC.
[Mh] MeSH terms primary: Carcinoma, Non-Small-Cell Lung/metabolism
Epithelial-Mesenchymal Transition
Geranyltranstransferase/metabolism
Lung Neoplasms/metabolism
Transforming Growth Factor beta1/metabolism
rho-Associated Kinases/metabolism
rhoA GTP-Binding Protein/metabolism
[Mh] MeSH terms secundary: Aged
Carcinoma, Non-Small-Cell Lung/genetics
Carcinoma, Non-Small-Cell Lung/pathology
Cell Line, Tumor
Female
Gene Expression Regulation, Neoplastic
Geranyltranstransferase/analysis
Geranyltranstransferase/genetics
Humans
Lung/metabolism
Lung/pathology
Lung Neoplasms/genetics
Lung Neoplasms/pathology
Male
Middle Aged
Neoplasm Invasiveness/genetics
Neoplasm Invasiveness/pathology
Signal Transduction
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Transforming Growth Factor beta1); EC 2.5.1.10 (Geranyltranstransferase); EC 2.7.11.1 (ROCK1 protein, human); EC 2.7.11.1 (rho-Associated Kinases); EC 3.6.5.2 (rhoA GTP-Binding Protein)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180117
[St] Status:MEDLINE


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