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[PMID]: 29505542
[Au] Autor:Shi Z; Ding H; Shen QW; Lu XG; Chen JY; Chen X; Tang X
[Ad] Address:Department of Medical Oncology.
[Ti] Title:The clinical manifestation, survival outcome and predictive prognostic factors of 137 patients with primary gastrointestinal lymphoma (PGIL): Strobe compliant.
[So] Source:Medicine (Baltimore);97(1):e9583, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:This retrospective study aimed to investigate clinical characteristics and prognostic factors in patients with primary gastrointestinal lymphoma (PGIL) of Chinese population.From January 2001 to December 2015, 137 patients diagnosed with PGIL were recruited. The clinical features, treatment, and follow-up information were analysed.The median patient age was 62.3 years. With 18.47 months follow-up, the 2-year progress-free survival and overall survival rate was 74.9% and 75.5%, respectively. The overall response rate was 33.6%. Age≥60 years, advanced Lugano staging (≥stage IIE), elevated lactate dehydrogenase (LDH) levels, ≥2 extra-nodal involved sites, National Comprehensive Cancer Network International Prognostic Index (NCCN-IPI)≥4, Ki-67≥50% were associated with worse prognosis in univariate analysis (P < .05). By multivariate analyses, we determined that the involvement of extra-nodal involved sites was the only statistically significant poor prognostic factor in PGIL.Age, staging, LDH levels, NCCN-IPI, Ki-67 especially involvement of multiple extra-nodal sites were associated with poor overall survival of PGIL.
[Mh] MeSH terms primary: Gastrointestinal Neoplasms/mortality
Lymphoma/mortality
[Mh] MeSH terms secundary: Adult
Aged
Aged, 80 and over
Antineoplastic Combined Chemotherapy Protocols
China/epidemiology
Female
Gastrointestinal Neoplasms/diagnosis
Gastrointestinal Neoplasms/pathology
Gastrointestinal Neoplasms/therapy
Gastrointestinal Tract/pathology
Humans
Lymphoma/diagnosis
Lymphoma/pathology
Lymphoma/therapy
Male
Middle Aged
Retrospective Studies
Survival Analysis
Treatment Outcome
Young Adult
[Pt] Publication type: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.0000000000009583

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[PMID]: 29482389
[Au] Autor:Elzahabi HSA; Nossier ES; Khalifa NM; Alasfoury RA; El-Manawaty MA
[Ad] Address:a Department of Pharmaceutical Chemistry , Faculty of Pharmacy (Girls), Al-Azhar University , Cairo , Egypt.
[Ti] Title:Anticancer evaluation and molecular modeling of multi-targeted kinase inhibitors based pyrido[2,3-d]pyrimidine scaffold.
[So] Source:J Enzyme Inhib Med Chem;33(1):546-557, 2018 Dec.
[Is] ISSN:1475-6374
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:An efficient synthesis of substituted pyrido[2,3-d]pyrimidines was carried out and evaluated for in vitro anticancer activity against five cancer cell lines, namely hepatic cancer (HepG-2), prostate cancer (PC-3), colon cancer (HCT-116), breast cancer (MCF-7), and lung cancer (A-549) cell lines. Regarding HepG-2, PC-3, HCT-116 cancer cell lines, 7-(4-chlorophenyl)-2-(3-methyl-5-oxo-2,3-dihydro-1H-pyrazol-1-yl)-5-(p-tolyl)- pyrido[2,3-d]pyrimidin-4(3H)-one (5a) exhibited strong, more potent anticancer (IC : 0.3, 6.6 and 7 µM) relative to the standard doxorubicin (IC : 0.6, 6.8 and 12.8 µM), respectively. Kinase inhibitory assessment of 5a showed promising inhibitory activity against three kinases namely PDGFR ß, EGFR, and CDK4/cyclin D1 at two concentrations 50 and 100 µM in single measurements. Further, a molecular docking study for compound 5a was performed to verify the binding mode towards the EGFR and CDK4/cyclin D1 kinases.
[Mh] MeSH terms primary: Antineoplastic Agents/pharmacology
Cyclin-Dependent Kinase 4/antagonists & inhibitors
Protein Kinase Inhibitors/pharmacology
Pyridines/pharmacology
Pyrimidines/pharmacology
Receptor, Epidermal Growth Factor/antagonists & inhibitors
Receptor, Platelet-Derived Growth Factor beta/antagonists & inhibitors
[Mh] MeSH terms secundary: Antineoplastic Agents/chemical synthesis
Antineoplastic Agents/chemistry
Cell Line, Tumor
Cell Proliferation/drug effects
Cyclin-Dependent Kinase 4/metabolism
Dose-Response Relationship, Drug
Drug Screening Assays, Antitumor
Humans
Models, Molecular
Molecular Structure
Protein Kinase Inhibitors/chemical synthesis
Protein Kinase Inhibitors/chemistry
Pyridines/chemical synthesis
Pyridines/chemistry
Pyrimidines/chemical synthesis
Pyrimidines/chemistry
Receptor, Epidermal Growth Factor/metabolism
Receptor, Platelet-Derived Growth Factor beta/metabolism
Structure-Activity Relationship
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antineoplastic Agents); 0 (Protein Kinase Inhibitors); 0 (Pyridines); 0 (Pyrimidines); 0 (pyrido(3,2-d)pyrimidine); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta); EC 2.7.11.22 (CDK4 protein, human); EC 2.7.11.22 (Cyclin-Dependent Kinase 4)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180228
[St] Status:MEDLINE
[do] DOI:10.1080/14756366.2018.1437729

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[PMID]: 29455234
[Au] Autor:Wang S; Wang X; Liu M; Bai O
[Ad] Address:Department of Hematology, The First Hospital of Jilin University, No. 71 Xinmin Street, Chaoyang District, Changchun, 130021, Jilin, People's Republic of China.
[Ti] Title:Blastic plasmacytoid dendritic cell neoplasm: update on therapy especially novel agents.
[So] Source:Ann Hematol;97(4):563-572, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and aggressive hematopoietic malignancy mainly affecting elderly patients. Most patients present with asymptomatic skin lesions as the first symptom and has a high frequency of bone marrow involvement. BPDCN is typically characterized by CD4+ and CD 56+ co-expression without common lymphoid or myeloid lineage markers. There is no consensus on the optimal therapeutic strategy for BPDCN. It is highly responsive to chemotherapy but the median event-free survival is very short. Allogeneic stem cell transplantation may improve the prognosis of BPDCN but the rate of relapse is still high. There are no specific targeted agents approved for patients with BPDCN, but advances in the understanding of the pathobiology of BPDCN and the results of early clinical studies have revealed novel targets and potentially effective agents. Novel targeted therapies may improve outcomes for patients with BPDCN in the future.
[Mh] MeSH terms primary: Antineoplastic Agents/therapeutic use
Dendritic Cells/drug effects
Drugs, Investigational/therapeutic use
Hematologic Neoplasms/drug therapy
[Mh] MeSH terms secundary: Animals
Antineoplastic Agents/pharmacology
Antineoplastic Combined Chemotherapy Protocols/pharmacology
Antineoplastic Combined Chemotherapy Protocols/therapeutic use
Cell Line, Tumor
Central Nervous System Neoplasms/diagnosis
Central Nervous System Neoplasms/prevention & control
Central Nervous System Neoplasms/secondary
Dendritic Cells/pathology
Drugs, Investigational/pharmacology
Hematologic Neoplasms/diagnosis
Hematologic Neoplasms/pathology
Hematologic Neoplasms/surgery
Hematopoietic Stem Cell Transplantation/adverse effects
Humans
Prognosis
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Antineoplastic Agents); 0 (Drugs, Investigational)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180219
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-018-3259-z

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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 5 years, 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

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[PMID]: 29409738
[Au] Autor:Li XP; Lan JY; Liu DQ; Zhou H; Qian MM; Wang WW; Yang M
[Ad] Address:Department of Laboratory Medicine, The Hospital Of Hangzhou Dianzi University, Hangzhou, Zhejiang, China.
[Ti] Title:OCA2 rs4778137 polymorphism predicts survival of breast cancer patients receiving neoadjuvant chemotherapy.
[So] Source:Gene;651:161-165, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Genome-wide association study (GWAS) studies have showed that single nucleotide polymorphisms (SNPs) in OCA2 gene were associated with the survival of breast cancer patients treated with adjuvant chemotherapy. To further explain the association between OCA2 SNPs and breast cancer survival, we investigated the predictive value of rs4778137 located in OCA2 in local advanced breast cancer patients receiving neoadjuvant chemotherapy. PATIENTS AND METHODS: A case-cohort with 150 breast cancer patients was performed to evaluate the effects of the OCA2 rs4778137 on breast cancer survival. The association between rs4778137 genotypes and pathological complete response (pCR, defined that the postoperative pathology indicating no residual invasive breast cancer in the breast or the axillary lymph node) were analyzed. Logistic regression analysis was performed to identify the independent predictors of pCR. Survival was assessed by Kaplan-Meier method and Cox regression analysis according to the rs4778137 genotypes. RESULTS: The differences between pCR and the rs4778137 genotypes were statistically significant (p < 0.05). The patients with genotype GG harbored a better disease-free survival (HR: 2.358, p = 0.000) and overall survival (HR: 1.578, p = 0.008) than the patients with genotype CC in rs4778137. The further Univariate and Multivariate survival analysis revealed that SNP rs4778137 was an independent predictive factor of disease-free survival (p = 0.000/p = 0.001) and overall survival (p = 0.006/p = 0.045). CONCLUSION: The OCA2 rs4778137 may be a predictor for the clinical response and survival in local advanced breast cancer patients who received neoadjuvant chemotherapy.
[Mh] MeSH terms primary: Antineoplastic Agents/therapeutic use
Breast Neoplasms/genetics
Breast Neoplasms/therapy
Membrane Transport Proteins/genetics
Neoadjuvant Therapy
Polymorphism, Single Nucleotide
[Mh] MeSH terms secundary: Adult
Breast Neoplasms/mortality
Chemotherapy, Adjuvant
Cohort Studies
Combined Modality Therapy
Epirubicin/therapeutic use
Female
Follow-Up Studies
Humans
Middle Aged
Prognosis
Survival Analysis
Taxoids/therapeutic use
Young Adult
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antineoplastic Agents); 0 (Membrane Transport Proteins); 0 (OCA2 protein, human); 0 (Taxoids); 3Z8479ZZ5X (Epirubicin)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180208
[St] Status:MEDLINE

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Clinical Trials Registry
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[PMID]: 29396713
[Au] Autor:Kiladjian JJ; Guglielmelli P; Griesshammer M; Saydam G; Masszi T; Durrant S; Passamonti F; Jones M; Zhen H; Li J; Gadbaw B; Perez Ronco J; Khan M; Verstovsek S
[Ad] Address:Centre d'Investigations Cliniques (CIC1427), Hôpital Saint-Louis, AP-HP, INSERM, CLIP2 "Saint-Louis - Paris Nord," Early Phase Research Center, Université Paris Diderot, 1, Avenue Claude Vellefaux, 75010, Paris, France. jean-jacques.kiladjian@aphp.fr.
[Ti] Title:Efficacy and safety of ruxolitinib after and versus interferon use in the RESPONSE studies.
[So] Source:Ann Hematol;97(4):617-627, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Ruxolitinib was well tolerated and superior to best available therapy (including interferon [IFN]) in controlling hematocrit without phlebotomy eligibility, normalizing blood counts, and improving polycythemia vera-related symptoms in the Study of Efficacy and Safety in Polycythemia Vera Subjects Who Are Resistant to or Intolerant of Hydroxyurea: JAK Inhibitor INC424 (INCB018424) Tablets Versus Best Available Care (RESPONSE) studies. This ad hoc analysis focuses on ruxolitinib in relation to IFN in the RESPONSE studies, with attention on the following: (1) safety and efficacy of ruxolitinib and best available therapy in patients who received IFN before study randomization, (2) safety and efficacy of IFN during randomized treatment in best available therapy arm, and (3) use of ruxolitinib after crossover from best available therapy in IFN-treated patients. IFN exposure before randomization had little effect on the efficacy or safety of ruxolitinib. In the randomized treatment arms, ruxolitinib was superior to IFN in efficacy [hematocrit control (RESPONSE = 60% of ruxolitinib vs 23% of IFN patients; RESPONSE-2 = 62% of ruxolitinib vs 15% of IFN patients)] and was tolerated better in hydroxyurea-resistant or hydroxyurea-intolerant patients. After crossing over to receive ruxolitinib, patients who had initially received IFN and did not respond had improved hematologic and spleen responses (62% of patients at any time after crossover) and an overall reduction in phlebotomy procedures. Rates and incidences of the most common adverse events decreased after crossover to ruxolitinib, except for infections (primarily grade 1 or 2). These data suggest that ruxolitinib is efficacious and well tolerated in patients who were previously treated with IFN. The RESPONSE (NCT01243944) and RESPONSE-2 (NCT02038036) studies were registered at clinicaltrials.gov .
[Mh] MeSH terms primary: Antineoplastic Agents/therapeutic use
Interferons/therapeutic use
Janus Kinases/antagonists & inhibitors
Polycythemia Vera/drug therapy
Protein Kinase Inhibitors/therapeutic use
Pyrazoles/therapeutic use
[Mh] MeSH terms secundary: Adult
Aged
Antineoplastic Agents/adverse effects
Bloodletting/adverse effects
Combined Modality Therapy/adverse effects
Cross-Over Studies
Drug Monitoring
Drug Resistance, Multiple
Drug Resistance, Neoplasm
Female
Humans
Hydroxyurea/adverse effects
Hydroxyurea/therapeutic use
Interferons/adverse effects
Janus Kinases/metabolism
Male
Middle Aged
Polycythemia Vera/metabolism
Polycythemia Vera/physiopathology
Polycythemia Vera/therapy
Practice Patterns, Physicians'
Protein Kinase Inhibitors/adverse effects
Pyrazoles/adverse effects
Reproducibility of Results
Splenomegaly/etiology
Splenomegaly/prevention & control
[Pt] Publication type:CLINICAL TRIAL; CLINICAL TRIAL, PHASE III; COMPARATIVE STUDY; EQUIVALENCE TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Name of substance:0 (Antineoplastic Agents); 0 (INCB018424); 0 (Protein Kinase Inhibitors); 0 (Pyrazoles); 9008-11-1 (Interferons); EC 2.7.10.2 (Janus Kinases); X6Q56QN5QC (Hydroxyurea)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180204
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3225-1

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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

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[PMID]: 29363351
[Au] Autor:Faghfuri E; Nikfar S; Niaz K; Faramarzi MA; Abdollahi M
[Ad] Address:a Pharmaceutical Biotechnology, Faculty of Pharmacy , Tehran University of Medical Sciences , Tehran , Iran.
[Ti] Title:Mitogen-activated protein kinase (MEK) inhibitors to treat melanoma alone or in combination with other kinase inhibitors.
[So] Source:Expert Opin Drug Metab Toxicol;14(3):317-330, 2018 Mar.
[Is] ISSN:1744-7607
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Malignant melanoma (MM) is an aggressive disease with a rapidly rising incidence due to neoplasm of melanocytes. Molecular targeted therapies have demonstrated lower toxicity and improved overall survival versus conventional therapies of MM. The revealing of mutations in the BRAF/MEK/ERK pathway has led to the development of BRAF inhibitors such as vemurafenib and dabrafenib for the treatment of cutaneous MM. Though, progression of resistance to these agents has prompted attempts to target downstream proteins in this pathway. Trametinib, a MEK1/2 inhibitor, was approved in 2013 for the treatment of BRAF V600E/K mutation-positive unresectable or metastatic cutaneous melanoma patients. Areas covered: The aim of the current review is to present an update on the role of MEK in progressive melanomas and summarize latest results of clinical studies with innovative MEK inhibitors and/or combined approaches with other kinase inhibitors such as BRAF inhibitors in the treatment of MM. Expert opinion: Two combined treatments (i.e. trametinib plus dabrafenib and vemurafenib plus cobimetinib) target two different kinases in the BRAF/MEK/ERK pathway. The simultaneous prohibition of both MEK and BRAF is associated with more durable response rate than BRAF monotherapy and can overcome acquired resistance.
[Mh] MeSH terms primary: Melanoma/drug therapy
Protein Kinase Inhibitors/administration & dosage
Skin Neoplasms/drug therapy
[Mh] MeSH terms secundary: Animals
Antineoplastic Combined Chemotherapy Protocols/administration & dosage
Antineoplastic Combined Chemotherapy Protocols/pharmacology
Drug Resistance, Neoplasm
Humans
Melanoma/genetics
Melanoma/pathology
Mitogen-Activated Protein Kinases/antagonists & inhibitors
Molecular Targeted Therapy
Mutation
Protein Kinase Inhibitors/pharmacology
Proto-Oncogene Proteins B-raf/genetics
Skin Neoplasms/genetics
Skin Neoplasms/pathology
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Protein Kinase Inhibitors); EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf); EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
[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:10.1080/17425255.2018.1432593

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[PMID]: 29351887
[Au] Autor:Jin R; Chen Q; Yao S; Bai E; Fu W; Wang L; Wang J; Du X; Wei T; Xu H; Jiang C; Qiu P; Wu J; Li W; Liang G
[Ad] Address:Department of Digestive Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China; Chemical Biology Research Center, College of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.
[Ti] Title:Synthesis and anti-tumor activity of EF24 analogues as IKKß inhibitors.
[So] Source:Eur J Med Chem;144:218-228, 2018 Jan 20.
[Is] ISSN:1768-3254
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:EF24 is an IKKß inhibitor (IC : 72 µM) containing various anti-tumor activities. In this study, a series of EF24 analogs targeting IKKß were designed and synthesized. Several IKKß inhibitors with better activities than EF24 were screened out and B3 showed best IKKß inhibitory (IC : 6.6 µM). Molecular docking and dynamic simulation experiments further confirmed this inhibitory effect. B3 obviously suppressed the viability of Hela229, A549, SGC-7901 and MGC-803 cells. Then, in SGC-7901 and MGC-803 cells, B3 blocked the NF-κB signal pathway by inhibiting IKKß phosphorylation, and followed arrested the cell cycle at G2/M phase by suppressing the Cyclin B1 and Cdc2 p34 expression, induced the cell apoptosis by down-regulating Bcl-2 protein and up-regulating cleaved-caspase3. Moreover, B3 significantly reduced tumor growth and suppressed the IKKß-NF-κB signal pathway in SGC-7901 xenograft model. In total, this study present a potential IKKß inhibitor as anti-tumor precursor.
[Mh] MeSH terms primary: Antineoplastic Agents/chemistry
Antineoplastic Agents/pharmacology
Benzylidene Compounds/chemistry
Benzylidene Compounds/pharmacology
I-kappa B Kinase/antagonists & inhibitors
Piperidones/chemistry
Piperidones/pharmacology
[Mh] MeSH terms secundary: Animals
Antineoplastic Agents/chemical synthesis
Antineoplastic Agents/therapeutic use
Apoptosis/drug effects
Benzylidene Compounds/chemical synthesis
Benzylidene Compounds/therapeutic use
Cell Line, Tumor
G2 Phase Cell Cycle Checkpoints/drug effects
Humans
I-kappa B Kinase/metabolism
Mice, Nude
Molecular Docking Simulation
NF-kappa B/metabolism
Neoplasms/drug therapy
Neoplasms/metabolism
Neoplasms/pathology
Phosphorylation/drug effects
Piperidones/chemical synthesis
Piperidones/therapeutic use
Signal Transduction/drug effects
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (3,5-bis(2-fluorobenzylidene)piperidin-4-one); 0 (Antineoplastic Agents); 0 (Benzylidene Compounds); 0 (NF-kappa B); 0 (Piperidones); EC 2.7.11.10 (I-kappa B Kinase)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180121
[St] Status:MEDLINE

  10 / 403881 MEDLINE  
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[PMID]: 29331379
[Au] Autor:Shinagawa-Kobayashi Y; Kamimura K; Goto R; Ogawa K; Inoue R; Yokoo T; Sakai N; Nagoya T; Sakamaki A; Abe S; Sugitani S; Yanagi M; Fujisawa K; Nozawa Y; Koyama N; Nishina H; Furutani-Seiki M; Sakaida I; Terai S
[Ad] Address:Division of Gastroenterology and Hepatology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, Niigata, Japan.
[Ti] Title:Effect of histidine on sorafenib-induced vascular damage: Analysis using novel medaka fish model.
[So] Source:Biochem Biophys Res Commun;496(2):556-561, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Sorafenib (SFN) is an anti-angiogenic chemotherapeutic that prolongs survival of patients with hepatocellular carcinoma (HCC); its side effects, including vascular damages such as hand-foot syndrome (HFS), are a major cause of therapy discontinuation. We previously reported that maintenance of peripheral blood flow by intake of dried bonito broth (DBB) significantly prevented HFS and prolonged the administration period. The amino acids contained in DBB probably contribute to its effects, but the mechanism has not been clarified. We hypothesized that histidine, the largest component among the amino acids contained in DBB, has effects on SFN-induced vascular damage, and evaluated this possibility using a novel medaka fish model. METHODS: The fli::GFP transgenic medaka fish model has a fluorescently visible systemic vasculature. We fed the fish with SFN with and without histidine to compare blood flow and vascular structure among the differently fed models. The vascular cross-sectional area of each fish was measured to determine vascular diameter changes. RESULTS: Our results demonstrated that SFN-fed medaka developed a narrower vascular diameter. In addition, this narrowing was counteracted by addition of histidine to the medaka diet. We observed no positive effect of histidine on regeneration of cut vessels or on cell growth of endothelial cells and HCC cell lines. CONCLUSION: We proved the efficacy of the medaka model to assess vascular changes after administration of specific chemicals. And our results suggest that SFN causes vascular damage by narrowing peripheral vessel diameter, and that histidine effectively counteracts these changes to maintain blood flow.
[Mh] MeSH terms primary: Antineoplastic Agents/adverse effects
Blood Flow Velocity/drug effects
Blood Vessels/drug effects
Blood Vessels/pathology
Histidine/pharmacology
Niacinamide/analogs & derivatives
Phenylurea Compounds/adverse effects
[Mh] MeSH terms secundary: Animals
Carcinoma, Hepatocellular/drug therapy
Humans
Liver Neoplasms/drug therapy
Niacinamide/adverse effects
Oryzias
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Antineoplastic Agents); 0 (Phenylurea Compounds); 25X51I8RD4 (Niacinamide); 4QD397987E (Histidine); 9ZOQ3TZI87 (sorafenib)
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:IM
[Da] Date of entry for processing:180115
[St] Status:MEDLINE


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