Search results for "Pancreatic cancer"

showing 10 items of 177 documents

1,2,4-Amino-triazine derivatives as pyruvate dehydrogenase kinase inhibitors: Synthesis and pharmacological evaluation

2023

: Among the different hallmarks of cancer, deregulation of cellular metabolism turned out to be an essential mechanism in promoting cancer resistance and progression. The pyruvate dehydrogenase kinases (PDKs) are well known as key regulators in cells metabolic process and their activity was found to be overexpressed in different metabolic alerted types of cancer, including the high aggressive pancreatic ductal adenocarcinoma (PDAC). To date few PDK inhibitors have been reported, and the different molecules developed are characterized by structural chemical diversity. In an attempt to find novel classes of potential PDK inhibitors, the molecular hybridization approach, which combine two or m…

PharmacologyPDK inhibitors4-Amino-triazines1Organic ChemistryDrug Discovery2124-Amino-triazinesGeneral MedicineKRAS-mutated pancreatic cancerLigand-based homology modelingSettore CHIM/08 - Chimica Farmaceutica124-Amino-triazines; KRAS-mutated pancreatic cancer; Ligand-based homology modeling; PDK inhibitorsEuropean Journal of Medicinal Chemistry
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Hereditäre Pankreatitis - Eine klinisch relevante Ursache des Pankreaskarzinoms? -

2001

UNLABELLED Hereditary pancreatitis is an autosomal dominant disease. Recently, the genetic defect has been mapped to chromosome 7q35 and consists mainly of a point mutation in exon 3 of the cationic trypsinogen gene which causes an Arg(CGC)-His(CAC) substitution at residue 117. In patients with hereditary pancreatitis the estimated cumulative risk for pancreatic carcinoma to age 70 approaches 40 %. Thus, the role of hereditary pancreatitis in the pathogenesis of pancreatic carcinoma is of interest. PATIENTS AND METHODS DNA was extracted from peripheral blood (n = 16), fresh tumor tissue (n = 29) and formalin fixed and paraffin embedded tumor tissue (n = 5) of 50 patients with ductal adenoca…

Hereditary pancreatitismedicine.medical_specialtyTrypsinogenbusiness.industryGeneral surgeryPoint mutationAutosomal dominant traitmedicine.diseasechemistry.chemical_compoundExonmedicine.anatomical_structurechemistryPancreatic cancermedicineCancer researchAdenocarcinomaSurgeryPancreasbusinessZentralblatt für Chirurgie
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Retrospective Cohort Study of Cancer Mortality at the Minsk Leather Tannery

2006

The cohort of 768 workers who were actively employed for a minimum of 6 months and died was retrospectively followed from 1 January 1953 to 31 December 2000. There were 328 women and 440 men observed. Proportionate mortality ratios (PMRs) were calculated using the Minsk-city population mortality proportions to generate expected numbers. The significant excess of pancreatic cancer (PMR=366%; 95%CI=134-800) and melanoma and skin cancer (PMR=455%; 95% CI=123-1,164) in women-workers of Dyeing and stuffing workshops was shown. The significantly high mortality from pancreatic cancer among Dyeing and stuffing workshops' female workers hired and discharged between 1958 and 1984 (PMR=1,024%; 95% CI=…

AdultMalemusculoskeletal diseasesmedicine.medical_specialtyRepublic of BelarusHealth Toxicology and MutagenesiseducationPopulationCohort StudiesUterine cancerNeoplasmsOccupational ExposureInternal medicinePancreatic cancermedicineHumanseducationCervixAgedRetrospective StudiesAged 80 and overGynecologyeducation.field_of_studybusiness.industryPublic Health Environmental and Occupational HealthTanningRetrospective cohort studyMiddle Agedmedicine.diseasemedicine.anatomical_structureCohortFemaleSkin cancerbusinessCohort studyIndustrial Health
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Malignant epithelial/exocrine tumors of the pancreas

2020

Summary Pancreatic malignant exocrine tumors represent the most important cause of cancer-related death for pancreatic neoplasms. The most common tumor type in this category is represented by pancreatic ductal adenocarcinoma (PDAC), an ill defined, stroma-rich, scirrhous neoplasm with glandular differentiation. Here we present the relevant characteristics of the most important PDAC variants, namely adenosquamous carcinoma, colloid carcinoma, undifferentiated carcinoma, undifferentiated carcinoma with osteoclast-like giant cells, signet ring carcinoma, medullary carcinoma and hepatoid carcinoma. The other categories of malignant exocrine tumors, characterized by fleshy, stroma-poor, circumsc…

acinarPathologymedicine.medical_specialtyAdenosquamous carcinomapancreatic cancerPancreatoblastomapancreatic ductal adenocarcinomaReviewAdenocarcinomaGlandular DifferentiationPathology and Forensic MedicinePancreatic cancersolid pseudopapillary.medicineCarcinomaNeoplasmHumansacinar; pancreatic cancer; pancreatic ductal adenocarcinoma; PDAC; solid pseudopapillaryPancreasbusiness.industryPDACPDAC; acinar; pancreatic cancer; pancreatic ductal adenocarcinoma; solid pseudopapillarymedicine.diseasePancreas ExocrinePancreatic Neoplasmssolid pseudopapillarymedicine.anatomical_structureMedullary carcinomaPancreasbusinessCarcinoma Pancreatic Ductal
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Prognostic Role of High-Grade Tumor Budding in Pancreatic Ductal Adenocarcinoma: A Systematic Review and Meta-Analysis with a Focus on Epithelial to …

2019

This study aims at clarifying the prognostic role of high-grade tumor budding (TB) in pancreatic ductal adenocarcinoma (PDAC) with the first systematic review and meta-analysis on this topic. Furthermore, we analyzed with a systematic review the relationship between TB and a recently suggested TB-associated mechanism: the epithelial to mesenchymal transition (EMT). Analyzing a total of 613 patients, 251 of them (40.9%) with high grade-TB, we found an increased risk of all-cause mortality (RR, 1.46; 95% CI, 1.13-1.88, p = 0.004; HR, 2.65; 95% CI, 1.79-3.91; p < 0.0001) and of recurrence (RR, 1.61; 95% CI, 1.05-2.47, p = 0.03) for PDAC patients with high-grade TB. Moreover, we found that E…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyPancreatic ductal adenocarcinomapancreatic cancerHigh grade tumorReviewEMT; budding; buds; epithelial to mesenchymal transition; pancreatic cancerbuddinglcsh:RC254-28203 medical and health sciences0302 clinical medicineTumor buddingPancreatic cancerInternal medicineMedicineClinical significanceEpithelial–mesenchymal transitionbusiness.industryEMTepithelial to mesenchymal transitionbudslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasebud3. Good health030104 developmental biologyIncreased riskOncology030220 oncology & carcinogenesisMeta-analysisbusinessCancers
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Treatment of pancreatic cancer: A narrative review of cost-effectiveness studies.

2013

Cancer of the pancreas is the second most frequent digestive cancer in the US, accounting for about 44,000 new cases per year. In Europe, it is the sixth most frequent cancer, accounting for 2.8% of cancers in men and 3.2% in women. With a five-year survival of less than 10%, it is the fifth leading cause of cancer-related death. The majority of cases are diagnosed above the age of 65 and in about 60% of cases at an advanced stage, explaining that little improvement has been observed in survival over the past 30 years. Radical surgery offers the only curative treatment of pancreatic cancer. Alternative or combined therapeutic options in particular consist of adjuvant or neoadjuvant chemothe…

Oncologymedicine.medical_specialtyCost effectivenessmedicine.medical_treatmentCost-Benefit AnalysisAntineoplastic AgentsQuality of lifePancreatic cancerInternal medicineAdjuvant therapyMedicineCombined Modality TherapyHumansRadical surgeryIntensive care medicineDigestive System Surgical Proceduresbusiness.industryPalliative CareGastroenterologyCancermedicine.diseaseCombined Modality TherapyRadiation therapyEconomics MedicalEuropePancreatic NeoplasmsQuality of LifeHealth ResourcesbusinessBest practiceresearch. Clinical gastroenterology
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FOXP3 Inhibitory Peptide P60 Increases Efficacy of Cytokine-induced Killer Cells Against Renal and Pancreatic Cancer Cells

2019

Background/aim Cytokine-induced killer (CIK) cells are ex vivo expanded major histocompatibility complex (MHC)-unrestricted cytotoxic cells with promising effects against a variety of cancer types. Regulatory T-cells (T-reg) have been shown to reduce the effectiveness of CIK cells against tumor cells. Peptide P60 has been shown to inhibit the immunosuppressive functions of T-regs. This study aimed at examining the effect of p60 on CIK cells efficacy against renal and pancreatic cancer cells. Materials and methods The effect of P60 on CIK cytotoxicity was examined using flow cytometry, WST-8-based cell viability assay and interferon γ (IFNγ) ELISA. Results P60 treatment resulted in a signifi…

Cytotoxicity ImmunologicCancer ResearchFOXP3Cell SurvivalImmunotherapy.KidneyMajor histocompatibility complexT-Lymphocytes RegulatoryInterferon-gamma03 medical and health sciencesCytokine-Induced Killer Cells0302 clinical medicineCytokine-induced killer (CIK) cellCell Line TumorPancreatic cancermedicineHumansCytotoxic T cellViability assayCytotoxicityPancreasCancerCytokine-induced killer cellbiologyChemistryFOXP3Forkhead Transcription FactorsGeneral Medicinemedicine.diseaseCoculture TechniquesKidney NeoplasmsPancreatic NeoplasmsOncologyCell culture030220 oncology & carcinogenesisAdoptive cell transferCancer researchbiology.proteinCytokinesPeptidesAnticancer Research
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Moving the target on the optimal adjuvant strategy for resected pancreatic cancers: A systematic review with meta-analysis

2020

Combination regimens have shown superiority over single agents in the adjuvant treatment of resected pancreatic cancer (PC), but there are no data supporting definition of the best regimen. This work aimed to compare the efficacy and safety of mFOLFIRINOX, gemcitabine+capecitabine, and gemcitabine+nab/paclitaxel in PC patients. A meta-analysis was performed for direct comparison between trials comparing combination regimens and gemcitabine monotherapy. Subsequently, an indirect comparison was made between trials investigating the efficacy and safety of mFOLFIRINOX, gemcitabine+capecitabine, and gemcitabine+nab/paclitaxel because of the same control arm (gemcitabine). A total of three studie…

OncologyCancer Researchmedicine.medical_specialtymedicine.medical_treatmentReviewNeutropenialcsh:RC254-282Capecitabine03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePancreatic cancerInternal medicinemedicineChemotherapyMeta-analysi030212 general & internal medicineAdjuvantChemotherapybusiness.industryMFOLFIRINOXPancreatic cancerlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseGemcitabineRegimenMeta-analysisOncologyPaclitaxelchemistryAdjuvant Chemotherapy Meta-analysis MFOLFIRINOX Pancreatic cancer Systematic review030220 oncology & carcinogenesisSystematic reviewbusinessAdjuvantmedicine.drug
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HGF/MET Axis Induces Tumor Secretion of Tenascin-C and Promotes Stromal Rewiring in Pancreatic Cancer

2021

Simple Summary It has been previously shown that activation of the MET receptor by its ligand, the hepatocyte growth factor (HGF), modulates the tumor-stroma cross-talk in models of pancreatic cancer. We now wish to cast light on the molecular mechanisms by which this ligand/receptor pair sustains the interaction between cancer cells and the tumor microenviroment. To this end, we compared data obtained by large-scale analysis of gene expression in pancreatic cancer cells grown in the presence of HGF versus cells grown in the presence of HGF and treated with specific inhibitors of HGF/MET signaling. By clustering differentially expressed genes according to functional groups, we identified ca…

0301 basic medicineCancer ResearchStromal cellpancreatic ductal adenocarcinomaArticle03 medical and health sciences0302 clinical medicinePancreatic tumorPancreatic cancerMET oncogenemedicinetumor microenvironmentmetastasisHepatocyte growth factor; MET oncogene; Metastasis; Pancreatic ductal adenocarcinoma; Tenascin C; Tumor microenvironmentRC254-282Tumor microenvironmentbiologyChemistryTenascin Ctenascin CNeoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease030104 developmental biologyhepatocyte growth factorOncology030220 oncology & carcinogenesisCancer cellHepatic stellate cellbiology.proteinCancer researchHepatocyte growth factormedicine.drugCancers
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Abstract LB061: On-target peripheral and tumor immune microenvironment modulation in patients treated with lacnotuzumab (anti-CSF1, MCS110) + spartal…

2021

Abstract Background: The CSF-1/CSF-1R (colony-stimulating factor-1) pathway plays a significant role in the tumor microenvironment via regulation of tumor-associated macrophages (TAMs). Lacnotuzumab (MCS110) is a humanized monoclonal antibody against CSF-1. Lacnotuzumab may counteract the tumor suppressive microenvironment induced by CSF-1, potentially enhancing the efficacy of PD-1 inhibition. Methods: MCS110Z2102 is a phase 1b/2 study in cancer patients with advanced malignancies treated by lacnotuzumab combined with the PD-1 inhibitor spartalizumab. Eligible patients with previously treated advanced/metastatic solid tumors received 1, 3, 5, 7.5 and 10 mg/kg intravenous doses of lacnotuzu…

Cancer ResearchTumor microenvironmentbusiness.industryEndometrial cancerMelanomaCancermedicine.diseaseGene expression profilingBreast cancerOncologyPancreatic cancermedicineCancer researchCytotoxic T cellbusinessCancer Research
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