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Insights into gemcitabine resistance and the potential for therapeutic monitoring [PDF]

open access: yesMetabolomics, 2018
Gemcitabine is an important component of pancreatic cancer clinical management. Unfortunately, acquired gemcitabine resistance is widespread and there are limitations to predicting and monitoring therapeutic outcomes.To investigate the potential of metabolomics to differentiate pancreatic cancer cells that develops resistance or respond to gemcitabine ...
Vinee Purohit   +2 more
exaly   +3 more sources

SLC38A5 Modulates Ferroptosis to Overcome Gemcitabine Resistance in Pancreatic Cancer

open access: yesCells, 2023
Pancreatic cancer is characterized by a poor prognosis, with its five-year survival rate lower than that of any other cancer type. Gemcitabine, a standard treatment for pancreatic cancer, often has poor outcomes for patients as a result of ...
Joon Seong Park   +2 more
exaly   +2 more sources
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Combination of hydroxyurea and tranilast suppresses gemcitabine resistance induced by ribonucleotide reductase M1 in gemcitabine‐resistant cells

Oral Science International, 2020
AbstractIntroductionGemcitabine (GEM; 2′,2′‐difluorodeoxycytidine) is widely used to treat pancreatic, biliary tract, non‐small cell lung, bladder, mammary, and ovarian cancers. Chemoradiotherapy with GEM is a promising treatment for patients with advanced and locally recurrent head and neck cancers, including those with oral cavity cancer.
Noriho Shinagawa   +7 more
openaire   +1 more source

S100A14 promotes progression and gemcitabine resistance in pancreatic cancer

Pancreatology, 2021
S100 calcium binding protein A14 (S100A14) plays an important role in the progression of several types of cancer. However, its roles in pancreatic ductal adenocarcinoma (PDAC) are largely unexplored. Here, we characterized the functional roles of S100A14 in the progression and chemoresistance of PDAC.
Hongwei, Zhu   +6 more
openaire   +2 more sources

Cytosolic 5′-nucleotidase 1A is overexpressed in pancreatic cancer and mediates gemcitabine resistance by reducing intracellular gemcitabine metabolites [PDF]

open access: yesEBioMedicine, 2019
BACKGROUND: Cytosolic 5'-nucleotidase 1A (NT5C1A) dephosphorylates non-cyclic nucleoside monophosphates to produce nucleosides and inorganic phosphates.
Volker Ellenrieder   +2 more
exaly   +3 more sources

Acquired resistance to gemcitabine and cross-resistance in human pancreatic cancer clones

Anti-Cancer Drugs, 2015
The efficacy of gemcitabine (GEM), a standard treatment agent for pancreatic cancer, is insufficient because of primary or acquired resistance to this drug. Patients with tumors intrinsically sensitive to GEM gradually acquire resistance and require a shift to second agents, which are associated with the risk of cross-resistance. However, whether cross-
Hiroshi, Yoneyama   +7 more
openaire   +2 more sources

Inference and Modelling of the Gemcitabine Pharmacokinetics and Resistance

2012
Context Integrative network inference methods and modelling approaches could support the experimental activity devoted to the identification of mechanisms of action of oncological drugs as well as the identification of pathways entailing with the chemoresistance.
Lecca, Paola, Priami, Corrado
openaire   +4 more sources

Abstract 3122: Combination effect of metformin with gemcitabine for gemcitabine-resistant pancreatic adenocarcinoma

Cancer Research, 2014
Abstract Metformin (MET) is the first-line treatment for type-2 diabetes mellitus. Several epidemiological studies have revealed the anti-cancer effects of metformin, including against pancreatic ductal carcinoma (PDC). Gemcitabine (GEM) has become the standard chemotherapy for PDC but tolerance to GEM is an important issue.
Keiichi Suzuki   +3 more
openaire   +1 more source

Development and Characterization of Gemcitabine-Resistant Pancreatic Tumor Cells

Annals of Surgical Oncology, 2007
Pancreatic cancer is an exceptionally lethal disease with an annual mortality nearly equivalent to its annual incidence. This dismal rate of survival is due to several factors including late presentation with locally advanced, unresectable tumors, early metastatic disease, and rapidly arising chemoresistance.
Ami N, Shah   +5 more
openaire   +2 more sources

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