Results 301 to 310 of about 85,787 (336)
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TRIM29 facilitates gemcitabine resistance via MEK/ERK pathway and is modulated by circRPS29/miR-770-5p axis in PDAC.

Drug resistance updates
AIMS Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal disease. Chemotherapy based on gemcitabine (GEM) remains the first-line drug for patients with advanced PDAC. However, GEM resistance impairs its therapeutic effectiveness.
Wenjie Huang   +9 more
semanticscholar   +1 more source

PDAC Subtypes/Stratification

2020
Large-scale sequencing analyses have transformed our understanding of PDAC and have defined several molecular taxonomies that now guide pre-clinical and clinical therapeutic development. The identification of molecularly defined subgroups of patients with distinct biological underpinnings and potential therapeutic vulnerabilities promises a step change
Holly Brunton   +3 more
openaire   +1 more source

Epigenomic Changes Prime PDAC Metastasis

Cancer Discovery, 2017
Abstract Widespread chromatin modifications and DNA methylation could be responsible for inducing the spread of pancreatic ductal adenocarcinoma cells to distant sites, according to recent research. The findings also implicate glucose metabolism as a driver of metastasis.
openaire   +2 more sources

S100A16 induces epithelial-mesenchymal transition in human PDAC cells and is a new therapeutic target for pancreatic cancer treatment that synergizes with gemcitabine.

Biochemical Pharmacology, 2020
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers, with a poor 5-year survival rate of approximately 6%, mostly due to poor treatment response and early progression.
Ting Li   +10 more
semanticscholar   +1 more source

KRAS degradation averts PDAC chemoresistance

Nature Cancer
Effectively targeting deregulated KRAS signaling remains an unmet clinical need, as current approaches commonly lead to the development of chemoresistance in clinical settings. ADAM9-mediated lysosomal KRAS degradation is now shown to counteract PDAC chemoresistance independently of mutational status.
Laura Leonhardt, Matthias Hebrok
openaire   +3 more sources

A Bacterial-Based Immunotherapy for PDAC

Cancer Discovery, 2022
Abstract Researchers have used the bacterium Listeria monocytogenes to deliver tetanus toxoid to mice with pancreatic ductal adenocarcinoma. In these mice, previously vaccinated for tetanus, memory T cells were reactivated to subsequently destroy the tumors. Plans are underway to evaluate this approach in a phase I trial.
openaire   +2 more sources

Neoantigen-based immunotherapy in pancreatic ductal adenocarcinoma (PDAC).

Cancer Letters, 2020
Neoantigens generated in neoplasms are a type of protein completely absent in healthy tissues. Therefore, anti-tumor immunity targeting neoantigens is highly specific, which provides an optional approach to boost tumor immunotherapy.
Hao Chen   +5 more
semanticscholar   +1 more source

Toward Ablative SBRT for Nonmetastatic PDAC

Cancer Discovery, 2023
Abstract Combining a superoxide dismutase mimetic, avasopasem manganese, with stereotactic body radiation therapy may enable safe delivery of higher than standard radiation doses for patients with nonmetastatic, inoperable pancreatic adenocarcinoma.
openaire   +2 more sources

PDAC-GENOME

DNA sequencing data of 41 paired PDAC patients and RNA-seq encing data of 41 normal PDAC ...
openaire   +1 more source

Glutamine metabolism drives PDAC

Science-Business eXchange, 2013
Dana-Farber researchers have identified a glutamine metabolism pathway activated by oncogenic K-Ras in pancreatic cancers. The team found three different enzyme targets within the pathway that could be targeted to specifically inhibit tumor proliferation.
openaire   +1 more source

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