A5030298957- Epigenetics and DNA Methylation
- Adenosine and Purinergic Signaling
- Pancreatic and Hepatic Oncology Research
- Biochemical and Molecular Research
- Cancer Genomics and Diagnostics
- Pancreatitis Pathology and Treatment
- DNA Repair Mechanisms
- Angiogenesis and VEGF in Cancer
- Pancreatic function and diabetes
- Phagocytosis and Immune Regulation
- Cancer Research and Treatments
- Virus-based gene therapy research
- CRISPR and Genetic Engineering
- Lymphatic System and Diseases
- Cancer, Hypoxia, and Metabolism
- Gastric Cancer Management and Outcomes
- Genetic factors in colorectal cancer
- Animal Virus Infections Studies
- Cancer Cells and Metastasis
- Genomics and Chromatin Dynamics
- Neuroendocrine Tumor Research Advances
- Ubiquitin and proteasome pathways
- RNA modifications and cancer
Centre de Recherche en Cancérologie de Toulouse
2021-2025
Inserm
2021-2024
Université de Toulouse
2021-2024
Centre National de la Recherche Scientifique
2021-2024
Université Toulouse III - Paul Sabatier
2021-2024
Abstract Cytidine deaminase (CDA) functions in the pyrimidine salvage pathway for DNA and RNA syntheses has been shown to protect cancer cells from deoxycytidine-based chemotherapies. In this study, we observed that CDA was overexpressed pancreatic adenocarcinoma patients at baseline essential experimental tumor growth. Mechanistic investigations revealed localized replication forks where it increased speed, improved fork restart efficiency, reduced endogenous stress, minimized breaks,...
In pancreatic ductal adenocarcinoma (PDAC), fibroblast activation leads to excessive secretion of extracellular matrix (ECM) and soluble factors that regulate tumor progression, prompting investigation into endoplasmic reticulum (ER)-resident proteins may support this activation. We identified FKBP7, a peptidyl-prolyl isomerase in the ER, as overexpressed PDAC stroma compared cancer cells, patients with favorable prognosis. Analysis single-cell RNA sequencing databases revealed FKBP7...
Pancreatic cancer will soon become the second cause of death by in Western countries. The main barrier to increase survival patients with this disease requires development novel and efficient therapeutic strategies that better consider tumor biology. In context, oncolytic viruses emerge as promising therapeutics. Among them, fibrotropic minute virus mice prototype (MVMp) preferentially infects migrating undifferentiated cells highly resemble poorly differentiated, basal-like pancreatic...
Abstract The E3 ubiquitin ligase thyroid hormone receptor interacting protein 12 (TRIP12) has been implicated in pancreatic adenocarcinoma (PDAC) through its role mediating the degradation of pancreas transcription factor 1a (PTF1a). PTF1a is a essential for acinar differentiation state that notably diminished during early steps carcinogenesis. Despite these findings, direct involvement TRIP12 onset cancer yet to be established. In this study, we demonstrated was significantly upregulated...
Triple-negative breast cancer (TNBC) is notoriously aggressive with a high metastatic potential, and targeted therapies are lacking. Using transcriptomic histologic analysis of TNBC samples, we found that expression thrombospondin-1 (TSP1), potent endogenous inhibitor angiogenesis an activator latent transforming growth factor beta (TGF-β), associated (i) gene signatures epithelial-mesenchymal transition TGF-β signaling, (ii) metastasis (iii) reduced survival in patients. In contrast, tumors...
Abstract The exonuclease domain of DNA polymerases epsilon's catalytic subunit (POLE) removes misincorporated nucleotides, called proofreading. POLE-exonuclease mutations cause colorectal- and endometrial cancers with an extreme burden single nucleotide substitutions. We recently reported that particularly the hereditary POLE mutation N363K predisposes in addition to aggressive giant cell glioblastomas. knocked-in this homozygously into human lines compared its properties knock-ins likewise...
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<div>Abstract<p>Cytidine deaminase (CDA) functions in the pyrimidine salvage pathway for DNA and RNA syntheses has been shown to protect cancer cells from deoxycytidine-based chemotherapies. In this study, we observed that CDA was overexpressed pancreatic adenocarcinoma patients at baseline essential experimental tumor growth. Mechanistic investigations revealed localized replication forks where it increased speed, improved fork restart efficiency, reduced endogenous stress,...
<p>Figure S2</p>
<div>Abstract<p>Cytidine deaminase (CDA) functions in the pyrimidine salvage pathway for DNA and RNA syntheses has been shown to protect cancer cells from deoxycytidine-based chemotherapies. In this study, we observed that CDA was overexpressed pancreatic adenocarcinoma patients at baseline essential experimental tumor growth. Mechanistic investigations revealed localized replication forks where it increased speed, improved fork restart efficiency, reduced endogenous stress,...
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ABSTRACT Chronic DNA replication stress and genome instability are two hallmarks of cancer that fuel oncogenesis tumor diversity. Therapeutic approaches aimed to leverage tumor-specific intolerable levels or expose vulnerabilities for synthetic lethality purposes have recently gained momentum, especially pancreatic cancer, a disease with no cure. However, the current knowledge regarding molecular mechanisms involved in response tumors is limited. Cytidine deaminase (CDA) pyrimidine salvage...