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Marta Palmieri

Researcher at University of Verona

Publications -  73
Citations -  9230

Marta Palmieri is an academic researcher from University of Verona. The author has contributed to research in topics: Pancreatic cancer & Gene. The author has an hindex of 35, co-authored 72 publications receiving 7850 citations.

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“Proteomic profiling of pancreatic ductal carcinoma cell lines treated with trichostatin-A”

TL;DR: Modulation of four proteins, of particular interest are the two downregulated proteins nucleophosmin and translationally controlled tumor protein, as well as the upregulated proteins programmed cell death protein 5 and stathmin, are consistent with the observation that TSA is able to inhibit cell growth of Paca44 by causing cell cycle arrest at the G2 phase and apoptotic cell death.
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Proteomic analysis of pancreatic endocrine tumor cell lines treated with the histone deacetylase inhibitor trichostatin A

TL;DR: The present data are in agreement with previous proteomic analyses performed on pancreatic ductal carcinoma cell lines and place histone‐deacetylases inhibitors among the potentially most powerful drugs for the treatment of pancreatic tumors.
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Gemcitabine response in pancreatic adenocarcinoma cells is synergistically enhanced by dithiocarbamate derivatives.

TL;DR: Results and the consideration that DSF is already used in clinics strongly support the GEM and DSF/Zn combination as a new approach to overcoming pancreatic cancer resistance to standard chemotherapy.
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Extracellular matrix composition modulates PDAC parenchymal and stem cell plasticity and behavior through the secretome.

TL;DR: A concerted high local invasion of parenchymal cells into the CSC‐derived vascular network suggests that a symbiotic relationship between the parenchymal cells and theCSCs underlies the initiation and maintenance of early PDAC infiltration and metastasis.
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Increased stability of P21(WAF1/CIP1) mRNA is required for ROS/ERK-dependent pancreatic adenocarcinoma cell growth inhibition by pyrrolidine dithiocarbamate.

TL;DR: The results suggest that the resistance of fibroblasts to the cytotoxic action of PDTC may be related to the up-regulation of p53-dependent antioxidant genes.