Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive type of solid tumor that is becoming more common. -[PtCl (NH)] (in short cisplatin or CDDP) has been shown to be effective in treating various cancers, including PDAC. However, the development of resistance to chemotherapy drugs has created a need for the synthesis of new anticancer agents. Platinum-based drugs containing the bidentate ligand phenanthroline have been found to have strong antitumor activity due to their ability to cause DNA damage. In this study, we examined the ability of two Pt (II) cationic complexes, [Pt( -CHOR) (DMSO) (phen)] (in short Pt-EtORSOphen; = Me, ; Et, ), to inhibit the growth and spread of BxPC-3 PDAC cells, in comparison to CDDP. The length of the alkyl chain and its associated lipophilic properties did not affect the anticancer effects of complexes and in BxPC-3 cells. However, it did appear to influence the rapid loss of mitochondrial membrane potential (ΔΨ), suggesting that these complexes could potentially be used as mitochondria-targeted lipophilic cations in anticancer therapy.
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http://dx.doi.org/10.1155/bca/5588491 | DOI Listing |
Ann Surg
January 2025
Department of General, Visceral and Transplantation Surgery, Heidelberg University Hospital, Heidelberg, Germany.
Aim: To validate the prognostic value of the PAncreatic NeoAdjuvant MAssachusetts (PANAMA)-score and to determine its predictive ability for survival benefit derived from adjuvant treatment in patients after resection of pancreatic ductal adenocarcinoma (PDAC) following neoadjuvant FOLFIRINOX.
Background: The PANAMA-score was developed to guide prognostication in patients after neoadjuvant therapy and resection for PDAC. As this score focuses on the risk for residual disease after resection, it might also be able to select patients who benefit from adjuvant after neoadjuvant therapy.
Bioinorg Chem Appl
December 2024
Department of Biological and Environmental Sciences and Technologies (DiSTeBA), University of Salento, Lecce, Via Monteroni I-73100, Italy.
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive type of solid tumor that is becoming more common. -[PtCl (NH)] (in short cisplatin or CDDP) has been shown to be effective in treating various cancers, including PDAC. However, the development of resistance to chemotherapy drugs has created a need for the synthesis of new anticancer agents.
View Article and Find Full Text PDFFront Immunol
January 2025
Division of Pharmacology, Otto Loewi Research Center, Medical University of Graz, Graz, Austria.
Background: The G protein-coupled receptor 55 (GPR55) is part of an expanded endocannabinoid system (ECS), and plays a pro-tumorigenic role in different cancer models, including pancreatic cancer. Next to cancer cells, various cells of the immune tumor microenvironment (TME) express receptors of the ECS that critically determine tumor growth. The role of GPR55 in cancer cells has been widely described, but its role in the immune TME is not well understood.
View Article and Find Full Text PDFFuture Med Chem
January 2025
Department of Organic Chemistry, Faculty of Pharmacy, University of Belgrade, Belgrade, Serbia.
Aim: With the aim of simultaneously modulating the epigenetic system and the protein kinase pathway, we selected the enzyme histone deacetylase (HDAC) and the Rho-associated protein kinases (ROCK) as desired targets to develop potential multitarget anticancer agents with additional antimetastatic properties. We report here the rational design, synthesis, and biological evaluation of the HDAC/ROCK multitarget inhibitors in pancreatic ductal adenocarcinoma (PDAC) and triple-negative breast cancer (TNBC).
Materials And Methods: A molecular docking study performed with the Gold software was used to develop HDAC/ROCK multitarget inhibitors.
Background: Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal cancer with a 5-year survival rate of 12%. It has two major molecular subtypes: classical and basal, regulated by the master transcription factors (MTFs) GATA6 and ΔNp63, respectively.
Objective: This study sought to uncover the transcriptional regulatory mechanisms controlling PDAC subtype identity.
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