Home Men Health PI3K/AKT and MEK/ERK pathways targeted in latest therapy for docetaxel-resistant prostate cancer

PI3K/AKT and MEK/ERK pathways targeted in latest therapy for docetaxel-resistant prostate cancer

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PI3K/AKT and MEK/ERK pathways targeted in latest therapy for docetaxel-resistant prostate cancer

A team of researchers from the Badalona Applied Research Group in Oncology (B·ARGO) and the Urologic Tumours Unit of the Institut Català d’Oncologia (ICO) and the Germans Trias i Pujol Research Institute (IGTP) have found a brand new therapeutic strategy for patients with a selected subtype of metastatic prostate cancer resistant to plain chemotherapy treatment with docetaxel.

On this study, published within the journal Frontiers in Pharmacology, they propose a brand new treatment based on a mix of kinase inhibitors in patients who inevitably stop responding to docetaxel. The team found that resistance to this drug is related to the hyperactivation of the cellular pathways PI3K/AKT and MEK/ERK and have explored the opportunity of inhibiting these pathways as a brand new therapeutic strategy in patients who maintain the function of PTEN, a negative regulatory protein of the PI3K/AKT pathway.

The outcomes of the study have been satisfactory and, for that reason, the team desires to conduct a clinical trial to evaluate the protection and efficacy of this mix in patients with prostate cancer proof against docetaxel. Vicenç Ruiz de Porras and Adrià Bernat-Peguera, ICO-IGTP researchers and co-first authors of the study, state that the outcomes of this study “open the door to a brand new therapeutic strategy for those patients with PTEN wild-type tumors, who’ve progressed to docetaxel and in whom, unlike PTEN null patients, the efficacy of AKT inhibitors in monotherapy has not been demonstrated.”

Source:

Journal reference:

Ruiz, V., et al. (2024). Dual inhibition of MEK and PI3Kβ/δ–a possible therapeutic strategy in PTEN-wild-type docetaxel-resistant metastatic prostate cancer. Frontiers in Pharmacology. doi.org/10.3389/fphar.2024.1331648.

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