Is 'miracle' cancer therapy all it's cracked up to be?
Nigel Lewis-Baker, 71, from Effingham in Surrey, was told he had just months to live three years ago after being diagnosed with prostate cancer.
Personalization of prostate cancer therapy through phosphoproteomics, Published online: 11 May 2018; doi:10.1038/s41585-018-0014-0Yang and colleagues discuss the clinical need and rationale for a phosphoproteomics approach to personalizing prostate cancer treatment. They describe current technologies, clinical findings, and challenges and strategies to realizing routine clinical application of phosphoproteomics.
Molecular PharmaceuticsDOI: 10.1021/acs.molpharmaceut.8b00152
In conclusion, we identify montelukast may be used as a novel agent for the treatment of prostate cancer by decreasing HIF-1α protein translation. PMID: 29708817 [PubMed - as supplied by publisher]
In this study, PEGylated bilirubin-based nanoparticles (BRNPs) were chosen as an appropriate delivery carrier because of their ability to release drugs in response to TME-associated reactive oxygen species (ROS) through rapid particle disruption. As a model SMDC, ACUPA-SN38 was synthesized by linking the prostate membrane-specific antigen (PSMA)-targeting ligand, ACUPA, to the chemotherapeutic agent, SN38. ACUPA-SN38 was loaded into BRNPs using a film-formation and rehydration method. The resulting ACUPA-SN38@BRNPs exhibited ROS-mediated particle disruption and rapid release of the SMDC, resulting in greater cytotoxicity t...
This study focused to clarify the roles of Metadherin (MTDH) and miR-342-3p in prostate cancer. We identified that MTDH was up-regulated and miR-342-3p was down-regulated in the prostate tissues, and there is an inverse correlation between MTDH and miR-342-3p. Functional studies revealed that miR-342-3p directly targets MTDH via binding to the 3’untranslated regions (UTRs) in the prostate cancer cells. Moreover, we also found MTDH overexpression in DU145 and PC3 cells inhibited apoptosis. Subsequently, miR-342-3p has been revealed to reverse the MTDH effect on the cellular apoptosis in the further studies. Our result...
Abstract The current paradigm in the development of new cancer therapies is the ability to target tumor cells while avoiding harm to noncancerous cells. Furthermore, there is a need to develop novel therapeutic options against drug-resistant cancer cells. Herein, we characterized the placental-derived stem cell (PLSC) exosomes (PLSCExo) and evaluated their anti-cancer efficacy in prostate cancer (PCa) cell lines. Nanoparticle tracking analyses revealed the size distribution (average size 131.4 ± 0.9 nm) and concentration of exosomes (5.23 × 1010±1.99 × 109 per ml) secreted b...
Conclusion: This study demonstrated that PSMA-11–derived dual-labeled dye conjugates are feasible for providing PSMA-specific pre-, intra-, and postoperative detection of prostate cancer lesions and have high potential for future clinical translation.
The ETS Related Gene (ERG) is dormant and non-detectable in normal prostate. Despite of significant advancements in prostate cancer treatment in recent years, hormone therapy remains the main treatment for advanced CaP. Unfortunately, late stage prostate cancers are highly prone to treatment resistance. Thus, there is an urgent need to develop effective and novel inhibitors to target CaP driver genes in the early stages of prostate tumorigenesis. ERG oncoprotein and ERG dependent pathways are promising targets for early stage cancer therapy.
To isolate cell-specific internalizing aptamers (Apt) against prostate cancer cells and evaluating their efficiency in vitro and in vivo. Engineering aptamer-targeted nanoparticles for prostate cancer therapy.
We examined the anticancer effects of NCL1 and NCD38, selective inhibitors of LSD1 (LSD1i) that were first discovered at our university.