Prostate Cancer: Emerging Modifiable Risk Factors and Therapeutic Strategies in the Management of Advanced Cancer
Abstract
:1. Introduction
2. Materials and Methods
3. Prostate Cancer and an Unhealthy Lifestyle
3.1. Diet
3.2. Smoking
3.3. Alcohol
3.4. Sedentary Lifestyle
Unhealthy Lifestyle | Effects on PCa Onset and Progression | References | |
---|---|---|---|
Diet | ROS production, Inflammation, Hyperinsulinemia, Gut microbiome disrupted | [18,19,20,21,22,23,24,25,26] | |
Smoking | High resistance to treatment | [28,29,30,31] | |
Alcohol | No correlation with PCa | [32,33] | |
Sedentary life | Active lifestyle reduces the risk of mortality. Poor sleep quality induces aggressive forms of PCa | [34,35,36,37,38] | |
Environmental Factors | Effects on PCa onset and progression | Mechanisms of action | References |
Heavy metals | Tumor progression | Increased levels of MMP-9; DNA metylation; K-RAS activation; apoptosis inhibition SUMOylation of AR | [39,40,41,42,43,44] |
Persistent Organic Pollutants | Increase in aggressiveness and metastasis progression | Activation/inhibition of transcriptional activity of target genes by AHR-XRE activation; up-regulation of ACAT1 by AHR activation; Up-regulation of MMP-9 exerted by AHR | [45,46] |
Environmental carcinogens | Excessive production of ROS drives the onset of PCa | Cellular damage, changes DNA sequence, proteins alterations | [47,48] |
4. Prostate Cancer and Environmental Factors
4.1. Heavy Metals
4.2. Persistent Organic Pollutants (POPs)
5. Preclinical Models and Emerging Therapies in the Treatment of Advanced Prostate Cancer
5.1. Preclinical Models of PCa
5.2. Novel Putative Therapies in the Management of Advanced PCa
Preclinical Models | Aims of Tool | Advances | Limitations | References | |
---|---|---|---|---|---|
PDX (Patient-derived xenograft model) | Transplantation of human tumor tissue into an immunodeficiency animal model | More accurate reproduction of tumor’s biology and complexity of TME by human tumor grown in animal model | Useful tool to a personalized therapeutic strategy | Lack of functionality of the human immune system in the host animal; loss of human stromal component in the animal model | [61] |
PDOs (Patient-derived organoids model) | 3D cultures of patient tissues by a basement membrane (Matrigel) | Development of organoids that reproduce the molecular and clinical diversity of PCa, as various genetic mutations | Mimic of the complexity of TME; a useful tool to test new drugs in PCa-resistant therapeutic strategies | High cost and further protocol standardization | [60,63,64,65] |
New therapeutic strategies | Aims | Advances | Limitations | References | |
CAR-T cell therapy | Genetic modification of patient’s T-cells expressing chimeric antigen receptor (CAR) targeting for PCa cells | CAR-T cells target and kill cancer cells | Low levels of PSA and improvement in imaging results; activation of peripheral blood endogenous, TCR repertoire diversity; alteration of TME | Collateral effects such as cytokine release syndrome and cystitis | [68] |
Cancer-Associated-Fibroblast (CAF) therapy | Co-culturing of human tumor tissue with CAF | Disruption of tumor progression and enhancement of cancer therapy | Useful tool for new treatment option of PCa; inhibition of chemokines/cytokines and growth factors | Complex interaction within TME due to the heterogeneity and plasticity of CAF | [69,70,71,72] |
Targeted Radionuclide therapy (TRT) | Radioactive isotope linked to a vector molecule specifically targeting tumor cell receptors or the tumor microenvironment (PSMA/GRPR) | Improving both overall survival and progression-free survival of patients with mCRPC | A useful tool for personalized treatment of mCRPC; Integration of TRT with other treatment modalities to optimize mCRPC therapy | Radiopharmaceuticals exhibit high tissue absorption, low energy transfer, and a broad radiation spectrum | [73,74,75,76] |
6. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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Bossio, S.; Urlandini, L.; Perri, A.; Conforti, F.; Aversa, A.; Di Agostino, S.; Rago, V. Prostate Cancer: Emerging Modifiable Risk Factors and Therapeutic Strategies in the Management of Advanced Cancer. Life 2024, 14, 1094. https://doi.org/10.3390/life14091094
Bossio S, Urlandini L, Perri A, Conforti F, Aversa A, Di Agostino S, Rago V. Prostate Cancer: Emerging Modifiable Risk Factors and Therapeutic Strategies in the Management of Advanced Cancer. Life. 2024; 14(9):1094. https://doi.org/10.3390/life14091094
Chicago/Turabian StyleBossio, Sabrina, Lidia Urlandini, Anna Perri, Francesco Conforti, Antonio Aversa, Silvia Di Agostino, and Vittoria Rago. 2024. "Prostate Cancer: Emerging Modifiable Risk Factors and Therapeutic Strategies in the Management of Advanced Cancer" Life 14, no. 9: 1094. https://doi.org/10.3390/life14091094