The Role of Genetic Polymorphisms in the Diagnosis and Management of Prostate Cancer: An Update

Dell’Atti, Lucio; Aguiari, Gianluca

doi:10.21873/anticanres.16166

Cited by 5 publications

(4 citation statements)

References 31 publications

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“…Unfortunately, after 2 to 3 years, resistance starts to develop in PC against ADT, which is then become castration-resistant prostate cancer (CRPC) (Zhang et al 2023 ). Several drugs have been used to overcome this resistance such as docetaxel, abiraterone acetate, cabazitaxel, enzalutamide, taxanes, radium-223, and sipuleucel-T (Dell’Atti and Aguiari 2023 ). All the previous drugs have demonstrated relatively small survival benefits and resistance developed eventually (Zhang et al 2023 ).…”

Section: Cannabis In Prostate Cancermentioning

confidence: 99%

Cannabis and cancer: unveiling the potential of a green ally in breast, colorectal, and prostate cancer

ALSalamat,

Abuarab,

Salamah

et al. 2024

J Cannabis Res

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Cancer comes in second place on the list of causes of death worldwide. In 2018, the 5-year prevalence of breast cancer (BC), prostate cancer (PC), and colorectal cancer (CRC) were 30%, 12.3%, and 10.9%, respectively. Cannabinoids are chemicals derived from the Cannabis sativa plant; the most investigated cannabinoids are cannabinol, delta 9-tetrahydrocannabinol (Δ9-THC), and cannabidiol. In humans, the endogenous endocannabinoid system consists of endocannabinoids, cannabinoids receptors (CBs), and enzymes that degrade the endocannabinoids. In this review, we will review the most recent literature for evidence that discusses the role of cannabis in the treatment of the three types of neoplasms mentioned. Studies have proved that BC cells express CB receptors; many in-vivo studies showed that cannabinoids cause apoptosis and inhibit proliferation and migration. Also, researchers found that treating BC mice with THC and JWH-133 (CB2 receptor agonist) slowed the tumor growth. Regarding CRC, cannabidiol was found to decrease the viability of chemotherapy-resistant CRC cells and inhibit metastasis by antagonizing the G-protein-coupled receptor 55 (GPR55; a novel cannabinoid receptor) necessary for metastasis. Moreover, cannabidiol had anti-angiogenetic effects by reducing the expression of vascular endothelial growth factor (VEGF) in addition to anti-inflammatory effects. Finally, studies demonstrated that PC cells highly express CB1 and CB2 receptors and that cannabinoids are capable of inhibiting the release of exosomes and microvesicles related to cancer progression. Cannabinoids also have antiproliferative, anti-invasive, anti-fibroblastic, cell cycle arrest, and proapoptotic effects on PC cells.

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Section: Cannabis In Prostate Cancermentioning

confidence: 99%

Cannabis and cancer: unveiling the potential of a green ally in breast, colorectal, and prostate cancer

ALSalamat,

Abuarab,

Salamah

et al. 2024

J Cannabis Res

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“…In diagnostics, prostate‐specific antigen (PSA) evaluation is widely used for PCa detection due to its relatively noninvasive nature. However, PSA is specific to the prostate gland rather than PCa, so elevated PSA levels in the bloodstream do not necessarily indicate PCa development and can be linked to benign prostatic hyperplasia or prostatitis 65–67 . Given the limited reliability of PSA screening, identifying robust biomarkers especially for early‐stage aggressive phenotypes, is a significant challenge in the treatment of PCa.…”

Section: Introductionmentioning

confidence: 99%

State‐of‐the‐art in transposable element modulation affected by drugs in malignant prostatic cancer cells

Terrazzan,

Vanini,

Ancona

et al. 2024

J of Cellular Biochemistry

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Over recent years, the investigation of transposable elements (TEs) has granted researchers a deeper comprehension of their characteristics and functions, particularly regarding their significance in the mechanisms contributing to cancer development. This manuscript focuses on prostate carcinoma cell lines and offers a comprehensive review intended to scrutinize the associations and interactions between TEs and genes, as well as their response to treatment using various chemical drugs, emphasizing their involvement in cancer progression. We assembled a compendium of articles retrieved from the PubMed database to construct networks demonstrating correlations with genes and pharmaceuticals. In doing so, we linked the transposition of certain TE types to the expression of specific transcripts directly implicated in carcinogenesis. Additionally, we underline that treatment employing different drugs revealed unique patterns of TE reactivation. Our hypothesis gathers the current understanding and guides research toward evidence‐based investigations, emphasizing the association between antiviral drugs, chemotherapy, and the reduced expression of TEs in patients affected by prostate cancer.

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“…Thus, there is a need to identify novel genetic markers which can be used as predictors for the most susceptible segments of the population to PCa or for genes that participate in PCa progression. Single‐nucleotide polymorphisms (SNPs) are variations in a genome's base pairs in a DNA sequence, with a variant frequency that occurs in more than 1% of the population and correlates with disease susceptibility, progression, or therapy responses 5–7 . Actually, in genome‐wide association studies (GWASs) and PCa case–control surveys, an enormous number of different SNPs in different genes were found to be correlated with PCa risk or progression 8 .…”

Section: Introductionmentioning

confidence: 99%

“…Single‐nucleotide polymorphisms (SNPs) are variations in a genome's base pairs in a DNA sequence, with a variant frequency that occurs in more than 1% of the population and correlates with disease susceptibility, progression, or therapy responses. 5 , 6 , 7 Actually, in genome‐wide association studies (GWASs) and PCa case–control surveys, an enormous number of different SNPs in different genes were found to be correlated with PCa risk or progression. 8 For example, SNPs located in genes such as caspase‐3 (CASP3), caspase‐9 (CASP9), hepatocyte nuclear factor 1‐beta (HNF1B), cancer susceptibility 8 (CASC8) and cyclin‐dependent kinase inhibitor 1B (CDKN1B) were implicated in regulation of cell apoptosis, the cell cycle, metabolism and cell division and were shown to be correlated with PCa susceptibility.…”

Section: Introductionmentioning

confidence: 99%

Genetic variants of dipeptidyl peptidase IV are linked to the clinicopathologic development of prostate cancer

Wen

Lin

Hsiao

et al. 2023

J Cellular Molecular Medi

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CD26/dipeptidyl peptidase IV (DPP4) is a multifunctional cell‐surface glycoprotein widely found in many cell types, and a soluble form is present in body fluids. There is longstanding evidence indicating a tumour‐promoting or ‐suppressive role of DPP4 in different cancer types. However, studies focusing on the impacts of genetic variants of DPP4 on cancers are very rare. Herein, we conducted a case–control study to evaluate whether single‐nucleotide polymorphisms (SNPs) of DPP4 were associated with the risk or clinicopathologic development of prostate cancer (PCa). We genotyped four loci of DPP4 SNPs, including rs7608798 (A/G), rs3788979 (C/T), rs2268889 (T/C) and rs6741949 (G/C), using a TaqMan allelic discrimination assay in 704 PCa patients and 704 healthy controls. Our results showed that PCa patients with the DPP4 rs7608798 AG+GG genotype or rs2268889 TC+CC genotype had a higher risk of developing an advanced clinical primary tumour (cT) stage (adjusted odds ratio (AOR): 1.680, 95% confidence interval (CI): 1.062–2.659, p = 0.025; AOR: 1.693, 95% CI: 1.092–2.624, p = 0.018). Additionally, in The Cancer Genome Atlas (TCGA) database, we observed that lower DPP4 expression levels were correlated with higher Gleason scores, advanced cT and pathological stages, tumour metastasis, and shorter progression‐free survival rates in PCa patients. Furthermore, overexpression of DPP4 suppressed migration/invasion of metastatic PC3 PCa cells. Our findings suggest that DPP4 levels may affect the progression of PCa, and the DPP4 rs7608798 and rs2268889 SNPs are associated with the clinicopathologic development of PCa in a Taiwanese population.

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The Role of Genetic Polymorphisms in the Diagnosis and Management of Prostate Cancer: An Update

Abstract: This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY-NC-ND) 4.0 international license (https://creativecommons.org/licenses/by-nc-nd/4.0).

Cited by 5 publications

References 31 publications

Cannabis and cancer: unveiling the potential of a green ally in breast, colorectal, and prostate cancer

Cannabis and cancer: unveiling the potential of a green ally in breast, colorectal, and prostate cancer

State‐of‐the‐art in transposable element modulation affected by drugs in malignant prostatic cancer cells

Genetic variants of dipeptidyl peptidase IV are linked to the clinicopathologic development of prostate cancer

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