Search Results (50,953)

Background: Intestinal failure-associated liver disease (IFALD) is a serious complication in patients receiving parenteral nutrition, often exacerbated by inflammation, lipid overload, and oxidative stress. Nobiletin (NOB), a polymethoxylated flavone, is known for its anti-inflammatory and lipid-regulating properties. Methods: We employed an in vitro model using THLE-2 human hepatocytes and primary human cholangiocytes exposed to Intralipid (INT) and lipopolysaccharide (LPS) to simulate IFALD conditions. NOB was tested at non-toxic concentrations (10 and 25 µM) to assess its protective effects. MTT viability assays, multiplex bead-based immunoassays (MAGPIX), RT-qPCR, and Western blotting were used to evaluate changes in inflammation markers, gene expression, and protein signaling. Moreover, ALT and AST activities were used to assess hepatocellular injury. Results: NOB maintained high cell viability in THLE-2 hepatocytes and cholangiocytes, confirming its low cytotoxicity. NOB normalized ALT and AST activities in both tested cell lines, but the effect reached statistical significance only for ALT in cholangiocytes. Under IFALD-like conditions (LPS+INT), NOB significantly preserved metabolic activity in both cell types. In THLE-2 and cholangiocytes, NOB markedly reduced the phosphorylation of pro-inflammatory proteins JNK, NF-κB, and STAT3, indicating a broad inhibition of inflammatory signaling. Moreover, in THLE-2 cells, NOB upregulated lipid metabolism-related genes (PRKAA2, CYP7A1, and ABCA1) and decreased oxidative stress, thereby enhancing the nuclear translocation of Nrf2 and increasing SOD1 level, which supports the activation of antioxidant defenses. Conclusions: NOB exhibits hepatoprotective properties under IFALD-like conditions in vitro, likely through modulation of inflammation-related signaling and lipid metabolism pathways. Full article

Background: Obesity is characterized by chronic low-grade inflammation and metabolic disturbances, including an altered tryptophan (Trp) catabolism through the kynurenine pathway (KP). Since the KP is closely linked to immune activity, energy metabolism, and hepatic function, modulating its flux through lifestyle interventions has gained interest as a potential therapeutic strategy. Objective: This exploratory study aimed to investigate the impact of a structured 12-week weight loss program (WLP) on serum KP metabolites in a sample of Mexican women with obesity. Methods: This study involved a pre–post-intervention design conducted in twenty-four women with clinically diagnosed obesity from the Mexican Navy who underwent a structured 12-week weight loss program combining a hypocaloric diet with moderate-intensity aerobic exercise; no control group was included. Anthropometric parameters, serum biochemistry, and circulating levels of Trp, kynurenine (KYN), kynurenic acid (KYNA), and 3-hydroxykynurenine (3-HK) were assessed before and after intervention. Psychological assessments of anxiety and depression were also conducted in a subset of participants. Results: The WLP significantly reduced body weight, BMI, fat mass, fasting insulin, and C-reactive protein levels. Serum concentrations of Trp, KYN, and KYNA decreased, while 3-HK showed a non-significant upward trend. Enzymatic indexes revealed a significant increase in the 3-HK/KYN ratio and a decrease in the KYNA/3-HK ratio, suggesting a shift toward kynurenine monooxygenase (KMO) branch. Notably, higher KYNA-related ratios were inversely associated with depressive symptoms. Conclusions: These findings position the KP as a responsive metabolic interface potentially linking improvements in body composition, liver function, and psychological status during structured weight loss efforts. Full article

Ocular allergy (OA) is a subtype of seasonal allergy that causes symptoms of itchiness, redness, swelling and irritation of the ocular surface and eyelids, often triggering allergy-induced eye rubbing and sustained inflammation for up to six months of the year during peak allergy season. These symptoms, coupled with reduced sleep quality, impaired daily productivity and decreased mood, highlight a significant yet underrepresented disease burden. Recent advances in tear-based multi-omics have enabled detailed characterisation of OA-associated biochemical changes on the ocular surface, highlighting human tears as a promising biospecimen for diagnostic biomarker and therapeutic target research. This review discusses emerging proteomic, lipidomic, metabolomic and miRNA findings comparing OA sufferers with healthy controls, and, where relevant, with comorbid conditions such as dry eye disease and keratoconus. Differential expression patterns across these analytes implicate key pathways involved in immune response, wound healing, angiogenesis, inflammation, oxidative stress and return to homeostasis on the ocular surface. By integrating these data into a stepwise model of OA biopathway activation, this review outlines candidate biomarkers and highlights methodological advances that may support translation of tear multi-omics into clinical tools for OA management. Full article

Background/Objectives: Periodontal disease is a prevalent chronic inflammatory condition that often progresses to irreversible tissue destruction. This study aimed to evaluate the clinical efficacy of a combined minimally invasive periodontal therapeutic protocol scaling and root planing (SRP) with injectable platelet-rich fibrin (i-PRF) and microneedling (MN) compared to conventional SRP with i-PRF alone in patients with stage II–III periodontitis. Methods: A prospective split-mouth clinical study was conducted on 54 patients diagnosed according to the 2018 EFP/AAP classification. Each participant received SRP + i-PRF in the upper arch (control) and SRP + i-PRF + MN in the lower arch (test). Periodontal parameters clinical attachment level (CAL), bleeding on probing (BOP), and plaque index (PI) were measured at baseline, 1, 3, and 6 months. Data were analyzed using Friedman and Wilcoxon tests with Bonferroni correction. Results: Both treatment protocols produced significant longitudinal improvements in CAL, BOP, and PI (p < 0.001). The most pronounced BOP reduction occurred within the first month, while CAL improvement was progressive and stabilized after six months. The Combined protocol achieved slightly greater CAL gain at 6 months (mean difference ≈ 0.46 mm; p = 0.0013), indicating a modest yet statistically significant advantage in attachment recovery. Correlation analyses confirmed a coherent healing trajectory characterized by early inflammation resolution, plaque control, and later tissue stabilization. Conclusions: Both i-PRF-based regenerative approaches significantly improved periodontal parameters. The addition of MN enhanced CAL recovery and may favor early vascularization and collagen remodeling. Although the clinical difference was limited, the biological plausibility and sustained improvement suggest that MN could represent a valuable adjunct to non-surgical regenerative periodontal therapy. Longer-term studies are warranted to assess the durability of these effects. Full article

Background: Ulcerative colitis (UC) is characterized by chronic mucosal inflammation, oxidative stress, and disruption of intestinal metabolic homeostasis. Immunomodulatory nutrients such as arginine, glutamine, and β-hydroxy β-methylbutyrate (HMB) have shown potential benefits; however, their combined molecular effects on UC remain insufficiently defined. Objective: To investigate the individual and combined effects of arginine, glutamine, and HMB on inflammatory and metabolic gene expression, oxidative stress markers, and histopathological outcomes in a dextran sulfate sodium (DSS)-induced colitis model. Methods: Female Sprague Dawley rats were assigned to six groups: control, DSS, DSS + arginine, DSS + glutamine, DSS + HMB, and DSS + mixture. Colitis was induced using 3% DSS. Colon tissues were examined histologically, serum MDA, MPO, and GSH levels were quantified, and mRNA expression of IL6, IL10, COX2, NOS2, ARG2, CCR1, and ALDH4A1 was measured by RT-qPCR. Pathway enrichment analyses were performed to interpret cytokine and metabolic network regulation. Results: DSS induced severe mucosal injury, elevated MDA and MPO, reduced GSH, and significantly increased IL6, COX2, NOS2, ARG2, and CCR1 expression. Glutamine demonstrated the strongest anti-inflammatory and antioxidant effects by decreasing IL6 and COX2 and restoring GSH. Arginine primarily modulated nitric oxide–related pathways, whereas HMB increased ALDH4A1 expression and metabolic adaptation. The combination treatment produced more balanced modulation across inflammatory, chemokine, and metabolic pathways, consistent with enrichment results highlighting cytokine signaling and amino acid metabolism. Histopathological improvement was greatest in the mixture group. Conclusions: Arginine, glutamine, and HMB ameliorate DSS-induced colitis through coordinated regulation of cytokine networks, oxidative stress responses, and metabolic pathways. Their combined use yields broader and more harmonized therapeutic effects than individual administration, supporting their potential as targeted immunonutritional strategies for UC. Rather than targeting a single inflammatory mediator, this study was designed to test whether combined immunonutrient supplementation could promote coordinated regulation of cytokine signaling, oxidative stress responses, and metabolic adaptation, thereby facilitating mucosal repair in experimental colitis. Full article

Atrial fibrillation (AF) is the most prevalent sustained arrhythmia worldwide and is now increasingly regarded as a disease of chronic inflammation and progressive atrial fibrosis. Understanding of molecular mechanisms that mediate the linkage between systemic metabolic dysregulation, inflammation, and structural atrial changes is crucial for informing risk stratification and targeting of prevention strategies. This review provides evidence from 105 studies focusing on the contributions of transforming growth factor-β1 (TGF-β1), tumor necrosis factor-a (TNF-α), interleukin-6 (IL-6), galectin-3, and galectin-1 to cardiac fibrogenesis, atrial fibrosis, and AF pathogenesis. We also link metabolic syndrome to these biomarkers and to atrial remodeling, as well as echocardiographic correlates of fibrosis. TGF-β1 is established as the central profibrotic cytokine and promotes Smad-based fibroblast activation, collagen accumulation, and structural atrial remodeling. Its role is highly potentiated by thrombospondin-1 by turning latent TGF-β1 into its potent form. TNF-α and IL-6 also play an integral role in the inflammatory fibrotic continuum by activating NF-κB and STAT3 signaling, promoting fibroblast proliferation, electrical uncoupling, and extracellular matrix accumulation. Galectin-3 is a potent profibrotic mediator that promotes TGF-β signaling and is a risk factor for negative outcomes, whereas Gal-1 seems to regulate inflammation resolution and may exert context-dependent protective or maladaptive roles. Metabolic syndrome is strongly associated with excessive levels of these biomarkers, chronic low-grade inflammation, oxidative stress, and ventricular and atrial fibrosis. Chronic clinical findings show that metabolic syndrome (MetS) increases AF risk, exacerbates atrial dilatation, and is associated with worse postoperative outcomes. Echocardiographic data are connected to circulating biomarkers and are non-invasive for evaluating atrial remodeling. The evidence to date supports that atrial fibrosis should be considered an end point of systemic inflammation, metabolic dysfunction, and activation of profibrotic molecular pathways. Metabolic syndrome, due to its chronic low-grade inflammatory environment and prolonged levels of metabolic stress, manifests as an important upstream factor of fibrotic remodeling, which continuously promotes the release of cytokines, oxidative stress, and fibroblast activation. Circulating fibrotic biomarkers, in comparison with metabolic syndrome, serve separate yet interdependent pathways that help orchestrate atrial structural remodeling through the simultaneous process but can also provide a long-term indirect measure of ongoing profibrotic activity. The integration of these biomarkers with superior atrial imaging enables a broader understanding of the fibrotic substrate of atrial fibrillation. This combined molecular imaging approach can facilitate risk stratification, refine therapeutic decisions, and facilitate early identification of higher-risk metabolic phenotypes, thus potentially facilitating directed antifibrotic and anti-inflammatory therapy in atrial fibrillation. Full article

Background: Sarcoidosis is a heterogeneous, multisystem inflammatory disease with an unpredictable clinical course and limited prognostic markers. Increasing attention has focused on nutritional and metabolic factors—particularly obesity, body composition, and calcium–vitamin D metabolism—as potentially modifiable elements associated with disease development and clinical phenotype. However, the available literature remains fragmented and methodologically heterogeneous. Objective: To systematically map current evidence on the relationship between nutritional status and the development, clinical course, and prognosis of sarcoidosis, and to identify key gaps requiring further research. Methods: A scoping review was conducted in accordance with the Joanna Briggs Institute methodology and the PRISMA-ScR guidelines. PubMed, Scopus, Web of Science, Cochrane Library, EBSCO, and Google Scholar were searched for studies published between 2015 and 2025. Eligible studies included adult patients with sarcoidosis and addressed nutritional status broadly defined, encompassing anthropometric measures, body composition, immunonutritional indices, nutrition-related biomarkers, dietary factors, and supplementation practices. Due to substantial heterogeneity in exposure definitions and outcome measures, no quantitative synthesis or formal methodological quality appraisal was performed. Results: Eighteen studies, predominantly observational, were included. The most consistent findings concerned anthropometric parameters, with overweight and obesity showing the strongest association with an increased risk of sarcoidosis and, in selected studies, with reduced exercise capacity and greater disease burden. Evidence linking nutritional status to prognosis was indirect, while direct data on sarcoidosis-specific survival were lacking. Disturbances in calcium–vitamin D metabolism were frequent and clinically relevant, particularly in the context of supplementation-related hypercalcemia. Conclusions: Current evidence suggests that nutritional status—particularly excess body weight—and selected metabolic and immunonutritional factors are associated with sarcoidosis. However, given the largely observational nature of the available data and the lack of formal assessment of methodological quality, these results should be interpreted as association mapping and hypothesis generation rather than as evidence of causality. Well-designed prospective and interventional studies using standardized nutritional assessment tools and clinically relevant endpoints are needed to clarify the role of nutritional factors in sarcoidosis. Full article

The preventive effect of leucine (Leu) against colonic damage in piglets infected with porcine epidemic diarrhea virus (PEDV) was examined in this study. Three groups (n = 6) were randomly assigned to eighteen 7-day-old Du-roc × Landrace × Large piglets (body weight [BW] = 2.58 ± 0.05 kg): Control, PEDV-infected (PEDV), and Leu-supplemented + PEDV-infected (Leu + PEDV). Following a three-day period of acclimatization, the Leu + PEDV group was given Leu (400 mg/kg BW) orally every day. On day eight, the PEDV and Leu + PEDV groups were challenged with PEDV, while the Control group was given Dulbecco’s Modified Eagle’s Medium. Colonic tissues were collected on day 11. PEDV infection induced severe colonic damage by an increase in crypt, disrupting intestinal homeostasis, including impaired barrier integrity (matrix metalloproteinase-7 and matrix metalloproteinase-13 upregulation), mucus disorganization (mucin 5AC elevation), oxidative stress (reduced catalase activity and increased malondialdehyde levels), inflammation, electrolyte imbalance and enhanced viral replication. Leu supplementation reversed these injuries by alleviating oxidative stress, suppressing inflammation, inhibiting viral replication and stabilizing ion homeostasis. This study provides a scientific basis for Leu as a nutritional intervention to alleviate PEDV-induced colonic damage in piglets. Full article

Resistance training (RT) influences endocrine pathways that control skeletal muscle (SM) growth. This review summarizes 25 years of evidence (January 2000–December 2025) from PubMed, Medline, and ScienceDirect, focusing on three aspects: (1) exercise types such as RT, speed, power, high-intensity interval training, and aerobic training at various intensities; (2) dietary factors, including caloric restriction, total protein, protein sources, amino acids, and carbohydrates; and (3) aging-related physiological factors that may impair the insulin/IGF-1 axis in SM, such as insulin resistance, fat infiltration, physical inactivity, mitochondrial dysfunction, and inflammation. The data from Grade A evidence in systematic reviews and RCTs are prioritized to develop practical recommendations and future research directions for young, middle-aged, older, and very old individuals. Evidence regarding the effects of anabolic amino acids in women, middle-aged, and very old individuals, as well as locally mediated IGF-1 effects of any type of exercise, is limited. Full article

Metabolic acidosis is common after kidney transplantation and has been linked to adverse renal outcomes. However, its relationship with histological injury in kidney allografts remains poorly characterized. We aimed to explore the association between metabolic acidosis and histopathological features in kidney allograft biopsies. This single-center, cross-sectional observational study included 63 adult kidney transplant recipients who underwent clinically indicated allograft biopsies. Metabolic acidosis was defined as a serum bicarbonate level < 22 mmol/L at the time of biopsy. Histological lesions were assessed according to the Banff classification. Lesion severity was evaluated using descriptive statistics, nonparametric comparisons, ordinal logistic regression, and multivariable logistic regression models adjusted for renal function, proteinuria, and time from transplantation. Sensitivity analyses additionally adjusted for hemoglobin and donor-related variables. Patients with metabolic acidosis exhibited numerically higher severity scores for both acute inflammatory lesions and chronic histological changes, including total inflammation and interstitial fibrosis/tubular atrophy (IFTA). Across ordinal analyses and multivariable regression models, consistent directional trends toward a greater histological injury burden were observed among acidotic patients; however, none of these associations reached statistical significance, and confidence intervals were wide. Sensitivity analyses yielded directionally consistent effect estimates. In this biopsy-based analysis, metabolic acidosis showed consistent directional trends toward a higher burden of inflammatory and chronic histological lesions, although these findings did not reach statistical significance. Full article

Background: Tracheobronchopathia osteochondroplastica (TO) is a rare benign disorder characterized by submucosal cartilaginous and osseous nodules of the tracheobronchial tree, typically sparing the posterior membranous wall. Involvement of the vocal cords is exceedingly rare and may result in critical airway obstruction. The underlying genetic and molecular mechanisms of TO remain largely unexplored. Case presentation: We report a rare case of TO extending from the vocal cords to the bronchi in a 76-year-old man who initially presented with pneumonia and later developed acute respiratory failure due to severe airway narrowing, necessitating emergency tracheostomy. Bronchoscopy and computed tomography revealed diffuse calcified nodules involving the anterior and lateral airway walls, including the subglottic region. Histopathology demonstrated chronic inflammatory cell infiltration with squamous metaplasia. To explore the molecular basis of this condition, whole-genome sequencing (WGS) was performed using peripheral blood samples—the first such application in TO. WGS identified 766 germline mutations (including 27 high-impact variants) and 66 structural variations. Candidate genes were implicated in coagulation and inflammation (KNG1), arachidonic acid metabolism and extracellular matrix remodeling (PLA2G4D), ciliary dysfunction and mineralization (TMEM67), vascular calcification (CDKN2B-AS1), smooth muscle function (MYLK4), abnormal calcification (TRPV2, SPRY2, BAZ1B), fibrotic signaling (AHNAK2), and mucosal barrier integrity (MUC12/MUC19). Notably, despite systemic germline mutations, calcification was restricted to the airway. Conclusions: This case highlights that TO with vocal cord involvement can progress beyond a benign course to cause life-threatening airway obstruction. Integrating clinical, histological, and genomic findings, we propose a novel pathophysiological model in which systemic genetic susceptibility interacts with local immune cell infiltration and fibroblast-driven extracellular matrix remodeling, resulting in airway-restricted dystrophic calcification. This first genomic characterization of TO provides new insights into its pathogenesis and suggests that multi-omics approaches may enable future precision medicine strategies for this rare airway disease. Full article

Sarcoidosis is an immune-mediated granulomatous disease whose etiology has remained unresolved despite more than a century of investigation. Accumulating microbiological and immunopathological evidence now implicates Cutibacterium acnes—a ubiquitous indigenous commensal—as the most consistent antigenic trigger. Its frequent detection within sarcoid granulomas by quantitative PCR, in situ hybridization, and species-specific immunohistochemistry suggests latent intracellular persistence and the potential for endogenous reactivation. To explain how a noncontagious commensal can drive granulomatous inflammation, this review proposes the concept of Endogenous Hypersensitivity Infection (EHI). EHI describes a host-centered process in which reactivation of latent intracellular microbes leads to the breakdown of immune tolerance and provokes Th1-dominant hypersensitivity responses in genetically and immunologically susceptible individuals. This framework bridges the traditional divide between infection and autoimmunity, reframing sarcoidosis as a disorder of disrupted host–commensal homeostasis rather than a classical infectious or autoimmune disease. By integrating microbiological, immunological, and pathological evidence, this review synthesizes the mechanistic basis of EHI and outlines how tolerance failure to C. acnes can account for the paradoxical clinical behavior of sarcoidosis. The EHI paradigm further provides a unifying conceptual lens through which related chronic inflammatory disorders—including Crohn’s disease, chronic rhinosinusitis, and atopic dermatitis—may be reinterpreted. Full article

Despite antiretroviral therapy, HIV proteins, such as Tat, persist in tissues, driving chronic inflammation. Cervical inflammation in females not only accelerates HIV progression but also increases the risk of other STIs; hence, understanding the underlying factors/regulators is vital. However, Tat-induced cervical inflammation and its regulation are hitherto poorly understood, which we investigated using TZM-bl cells. Tat stimulation in these cervical epithelial cells significantly increased the expression of various inflammatory mediators, including cytokines (IL-1β, TNF-α, IL-6, IL-17a, GM-CSF), chemokines (MIP-1α, MIP-1β), adhesion molecules (ICAM-1, P-Selectin, E-Selectin), and ROS. Further upregulation of inflammatory mediators (NF-κB, IRAK-4) along with TLR7 was observed in Tat-stimulated cells. Interestingly, Tat stimulation decreased miR-204-5p expression in these cells, suggesting a role in regulating Tat-mediated inflammatory processes. Using a gain-of-function approach, we further observed that the overexpression of miR-204-5p reduced the expression of IL-1β, TNF-α, IL-6, MIP-1α, MIP-1β, ICAM-1, P-Selectin, and ROS in the Tat-stimulated TZM-bl cells, along with NF-κB, IRAK-1, and IRAK-4. Using Western blotting and luciferase assays, miR-204-5p was further shown to directly target NF-κB. Here, we report that HIV-1 Tat stimulation in cervical epithelial cells downregulates hsa-miR-204-5p, thereby activating the pro-inflammatory TLR7/NF-κB axis, highlighting its relevance to understanding mechanisms underlying cervical inflammation. Full article

One highly consequential presentation of Venezuelan equine encephalitis virus (VEEV) infection is encephalitis. Here we considered anti-inflammatory interventions to limit the effects of this using a BALB/c subcutaneously challenged mouse model of disease. This disease model nearly ubiquitously presents with severe encephalitis, where viral neuroinvasion correlates with much of the outward clinical signs of disease. A selection of already licenced, commonly used anti-inflammatory drugs were tested in mice developing encephalitis (starting treatment at post challenge). Drug regimens were used that had previously been shown to have pharmacodynamic effects in mice for unrelated conditions. None of the treatment regimens tested reduced brain inflammation. A single anti-inflammatory drug (dexamethasone) was further tested utilising ascending doses in an effort to provide an effective anti-inflammatory regimen. Higher doses of dexamethasone ( and ) reduced inflammatory markers in the brain and lowered weight loss and clinical signs early on during infection. However, the regimen also caused the disease to become more severe at later time points when compared to controls. When combined with the antiviral drug molnupiravir, the negative effects of the dexamethasone treatment ( and ) were absent, and the positive disease severity-reducing effects remained. When combined with a specific VEEV monoclonal antibody (1A3B7), dexamethasone significantly reduced the antibody’s protective effects. These data present currently unique insights into how anti-inflammatory approaches might benefit patients with VEEV disease and where caution might be advised. Full article

Adiposity-Based Chronic Disease (ABCD) is known to increase the risk of aggressive prostate cancer (PCa), recurrent disease after treatment for localized PCa, and PCa mortality. A key mechanistic link contributing to this enhanced risk is chronic inflammation originating from excess white visceral adipose tissue (WAT; VAT) and periprostatic adipose tissue (ppWAT). Contributing to systemic inflammation is gut dysbiosis, which itself may be caused by ABCD as well as background local inflammation (prostatitis), which is common in aging men and may be exacerbated by the urinary microbiome. Investigating the molecular biology driving inflammation and its association with increased PCa risk, a recent paper applied a network and gene set enrichment to adipokine drivers in the ABCD-PCa network. It found prominent roles for MCP-1, IL-1β, and CXCL-1 in addition to confirming the importance of exposure to lipopolysaccharides and bacterial components, corroborating the role of gut dysbiosis. To further unravel the mechanistic links between ABCD and PCa risk, this critical review will discuss the current literature on prominent inflammatory signaling pathways activated in ABCD; the influence of gut dysbiosis, the urinary microbiome, and chronic prostatitis; and current hypotheses on how these domains may result in the development of aggressive PCa over a man’s life. Moreover, we performed a novel pathway enrichment analysis to further evaluate the associations between ABCD, PCa risk, gut dysbiosis, and the prostate microbiome, the results of which were partitioned into extracellular and intracellular signaling pathways. In the extracellular space, novel mechanistic links between gut dysbiosis and MCP-1, IL-1β, CXCL1, and leptin via bacterial pathogen signaling and the intestinal immune network (for IgA production), crucial for gut immune homeostasis, were found. Within the intracellular space, there were downstream signals activating chemokine and type 2 interferon pathways, focal adhesion PI3K/Akt/mTOR pathways, as well as the JAK/STAT, NF-κB, and PI3K/Akt pathways. Overall, these findings point to an emerging molecular pathway for PCa oncogenesis influenced by ABCD, gut dysbiosis, and inflammation, and further research, possibly with lifestyle program-based clinical trials, may discover novel biomarker panels and molecular targeted therapies for the prevention and treatment of PCa. Full article