Search Results (3,394)

Atherosclerosis is a chronic inflammatory arterial disease and the primary underlying cause of cardiovascular morbidity and mortality worldwide. Its development and progression are driven by a mechanistically interconnected triad of endothelial dysfunction, oxidative stress, and vascular inflammation. Current pharmacotherapy, primarily focused on low-density lipoprotein cholesterol (LDL-C) reduction through statin-based and adjunctive therapies, does not fully address the residual inflammatory and calcific components of atherosclerotic risk. Menaquinone-7 (MK-7), a long-chain isoform of vitamin K2 with superior bioavailability and extrahepatic tissue distribution, has emerged as a multi-target modulator of atherogenic processes. Its classical function is to serve as a cofactor for the gamma-carboxylation of vitamin K-dependent proteins (VKDPs), principally matrix Gla protein (MGP), the primary endogenous inhibitor of vascular calcification. Beyond this established pathway, a growing body of experimental evidence indicates that MK-7 may modulate endothelial nitric oxide (NO) production through carboxylation-dependent activation of Growth Arrest-Specific Protein 6 (Gas6) and suppress lipid peroxidation and ferroptosis via Ferroptosis Suppressor Protein 1 (FSP1)-mediated reduction of vitamin K hydroquinone (VKH₂). In addition, it may attenuate nuclear factor kappa-B (NF-κB)-driven inflammatory gene transcription in vascular cells. Previous reviews mainly focused on how vitamin K2 influences vascular calcification and cardiovascular outcomes. However, emerging mechanistic evidence linking MK-7 to endothelial dysfunction, oxidative stress, ferroptosis, and vascular inflammation has not been comprehensively integrated. This review summarizes the current knowledge of in vitro, animal, observational, and randomized controlled trial evidence for MK-7 in the context of atherosclerosis. It particularly emphasises mechanistic pathways, the strength of evidence, and translational limitations, highlighting the lack of direct human vascular evidence in several areas. Full article

Background/Objectives: Chronic inflammation is a key factor in the development and progression of colorectal cancer (CRC). When COX-2 levels and PGE₂ production increase, nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin (ASA) and selective COX-2 inhibitors, such as celecoxib and rofecoxib, are commonly employed. This paper presents the effect of anti-inflammatory drugs, primarilyNSAIDs, on the incidence of CRC. Methods: A comprehensive literature search (119 articles) was conducted with databases such as PubMed. During our research, we used keywords such as colorectal cancer (CRC), nonsteroidal anti-inflammatory drugs (NSAIDs), ASA, COX, precision oncology, and personalized medicine. Results: The development of CRC is primarily associated with chronic inflammation and the actions of COX-2 and prostaglandin E2 (PGE₂), which promote cancer cell proliferation and angiogenesis. Anti-inflammatory drugs act by inhibiting the secretion of COX-1 and COX-2 enzymes, which leads to reduced PGE₂ production and may limit tumor growth. Aspirin has the best-documented and studied anti-cancer effect; long-term use is associated with a reduced risk of CRC development and mortality through its anti-inflammatory and antiplatelet effects, thereby limiting metastasis. Particularly beneficial effects are observed in patients with mutations in the PIK3CA gene. Factors influencing the effectiveness of CRC treatment include molecular differences and tumor location. Conclusions: The future of CRC treatment and prevention lies in personalized medicine, which accounts for each patient’s genetic profile. Decisions regarding NSAIDs use and CRC prevention should consider the potential benefits and risks of side effects. Full article

Light availability is a primary determinant of plant growth and a key factor influencing the success of alien plant invasions. Although the phytohormone abscisic acid (ABA) is a known master regulator of abiotic stress responses, its specific role in the shade tolerance and competitive advantage of invasive species remains poorly understood. In this study, we conducted a comparative experiment using the highly invasive Wedelia trilobata and its native congener, Wedelia chinensis. We investigated their eco-physiological responses to normal (100%) and low-light (30%) intensities, coupled with the application of exogenous ABA (A1) and the biosynthesis inhibitor sodium tungstate (S1). Our results showed that low light significantly inhibited the growth and photosynthetic capacity of both species, reducing biomass and net photosynthetic rate P_n. However, exogenous ABA application specifically enhanced the P_n and biomass of the invasive W. trilobata under low-light stress, while reducing malondialdehyde (MDA) content and optimizing antioxidant enzyme activities (SOD, POD, and CAT). Conversely, the inhibition of endogenous ABA by sodium tungstate exacerbated oxidative damage and photosynthetic decline in both species, with a more pronounced negative impact on W. trilobata. Correlation analysis further revealed that W. trilobata maintains a superior capacity to coordinate stomatal regulation and antioxidant defense through ABA signaling. These findings suggest that the invasive success of W. trilobata in fluctuating light environments is significantly driven by its high sensitivity and efficiency in ABA-mediated physiological plasticity, providing a potential target for managing its spread through hormonal or metabolic interference. Full article

Background: Prostate cancer (PCa) is the most commonly diagnosed malignancy in men and a leading cause of cancer-related mortality worldwide. Growing evidence indicates that metabolic syndrome components, including obesity, insulin resistance, and hyperglycemia, contribute to PCa development, and progression to more aggressive form. At the same time, standard treatments such as androgen deprivation therapy (ADT) and androgen receptor pathway inhibitors (ARPIs) significantly improve oncologic outcomes but are associated with adverse metabolic effects, including increased fat mass, insulin resistance, and sarcopenia, potentially worsening patients’ overall metabolic profile and quality of life. Tumor progression in PCa is strongly driven by androgen receptor (AR) signaling, which is closely linked to cellular metabolic reprogramming, highlighting metabolism as a potential therapeutic target. Aim: The aim of this study was to evaluate and synthesize current evidence on the role of the ketogenic diet (KD) in PCa, with particular emphasis on its interaction with hormonal therapies, underlying metabolic and endocrine mechanisms, and its potential application as an adjunctive strategy in integrated oncologic care. Results: The KD, characterized by high fat and very low carbohydrate intake, induces a metabolic state of ketosis that reduces circulating glucose, insulin, and insulin-like growth factor 1 (IGF-1), potentially counteracting metabolic alterations associated with PCa and its treatments. Preclinical studies consistently demonstrate that carbohydrate restriction and KD can slow tumor growth, modulate key oncogenic pathways such as PI3K/AKT/mTOR, reduce systemic insulin signaling, and enhance survival in prostate cancer models. Additionally, emerging evidence suggests possible synergistic effects when KD is combined with standard therapies, including ADT and immunotherapy. Clinical data, although limited, indicate that low-carbohydrate dietary interventions may improve metabolic parameters and could delay biochemical progression, as suggested by increased prostate-specific antigen (PSA) doubling time. However, results across studies remain heterogeneous, and robust evidence on long-term oncologic outcomes is lacking. Conclusions: Overall, the KD represents a promising but still experimental strategy in PCa management, requiring careful nutritional supervision to avoid adverse effects such as unintended weight loss or sarcopenia. Further well-designed randomized clinical trials are needed to clarify its safety, efficacy, and role in routine clinical practice. Full article

Clear cell renal cell carcinoma (ccRCC) is driven by von Hippel-Lindau (VHL) tumor suppressor loss and persistent activation of hypoxia-inducible factors (HIFs), which coordinately regulate angiogenesis, metabolic reprogramming, redox balance, and tumor–immune interactions. Although immune checkpoint inhibitors and vascular endothelial growth factor-targeted therapies have improved outcomes, resistance remains common due to adaptive network plasticity. Selected natural products have been reported to exhibit multitarget regulatory activities that may influence interconnected oncogenic pathways. This review highlights how compounds such as curcumin, resveratrol, quercetin, and epigallocatechin-3-gallate modulate the VHL-HIF axis, disrupt metabolic and redox homeostasis, and influence tumor–immune system interactions in ccRCC. We propose a system-level framework in which natural products enhance therapeutic sensitivity; however, further validation is required for clinical translation. Full article

The increasing demand for resilient and multifunctional crops in the Mediterranean region has renewed interest in Urtica dioica L. as a potential alternative crop. This study evaluated the combined effects of fertilization and row spacing on the growth, yield, and nitrogen use efficiency of nettle in Athens, Greece. A split-plot experimental design was employed in a three-year experiment, with three fertilization treatments (C = control, U = urea, and I = urea with urease inhibitor) and two different row spacings (D1 = 30 cm × 20 cm, and D2 = 50 cm × 20 cm). Agronomic traits, seed yield, nitrogen content, vegetation indices (NDVI), chlorophyll content (SPAD), and nitrogen efficiency indices were assessed. Fertilization significantly enhanced plant performance, with the application of I consistently producing the highest values for plant height (increased by 10–30%), biomass (increased by 10–20%), and seed yield (increased up to 30%) compared to C. Row spacing influenced crop performance, with D2 favoring plant height (up to 9% compared to D1), while D1 generally increased biomass production per unit area (up to 20% compared to D2). Nitrogen-related indices (NUE, NAE, and NUtE) were markedly improved under fertilized treatments, particularly when I was applied (up to 20%, 100%, and 19% compared to U). NDVI and SPAD values were also influenced by fertilization and row spacing at early growth stages. The findings demonstrate that both factors play critical roles in optimizing nettle cultivation under Mediterranean conditions, highlighting the importance of integrated agronomic management practices. Full article

Triple-negative breast cancer is an aggressive and heterogeneous type of invasive breast cancer (BC) in which the cancer cells lack estrogen and progesterone receptors, as well as expression of the human epidermal growth factor 2 protein. This cancer tends to grow and spread faster than other BC subtypes, and is associated with a poor prognosis due to early visceral and neurological recurrences. Multidisciplinary management includes surgery, chemotherapy, radiation therapy, and immunotherapy with targeted immune checkpoint inhibitors (ICIs). The introduction of ICIs has improved outcomes in patients with TNBC, particularly in the metastatic and neoadjuvant settings. Despite these advances, a significant proportion of patients either do not respond to treatment or develop resistance to it. TNBC mortality remains high, underscoring the urgent need to identify novel prognostic and predictive biomarkers to overcome resistance to immunotherapy. Following a brief overview of the clinical features and established biomarkers of TNBC, the current review focuses on immune checkpoint proteins (ICPs) beyond PD-1 and PD-L1, and on the potential use of soluble ICPs rather than the well-established membrane-bound assays. These soluble ICPs are produced through the alternative splicing of messenger (m)RNA or the cleavage/shedding of membrane-bound proteins. This is followed by an overview of current treatment and novel predictive targets in TNBC. Additionally, the involvement of the B- and T-lymphocyte attenuator (BTLA)/herpes virus entry mediator (HVEM)/CD160 pathway and its role in the pathogenesis of BC and TNBC are reviewed, highlighting the potential use of BTLA and HVEM as biomarkers. Full article

Background: Aging profoundly alters host immunity, yet how age-associated immune changes in the liver influence the growth of metastatic tumors remains incompletely understood. Liver metastasis is a major cause of cancer-related mortality, particularly in elderly patients, for whom aggressive treatments are often not feasible. This study aimed to clarify how aging reshapes the hepatic immune microenvironment and to identify age-associated host factors that influence liver metastasis growth. Methods: Tumor-naïve and tumor-bearing young and aged mice were analyzed using a syngeneic MC38 liver metastasis model. Immune cell composition in the liver was assessed by flow cytometry, and gene expression was evaluated by quantitative reverse transcription PCR (RT–qPCR). Public transcriptomic datasets were screened to identify age-associated inflammatory factors. The functional relevance of the S100A8/A9 axis was examined using the small-molecule inhibitor paquinimod. Results: Aging was associated with a distinct baseline immune cell composition in the liver. During liver metastasis, overall growth was comparable between young and aged mice; however, metastatic lesions in aged hosts showed increased expression of multiple inflammation-related genes and prominent accumulation of Ly6G⁺ cells. In silico screening identified S100a9 as one of the most highly upregulated inflammation-related genes in aged livers, which was confirmed in both tumor-naïve and metastatic liver tissues. Pharmacological modulation of the S100A8/A9 axis with paquinimod significantly reduced liver metastasis growth in aged, but not young, mice, and was accompanied by a shift in immune cell composition, including an increased representation of CD8⁺ T cells. Conclusions: These findings indicate that aging is associated with a distinct hepatic immune context that shapes the inflammatory and cellular composition of the tumor microenvironment during liver metastasis. S100A9 emerges as a key age-associated, host-derived factor that is functionally relevant to the growth of liver metastases in aged hosts, supporting the S100A8/A9 axis as a context-specific therapeutic target. Full article

Background: Growth factor therapy often fails in diabetic foot ulcers (DFUs). The reason remains unclear. Standard differential expression analysis may miss functionally critical genes with modest expression changes. Methods: We performed a secondary computational analysis of a longitudinal DFU transcriptomic dataset (Dryad; 17 patients, 117 serial biopsy samples, 12-week follow-up). Co-expression networks were built separately for healed (n = 37) and non-healed (n = 80) samples. Virtual gene knockout (VGK) was used to rank genes by topological impact on network cohesion. Single-cell analysis (GSE165816) assessed the association between endogenous KIF13A expression and keratinocyte migration-related signatures. A conceptual Hill-equation simulation was used to illustrate the transport-signaling threshold relationship. Drug repurposing used DSigDB enrichment. An independent bulk DFU cohort (GSE134431) was used for external validation. Results: KIF13A showed no differential expression (log₂FC = 0.173, p = 0.263) yet ranked first by VGK topological impact. In keratinocytes, high KIF13A expression correlated with greater migration scores versus zero-detection cells (p = 0.0058). A clear threshold effect emerged: below the 30th expression percentile, EGF, PDGF, and FGF pathway activation scores remained near baseline. In a structural-equation model, transport activity negatively predicted inflammation (standardized β = −0.92, p < 0.001). HIF1A showed the strongest positive correlation with KIF13A in keratinocytes (Spearman ρ = 0.26, p < 0.001), and FOS showed a negative correlation in the single-cell analysis (ρ = −0.16, p < 0.001) and in the bulk longitudinal cohort (ρ = −0.32, p < 0.001, n = 117). Recurrent AKR1B1-related drug signatures nominated the aldose-reductase pathway, and epalrestat was therefore prioritized as a hypothesis-generating candidate compound rather than a direct top-ranked enrichment hit. External validation confirmed consistent upregulation of KIF13A (Fold-Change = 1.58, adj. p = 0.0075), EPN1, and CLIP1 in DFU tissue. Despite population-level upregulation, a subset of cells fell below the functional signaling threshold. Conclusions: These computational findings suggest that KIF13A-associated vesicle transport impairment may represent a candidate systems-level bottleneck for growth-factor responsiveness in DFUs, a network-level pattern not captured by standard differential-expression analysis. Epalrestat, an AKR1B1 inhibitor prioritized through recurrent AKR1B1-related drug signatures, is presented as a candidate compound for further evaluation. As the present analysis is observational and computational, the findings should be interpreted as hypothesis-generating; experimental perturbation studies and prospective clinical validation are required. Full article

Compound repurposing is an efficient method to save both time and costs by redirecting previously synthesized small molecules towards new biological targets. In this research, we employ computational methodologies to investigate and assess target engagement of small molecules as tyrosine kinase inhibitors (TKIs). Therefore, compounds TKI.2a, TKI.2b, TKI.6, TKI.16, TKI.19, and TKI.21b identified from our earlier research, undergo assessments of molecular similarity, docking studies, and pharmacophore modeling along with those discovered through database searches. Compounds TKI.2a, TKI.2b, TKI.6, and TKI.19 appear to exhibit multi-target tyrosine kinase inhibitory activities against VEGFR-2 (Vascular Endothelial Growth Factor Receptor), RET (proto-oncogene tyrosine–protein kinase receptor), PDGFRα (Platelet-Derived Growth Factor Receptor alpha), EGFR (Epidermal Growth Factor Receptor), and HER2 (Human Epidermal Receptor) receptors. Pharmacophore models were applied for ligand-based virtual screening using defined parameters to discover candidate compounds that exhibit drug-likeness with FDA (Food and Drug Administration)-approved tyrosine kinase inhibitors. Molecular docking studies identified lead compounds for each biological target based on their overall affinity values and established interactions. Compound ChEMBL2170947 was found to be the most promising candidate for the VEGFR-2 receptor, ChEMBL5019511 for PDGFRα, ChEMBL2216869 for EGFR, and ChEMBL3355044 for HER2. Full article

Background/Objectives: The prognostic significance of the uric acid-to-albumin ratio (UAR) in patients with hormone receptor-positive (HR+) and human epidermal growth factor receptor 2-negative (HER2−) metastatic breast cancer treated with cyclin-dependent kinase 4/6 (CDK4/6) inhibitors has not been adequately investigated. This study aimed to investigate the association between baseline UAR and survival outcomes in this patient population. Methods: This retrospective study included HR-positive/HER2-negative metastatic breast cancer patients treated with ribociclib or palbociclib at Necmettin Erbakan University between May 2020 and April 2025. UAR was calculated by dividing the serum uric acid level (mg/dL) by the serum albumin level (g/dL). Based on receiver operating characteristic (ROC) analysis, the optimal cut-off value for UAR was identified as 1.0 (AUC = 0.67; sensitivity 68%; specificity 58%). Patients were subsequently classified into two groups as UAR < 1 and UAR ≥ 1. Progression-free survival (PFS) and overall survival (OS) were estimated using the Kaplan–Meier method and compared with the log-rank test. Independent prognostic factors were evaluated using Cox regression analyses. Results: A total of 118 eligible patients were included in the analysis, including 34 (28.8%) in the UAR < 1 group and 84 (71.2%) in the UAR ≥ 1 group. The proportion of postmenopausal patients was significantly higher in the UAR ≥ 1 group (p = 0.01). Kaplan–Meier analysis showed that median PFS was not reached in the UAR < 1 group, whereas it was 33.05 months in the UAR ≥ 1 group (log-rank p = 0.06). Median OS was not reached in the UAR < 1 group and was 50.7 months in the UAR ≥ 1 group (p = 0.017). Multivariate Cox regression analysis demonstrated that UAR < 1 was associated with improved PFS (HR = 0.65; 95% CI: 0.34–0.89; p = 0.04). Postmenopausal status emerged as an independent adverse prognostic factor for PFS (HR = 1.92; 95% CI: 1.10–4.05; p = 0.04). In addition, UAR < 1 was associated with a reduced risk of mortality in the OS analysis (HR = 0.61; 95% CI: 0.26–0.87; p = 0.01). Conclusions: Lower baseline UAR was associated with more favorable survival outcomes in HR-positive/HER2-negative metastatic breast cancer patients treated with CDK4/6 inhibitors. As an inexpensive and easily accessible biomarker derived from routine laboratory parameters, UAR may provide additional prognostic information for clinical risk stratification. Full article

Background: Evaluation of gene-level copy number variants (CNVs) for diagnosis and therapeutic decision making has become standard of care with next-generation sequencing (NGS), immunohistochemistry (IHC), and/or fluorescence in situ hybridization (FISH) being used to detect gene amplifications/deletions in tumor tissue. In contrast to most solid tumors, CNS cancers are challenging to evaluate by resection and/or biopsy due to the associated risks with invasive brain surgery that can also result in death or associated morbidity and therefore alternate methods are required.Methods: This study presents the analytical validation of using quantitative PCR (qPCR) to detect gene CNVs directly from cerebrospinal fluid (CSF)-derived DNA and from the Ascent^TM low-pass whole genome sequencing (LP-WGS) libraries, demonstrating concordance with the gold standard of NGS/IHC/FISH used in tumor tissue. Results: The analytical sensitivity of qPCR to detect gene amplification calls for ERBB2 (erb-b2 receptor tyrosine kinase 2) was demonstrated to be 100% and that of EGFR (epidermal growth factor receptor) was 83%, with specificities of 96% and 100%, respectively. The analytical sensitivity of qPCR to detect gene deletions for CDKN2A/2B (cyclin-dependent kinase inhibitor 2A/2B) was 60% and that for MTAP (methylthioadenosine phosphorylase) was 100% with a specificity of 100% for all three genes. Ascent^TM was demonstrated to have a higher sensitivity (100%) when compared to qPCR for the same genes evaluated and demonstrated 100% positive agreement and 100% negative agreement with known CNV status. Conclusions: The results demonstrate that given the paucity of cells in CSF limiting the use of IHC and FISH, qPCR and Ascent^TM provide highly sensitive, novel, minimally invasive methods for the evaluation of gene copy number (CN) status to inform the diagnosis and management of CNS cancers. Full article

Background: Breast cancer remains a leading cause of cancer-related mortality in women, largely due to metastasis and treatment resistance. ELF3, an ETS transcription factor, has been linked to cancer progression; however, the mechanisms regulating its activity remain incompletely understood. Methods: ELF3 expression and its association with patient survival were analyzed using GEO datasets and the Kaplan–Meier Plotter platform. Functional studies were performed using ELF3 knockdown in breast cancer cell lines, followed by WST-1 assays and crystal violet staining. Protein–protein interactions were evaluated using co-expression analysis, immunofluorescence, split luciferase complementation, GST pull-down, and yeast two-hybrid assays. Cycloheximide chase assays were conducted to assess ELF3 protein stability. A panel of small molecules was screened to identify inhibitors of the ELF3-HSP27 interaction, and a lead compound was further validated using biochemical and functional assays. Antitumor activity was evaluated in a xenograft mouse model. Results: High ELF3 expression was associated with poorer overall survival in breast cancer patients. HSP27 was identified as a binding partner that stabilizes ELF3 protein, thereby promoting breast cancer cell proliferation. A novel small-molecule inhibitor disrupting the ELF3-HSP27 interaction suppressed cancer cell growth in vitro and reduced tumor growth in vivo. Conclusions: The ELF3-HSP27 interaction represents a previously unrecognized contributor to breast cancer progression, and its disruption provides a promising therapeutic strategy. Full article

Background: Patients with inflammatory bowel disease (IBD) exhibit a hypercoagulable state with increased thrombotic risk. Previous studies demonstrated elevated thrombin generation in pediatric IBD, paradoxically accompanied by prolonged lag time during active disease. We hypothesized that elevated tissue factor pathway inhibitor (TFPI) levels during active inflammation contribute to this paradox. Methods: We prospectively enrolled 25 pediatric patients (10 Crohn’s disease [CD], 15 ulcerative colitis [UC]) aged 7–18 years with newly diagnosed IBD. Blood samples were collected at diagnosis and in remission. Thrombin generation was assessed using calibrated automated thrombography. Plasma levels of TFPI, tissue factor activity (TFA), vascular endothelial growth factor (VEGF), and interleukin-6 (IL-6) were measured. Results: TFPI levels correlated positively with thrombin generation lag time (r = 0.43, $p_{\mathrm{adj}}$ < 0.05) and disease activity scores (r = 0.54, $p_{\mathrm{adj}}$ < 0.05) in patients with active disease (PCDAI/PUCAI > 0). Longitudinal analysis of 16 patients achieving remission revealed elevated TFPI and prolonged lag time during active disease compared to quiescence (both $p_{\mathrm{adj}}$ < 0.05), while TFA did not change significantly. VEGF decreased significantly upon remission ($p_{\mathrm{adj}}$ < 0.05), whereas IL-6 showed no significant change. Conclusions: Elevated TFPI levels during active IBD likely contribute to the paradoxical prolongation of thrombin generation lag time. TFPI normalization upon remission reflects vascular inflammation resolution, suggesting TFPI as a potential biomarker and therapeutic target. Full article

Background: Fibroblast growth factor 21 (FGF21) is a peptide hormone that is synthesized by several organs and regulates energy homeostasis, including reducing fat mass and lowering hyperglycemia, insulin resistance and dyslipidemia. It also increased metabolic syndrome (MS) and cardiovascular risk in breast cancer (BC) survivors treated with aromatase inhibitors (AIs) aimed at reducing cancer recurrence. We evaluated whether blood FGF21 concentration is associated with MS and its five criteria in postmenopausal women treated with AIs, and whether this persists after multimodal interventions that reduce MS. Methods: A quasi-experimental longitudinal study in 31 postmenopausal women with localized BC on Ais, assessed via a 12-week multimodal program. Their MS was evaluated per the NCEP-ATP III guidelines (waist circumference, blood pressure, fasting glucose, triglycerides, HDL-cholesterol). Plasma FGF21 was measured pre/post-intervention via fasting blood samples, centrifugation, and ELISA assay. Results: Pre-intervention FGF21 median: 377.62 pg/mL (38.40–1616.42). Plasma FGF21 concentrations positively correlated with MS criteria number pre- and post-intervention (all p < 0.05). Linear regression confirmed pre-intervention MS criteria (β = 127.262, p = 0.006) and antihypertensive drugs as predictors of post-FGF21 levels. Analysis of individual MS criteria revealed significant associations with blood pressure (p = 0.028 and p = 0.022 for systolic and diastolic pressure, respectively) and fasting glucose changes (p = 0.008). Conclusions: Plasma FGF21 may act as a biomarker for monitoring exercise-based interventions which reduce MSs, particularly hypertension and hyperglycemia, in AI-treated BC survivors. Full article