Prostate cancer is one of the most common malignant diseases in men, and it contributes significantly to the increased mortality rate in men worldwide. This study aimed to review the roles of p300 and TMPRSS2 (transmembrane protease, serine 2) in the AR (androgen receptor) pathway as they are closely related to the development and progression of prostate cancer. This paper represents a library-based study conducted by selecting the most suitable, up-to-date scientific published articles from online journals. We focused on articles that use similar techniques, particularly those that use prostate cancer cell lines and immunohistochemical staining to study the molecular impact of p300 and TMPRSS2 in prostate cancer specimens. The TMPRSS2:ERG fusion is considered relevant to prostate cancer, but its association with the development and progression as well as its clinical significance have not been fully elucidated. On the other hand, high p300 levels in prostate cancer biopsies predict larger tumor volumes, extraprostatic extension of disease, and seminal vesicle involvement at prostatectomy, and may be associated with prostate cancer progression after surgery. The inhibition of p300 has been shown to reduce the proliferation of prostate cancer cells with TMPRSS2:ETS (E26 transformation-specific) fusions, and combining p300 inhibitors with other targeted therapies may increase their efficacy. Overall, the interplay between the p300 and TMPRSS2 pathways is an active area of research.

Breast cancer ranks first in incidence and second in deaths worldwide, presenting alarmingly rising mortality rates. Imaging methodologies and/or invasive biopsies are routinely used for screening and detection, although not always with high sensitivity/specificity. MicroRNAs (miRNAs) could serve as diagnostic and prognostic biomarkers for breast cancer. We have designed a computational approach combining transcriptome profiling, survival analyses, and diagnostic power calculations from 1165 patients with breast invasive carcinoma from The Cancer Genome Atlas (TCGA-BRCA). Our strategy yielded two separate miRNA signatures consisting of four up-regulated and five down-regulated miRNAs in breast tumors, with cumulative diagnostic strength of AUC 0.93 and 0.92, respectively. We provide direct evidence regarding the breast cancer-specific expression of both signatures through a multicancer comparison of >7000 biopsies representing 19 solid cancer types, challenging their diagnostic potency beyond any of the current diagnostic methods. Our signatures are functionally implicated in cancer-related processes with statistically significant effects on overall survival and lymph-node invasion in breast cancer patients, which underlie their strong prognostic implication. Collectively, we propose two novel miRNA signatures with significantly elevated diagnostic and prognostic power as a functionally resolved tool for binary and accurate detection of breast cancer and other tumors of the female reproductive system.

Ulcerative colitis (UC) is a chronic immune-mediated inflammatory disease characterized by substantial heterogeneity in histologic activity, which is frequently uncoupled from clinical symptoms and endoscopic findings. Persistent microscopic inflammation is increasingly recognized as a critical determinant of relapse, therapeutic failure, and long-term disease outcomes, underscoring the need for molecular frameworks that align directly with tissue-level immune dysregulation. Interleukins (ILs) represent central regulators of mucosal immunity in UC, integrating innate and adaptive immune responses that govern epithelial injury and resolution. In this narrative review, we synthesize mechanistic, translational, genetic, and clinical evidence examining IL networks associated with histologic disease activity and persistence. Particular emphasis is placed on IL-23-driven inflammatory pathways, which consistently align with histologic severity, sustained microscopic inflammation, and resistance to immune resolution. In contrast, preserved IL-10-mediated regulatory signaling characterizes histologic remission and effective mucosal healing, whereas its insufficiency permits ongoing tissue-level inflammation. Downstream effector ILs, including IL-6, IL-1β, IL-8, and IL-17A, are discussed as mediators translating upstream immune imbalance into neutrophil recruitment and epithelial injury. Throughout this review, the term “prognostic” is used to denote alignment with histologic disease behavior rather than validated prediction of clinical outcomes. Collectively, the evidence supports the concept that coordinated IL patterns reflect distinct immunopathologic states underlying microscopic inflammation in UC, providing a biologically coherent framework for interpreting histologic activity and disease persistence beyond symptom-based assessment.

Background/Objectives: Deep remission, defined as the coexistence of endoscopic remission and histologic healing, has emerged as an advanced therapeutic target in ulcerative colitis (UC). However, reliable non-invasive biomarkers capable of accurately reflecting histologic inflammatory status remain limited. We aimed to evaluate the association between serum interleukin-10 (IL-10) concentrations and deep remission in UC and to assess its discriminatory performance. Methods: In this prospective single-center observational study, consecutive adult patients with ulcerative colitis undergoing clinically indicated colonoscopy were enrolled. Serum IL-10 concentrations were measured prior to endoscopy using an enzyme-linked immunosorbent assay. Histologic healing was defined as a Geboes score < 2.0, and deep remission as the coexistence of endoscopic remission and histologic healing. Associations were evaluated using Firth penalized logistic regression. Discrimination was assessed using receiver operating characteristic analysis with bootstrap internal validation (500 resamples). Results: Among 44 patients, 18 (40.9%) achieved deep remission. Serum IL-10 levels were significantly higher in patients with histologic healing compared with those with active histologic inflammation (p < 0.001). Log-transformed IL-10 was independently associated with deep remission in both univariable and multivariable models. The primary multivariable model demonstrated apparent good discrimination (apparent AUC 0.88; optimism-corrected AUC 0.85). Among patients in endoscopic remission, non-detectable IL-10 identified persistent histologic activity with high sensitivity (92.9%) and negative predictive value (94.4%), although these findings are exploratory. Conclusions: Serum IL-10 concentrations were independently associated with deep remission and showed potentially promising internally validated discriminatory performance within this cohort. These findings are hypothesis-generating and require external validation in larger cohorts before clinical application.

Small leucine-rich proteoglycans (SLRPs) are an important group of molecules in the extracellular matrix (ECM) that are involved in regulating collagen assembly, tissue homeostasis, and cell signalling pathways. Among them, Decorin represents the proto-type member and plays a central role in maintaining ECM integrity, regulating fibrosis, and controlling tumor progression. This review examines the structural and functional biology of SLRPs, with a special focus on Decorin, highlighting its involvement in fibrotic diseases, degenerative disorders and the tumor microenvironment. Decorin acts as a multifunctional regulator through its interactions with TGF-β, various tyrosine kinase receptors, and multiple ECM components, carrying out anti-fibrotic, anti-angiogenic, anti-cancer, and tumour-suppressive functions. Additionally, factors such as the contribution of SLRPs to the desmoplastic response of tumors, their potential use as biomarkers for extracellular matrix remodelling, and the emerging therapeutic prospects based on administering recombinant Decorin, gene therapies, mimetic molecules, and strategies targeting the ECM. Overall, SLRPs, especially Decorin, stand out as key molecules in integrating structural and molecular signals and as promising diagnostic and therapeutic targets in fibrotic and neoplastic diseases.

Background: Endoscopic remission is a central therapeutic target in inflammatory bowel disease (IBD); however, histologic inflammation may persist despite apparent mucosal healing. The biological mechanisms underlying endoscopic–histologic discordance remain incompletely defined. We aimed to characterize systemic cytokine patterns associated with discordant disease. Methods: In this prospective cross-sectional study, 59 patients with IBD undergoing clinically indicated colonoscopy underwent concurrent endoscopic and histologic assessment. Endoscopic remission was defined as a Mayo endoscopic subscore ≤ 1 for ulcerative colitis and SES-CD ≤ 2 for Crohn’s disease. Histologic healing was defined as a Geboes score < 2.0. Patients were classified into concordant remission, discordant disease (endoscopic remission with persistent histologic activity), and concordant active disease. Circulating interleukin (IL)-10, IL-23, and C-reactive protein (CRP) levels were compared across phenotypes using nonparametric methods. Associations with discordant disease were evaluated using Firth penalized logistic regression, and model discrimination was assessed using receiver operating characteristic (ROC) analysis with bootstrap internal validation. Results: Among 36 patients in endoscopic remission, 14 (38.9%) exhibited persistent histologic activity. Discordant patients demonstrated significantly lower IL-10 and higher IL-23 concentrations compared with concordant remission (both p < 0.001), whereas CRP did not differ significantly. Across phenotypes, IL-10 decreased progressively, while IL-23 increased stepwise (both p < 0.001). In multivariable analysis, lower IL-10 (OR 0.0014; 95% CI 0.000003–0.576; p = 0.032) and higher IL-23 (OR 16.94; 95% CI 1.90–151.32; p = 0.011) were independently associated with discordant disease. A model incorporating IL-10 and CRP demonstrated strong discrimination (AUC 0.925), with further improvement after inclusion of IL-23 (AUC 0.994), although these estimates should be interpreted with caution given the limited sample size. Conclusions: Endoscopic–histologic discordance is associated with a distinct systemic cytokine profile characterized by reduced IL-10 and elevated IL-23 levels, despite low CRP concentrations. These findings suggest incomplete restoration of immune regulatory balance and highlight the potential role of circulating cytokines, particularly IL-10, in identifying ongoing microscopic inflammation. These results are exploratory and hypothesis-generating and require validation in larger, prospective cohorts before clinical application.