Bladder cancer (BC) is one of the most common types of cancer worldwide, with significant differences in survival depending on the degree of muscle and surrounding tissue invasion. For this reason, the timely detection and monitoring of the disease are important. Surveillance cystoscopy is an invasive, costly, and uncomfortable procedure to monitor BC, raising the need for new, less invasive alternatives. In this scenario, microRNAs (miRNAs) represent attractive prognostic tools given their role as gene regulators in different biological processes, tissue expression, and their ease of evaluation in liquid samples. In cancer, miRNA expression is dynamically modified depending on the tumor type and cancer staging, making them potential biomarkers. This review describes the most recent studies in the last five years exploring the utility of miRNA-based strategies to monitor progression, stratify, and predict relevant clinical outcomes of bladder cancer. Several studies have shown that multimarker miRNA models can better predict overall survival, recurrence, and progression in BC patients than traditional strategies, especially when combining miRNA expression with clinicopathological variables. Future studies should focus on validating their use in different cohorts and liquid samples.

To date, prostate cancer remains the most common tumor diagnosed in males and the second most common cause of cancer-related mortality. While current screening protocols can detect early disease, t... Tweetable abstract In prostate cancer, there remains a need for more accurate diagnostic, prognostic and treatment-response strategies utilizing less invasive sources. As such, miRNAs are promising...

Background: The role of adjuvant chemotherapy in early-stage small cell lung cancer (SCLC) and large cell neuroendocrine carcinoma (LCNEC) remains unclear, particularly for small tumors. This study assesses the survival benefits of adjuvant chemotherapy after surgical resection with a novel focus on tumors less than 1 cm. Materials and methods: Data from the National Cancer Database (NCDB) was extracted for patients with SCLC (n = 11,962) and LCNEC (n = 6821) who underwent surgical resection between 2004 and 2020. Exclusion criteria were limited survival (< 30 days), positive lymph nodes, distant metastases, large tumors (> 5 cm), residual microscopic disease, and neoadjuvant therapy. The primary outcome was overall survival (OS) from diagnosis, which was evaluated using Kaplan–Meier methods and multivariate Cox regression analyses. A propensity score matching (PSM) analysis was performed to compare outcomes in patients with SCLC and tumors ≤ 1 cm who received adjuvant chemotherapy versus surgery alone. Results: The study involved 4114 SCLC and 3954 LCNEC patients. Adjuvant chemotherapy was associated with a significant increase median OS in both SCLC (6.26 vs. 4.18 years; p < 0.001) and LCNEC (7.02 years vs. 4.89 years; p < 0.001), while also being an independent predictor of better OS in SCLC (HR: 0.74) and LCNEC (HR: 0.75) (p < 0.001). The benefit was more noticeable in tumors ≤ 1 cm, showing a significant OS increase after PSM (median OS 7.34 vs. 5.02 years; p = 0.0048). Conclusion: Adjuvant chemotherapy after surgery is associated with improved overall survival in stage I SCLC and LCNEC, particularly in SCLC tumors of 1 cm or less.

Hodgkin lymphoma (HL) is a common neoplasm in adolescents and young adults, primarily treated with doxorubicin (DOX) and bleomycin (BLM), which may cause severe adverse effects. The cure rate decreases to 75% in advanced-stage disease, highlighting the need for improved treatment strategies. Pentoxifylline (PTX), an NF-κB pathway inhibitor, enhances chemotherapy-induced apoptosis in cancer cells, making it a promising candidate for HL therapy. This study assessed the effects of PTX, DOX, and BLM on apoptosis, proliferation, and senescence in Hs-445 HL cells. Cell viability and clonogenicity were measured by spectrophotometry and spectrofluorimetry, while apoptosis, caspase activity, cell cycle, mitochondrial membrane potential (ΔΨm), proliferation, and senescence were analyzed via flow cytometry. Gene expression was assessed by qPCR. PTX significantly induced apoptosis, especially when combined with BLM or BLM+DOX (triple therapy), and modulated gene expression by upregulating proapoptotic and downregulating antiapoptotic markers. PTX increased caspase-3, -8, and -9 activity and disrupted the ΔΨm, particularly with BLM or triple therapy. Furthermore, PTX abolished DOX-induced G2 cell cycle arrest, reduced proliferation, and clonogenicity, and reversed DOX- and BLM-induced senescence. In conclusion, PTX induces apoptosis in HL cells, enhances DOX and BLM cytotoxicity synergistically, and reverses senescence, suggesting its potential as an adjunct therapy for HL.

Rapidly progressive glomerulonephritis (GN) in the context of B-cell lymphoma is rare, with most cases involving diffuse-large B-cell lymphoma or marginal zone lymphoma. Kidney biopsies are infrequently performed in this population, further limiting diagnostic clarity. Here, we report a case of newly diagnosed follicular large B-cell lymphoma (FLBCL) presenting with a nephritic syndrome, characterised by haematuria, hypertension and heavy proteinuria, caused by C3 crescentic GN, requiring dialysis. The patient was treated with polatuzumab, bendamustine and rituximab, which was well tolerated. Renal function gradually improved, leading to dialysis discontinuation, coinciding with lymphoma remission. This case underscores the atypical presentation of FLBCL, including renal dysfunction as an early manifestation, and the importance of prompt diagnosis and targeted therapy.

Neoadjuvant systemic therapy (NST) is standard for locally advanced breast cancer (BC), yet predictors of pathological complete response (pCR) remain elusive. While Natural Killer (NK) cells are vital for anti-tumor response, their specific receptor dynamics during NST are poorly defined. This study provides a high-dimensional characterization of the peripheral NK cell landscape and immune signatures associated with therapeutic success. This prospective cohort study included 34 BC patients and 35 healthy donors (HD). Clinical characteristics were collected, and peripheral blood NK cell subsets were evaluated. We utilized high-parameter flow cytometry and unsupervised clustering (UMAP) to longitudinally track NK cell phenotypes (NKG2D, DNAM-1, PD-1, TIGIT) pre- and post-NST. NK cell cytotoxicity was evaluated, and serum levels of related IL-17A (interleukin), IL-2, IL-4, IL-10, IL-6, TNF-α (tumor necrosis factor-alpha), Fas, sFasL, IFN-γ (interferon-gamma), and Granzyme A were analyzed. Patients exhibited distinct NK cell profiles according to the pathological response. Only 12 BC patients achieved pCR. These patients showed improved NK cell cytotoxicity and higher concentrations of IL-2, TNF-α, sFASL, and Granzyme B after treatment compared with Non-pCR patients. In contrast, in Non-pCR patients, the percentages of CD56^bright NK cells increased after neoadjuvant therapy, whereas the more cytotoxic CD56^dim NK cell population decreased. Additionally, NK cells from Non-pCR patients exhibited higher co-expression of inhibitory checkpoints (TIGIT and PD-1), indicating reduced NK cell function. Otherwise, pCR patients displayed a more favorable balance of activating receptors (NKG2D and DNAM-1), and a favorable shift in the TIGIT/DNAM-1 activating-to-inhibitory axis. This study highlights the potential role of NK cells in determining the response to neoadjuvant therapy in BC patients. Those who achieved pCR showed enhanced NK cell activity and higher expression of activating receptors. Moreover, NK cells from Non-pCR patients showed lower cytotoxicity and higher expression of inhibitory receptors. These results suggest that NK cell phenotype evaluation could serve as a biomarker of treatment response in patients with BC. They also showed that the TIGIT/DNAM-1 axis can be a critical determinant of pCR.