The HCC constitutes one of the most frequent cancers, with a non-decreasing trend in disease mortality despite advances in systemic therapy and surgery. This trend is fueled by the rise of an obesity wave which is prominent the Western populations and has reshaped the etiologic landscape of HCC. Interest in the nucleotide-binding domain leucine-rich repeat containing (NLR) family member NLRP3 has recently been revived since it would appear that, by generating inflammasomes, it participates in several physiologic processes and its dysfunction leads to disease. The NLRP3 inflammasome has been studied in depth, and its influence in HCC pathogenesis has been extensively documented during the past quinquennial. Since inflammation comprises a major regulator of carcinogenesis, it is of paramount importance an attempt to evaluate the contribution of the NLRP3 inflammasome to the generation and management of HCC. The aim of this review was to examine the literature in order to determine the impact of the NLRP3 inflammasome on, and present a hypothesis about its input in, HCC.

Pancreatic Ductal Adenocarcinoma (PDAC) constitutes a leading cause of cancer death globally. Its mortality remains unaltered despite the considerable scientific progress made in the fields of diagnostics and treatment. Exosomes comprise of small extracellular vesicles secreted by nearly all cells; their cargo contains a vast array of biomolecules, such as proteins and microRNAs. It is currently established that their role as messengers is central to a plethora of both physiologic and pathologic processes. Accumulating data have shed light on their contributions to carcinogenesis, metastasis, and immunological response. Meanwhile, the advancement of personalized targeted therapies into everyday clinical practice necessitates the development of cost-efficient treatment approaches. The role of exosomes is currently being extensively investigated towards this direction. This review aims to summarize the current pre-clinical and clinical evidence regarding the effects of exosomal applications in the timely diagnosis, prognosis, and therapeutic management of pancreatic cancer.

Pancreatic ductal adenocarcinoma (PDAC) is a major concern for health care systems worldwide, since its mortality remains unaltered despite the surge in cutting-edge science. The EPH/ephrin signaling system was first investigated in the 1980s. EPH/ephrins have been shown to exert bidirectional signaling and cell-to-cell communication, influencing cellular morphology, adhesion, migration and invasion. Recent studies have highlighted the critical role of the EPH/ephrin system in various physiologic processes, including cellular proliferation, survival, synaptic plasticity and angiogenesis. Thus, it has become evident that the EPH/ephrin signaling system may have compelling effects on cell homeostasis that contribute to carcinogenesis. In particular, the EPH/ephrins have an impact on pancreatic morphogenesis and development, whereas several EPHs and ephrins are altered in PDAC. Several clinical and preclinical studies have attempted to elucidate the effects of the EPH/ephrin pathway, with multilayered effects on PDAC development. These studies have highlighted its highly promising role in the diagnosis, prognosis and therapeutic management of PDAC. The aim of this review is to explore the obscure aspects of the EPH/ephrin system concerning the development, physiology and homeostasis of the pancreas.

ERCC1 is a key regulator of nucleotide excision repair (NER) pathway that repairs bulky DNA adducts, including intrastrand DNA adducts and interstrand crosslinks (ICLs). Overexpression of ERCC1 has been linked to increased DNA repair capacity and platinum resistance in solid tumors. Multiple single nucleotide polymorphisms (SNPs) have been detected in ERCC1 gene that may affect ERCC1 protein expression. Platinum-based treatment remains the cornerstone of urothelial cancer treatment. Given the expanding application of neoadjuvant and adjuvant chemotherapy in locally advanced bladder cancer, there is an emerging need for biomarkers that could distinguish potential responders to cisplatin treatment. Extensive research has been done regarding the prognostic and predictive role of ERCC1 gene expression and polymorphisms in bladder cancer. Moreover, novel compounds have been recently developed to target ERCC1 protein function in order to maximize sensitivity to cisplatin. We aim to review all the existing literature regarding the role of the ERCC1 gene in bladder cancer and address future perspectives for its clinical application.

Ovarian cancer is the gynecologic malignancy that bears the highest mortality rate in the Western world. This is attributed to late diagnosis and limited therapeutic progress. Recent advances in molecular oncology have highlighted the pivotal role of epigenetic modifications—including DNA methylation, histone modifications, non-coding RNAs, chromatin remodeling, and RNA methylation—in ovarian cancer development, progression, and treatment resistance. DNA methylation patterns affect key tumor suppressors and oncogenes, while histone modifications alter chromatin accessibility, influencing gene expression. Chromatin remodeling complexes, particularly the SWI/SNF complex, are frequently mutated in specific ovarian cancer subtypes, which is central in shaping their biological behavior. Non-coding RNAs, including microRNAs and long non-coding RNAs, further regulate tumor cell behavior and the immunosuppressive tumor microenvironment. Epigenetic profiles vary among histological subtypes and hold promise for biomarker development, early detection, prognosis, and therapeutic monitoring. Liquid biopsy approaches leveraging circulating tumor DNA methylation show diagnostic potential superior to conventional markers. Moreover, targeting epigenetic regulators—such as DNMT and HDAC inhibitors, EZH2 antagonists, and RNA-modifying enzymes—offers novel avenues for treatment, particularly in reversing chemoresistance and sensitizing tumors to immunotherapy. While promising, these strategies require further validation through clinical research to translate into effective clinical interventions. This review aims to summarize the current literature and highlights potential applications of epigenetic manipulation in day-to-day practice.

Background/Objectives: Survival rates for ovarian cancer remain distressingly low. Despite established prognostic factors, the need to identify modifiable parameters to influence survival outcomes is imperative. Overweight and obesity, both prevalent conditions, have been implicated in cancer development and potentially poor survival. However, conflicting data on the associations of body mass index (BMI) with progression-free survival (PFS) and overall survival (OS) in ovarian cancer patients necessitate further exploration. This study aims to investigate the prognostic role of BMI before chemotherapy in women with ovarian cancer, specifically focusing on PFS and OS. Methods: A retrospective analysis encompassed 1,136 patients diagnosed with ovarian carcinomas between 1995 and 2018. Patients were categorized based on BMI at presentation, and a comprehensive examination of clinicopathological, treatment, and survival data was conducted. Results: In the patient population, normal weight patients (BMI < 25 kg/m²) demonstrated a median PFS of 12.8 months (95% CI 11.7–13.9 months), while overweight/obese patients (BMI ≥ 25 kg/m²) exhibited a significantly longer median PFS of 14.9 months (95% CI 13.6–16.4 months, P = 0.006). No statistically significant difference was noted in median OS between the two BMI groups. Subgroup analysis for different histological subtypes revealed a statistically significant benefit for overweight and obese patients with serous and endometrioid histology (mPFS 12.9 months, 95% CI 11.7–14.0 vs. 15.6 months, 95% CI 13.9–17.3, P = 0.012 and 14.6 months 95% CI 13.7–15.5 vs. 25.6 months, 95% CI 9.5–41.7, P = 0.031, respectively). Additionally, BMI ≥ 25 kg/m² demonstrated a significant advantage in advanced-stage disease. Conclusions: The study underscores the intricate association between BMI and ovarian cancer prognosis. While a statistically significant difference in progression-free survival was noted between normal weight and overweight/obese patients, with the latter group experiencing a survival benefit, no such difference was observed in overall survival.