Hepatocellular carcinoma (HCC) is characterized by high mortality, frequent recurrence, and limited long-term benefit from systemic therapy and radiotherapy. Circular RNAs (circRNAs), a class of covalently closed non-coding RNAs with high molecular stability and tissue-specific expression, have emerged as important regulators of HCC biology and treatment response.

To clarify the prevalence and clinical utility of molecular biomarkers in vulvar cancer, we performed a review of systematic and high-quality narrative reviews, complemented by interrogation of public repositories containing genomic datasets. Our objectives were to (i) quantify biomarker prevalence across vulvar cancer subtypes, (ii) evaluate their prognostic and predictive value, and (iii) identify actionable therapeutic targets.

Glioblastoma (GBM) is the most aggressive primary brain tumor with a poor prognosis. The current standard regimen of surgery combined with concurrent temozolomide chemoradiotherapy has limited efficacy. Multiple targeted therapies have been evaluated in randomized controlled trials (RCTs), but results are inconsistent and lack systematic comparisons. This review used network meta-analysis (NMA) to assess the relative efficacy and safety of different targeted drugs vs. standard treatment.

Molecular biomarkers are increasingly used for risk stratification, particularly in up-front surgery settings (Children's Oncology Group trials), whereas in preoperative chemotherapy setting, the ongoing International Society of Pediatric Oncology (SIOP)-Renal Tumor Study Group-2016 UMBRELLA study aims to validate selected biomarkers for future risk-adapted treatment strategies. This systematic review summarizes all literature on the prognostic value of these biomarkers.

The cystine/glutamate antiporter, also known as system Xc-, has two roles: (1) imports cystine used to form glutathione (GSH), (2) regulates the extracellular concentration of glutamate. These roles are essential for brain function, as GSH is the most important antioxidant in the brain, and glutamate is the main excitatory neurotransmitter. This antiporter is composed of two subunits: xCT (encoded by the gene Slc7a11) and a heavy chain, CD98 (encoded by the gene Slc3a2). xCT is the subunit responsible for cystine/glutamate transport, while CD98 is responsible for the translocation of system Xc- to the membrane. The antioxidant function of xCT has been highlighted by the discovery of ferroptosis, a distinctive form of programmed cell death triggered by lipid peroxidation and the accumulation of reactive oxygen species. In addition, numerous types of cancers have been shown to overexpress xCT to evade ferroptosis. The mechanisms by which healthy cells regulate xCT expression, the mechanisms responsible for xCT overexpression in cancer cells, and whether different types of cancers employ identical mechanisms to upregulate xCT have not been systematically studied. To answer these questions, we conducted a systematic review to consolidate the regulatory mechanisms governing xCT expression. We found that xCT expression is regulated at nearly all known levels, including epigenetic, transcriptional, post-transcriptional, translational, post-translational, and by protein-protein interactions, with some cell-type- and context-specific mechanisms. Overall, our work highlights the role of xCT and the breadth of axes through which its expression can be modulated.

The heterogeneous response to immunotherapy in diffuse large B-cell lymphoma (DLBCL) is largely attributable to the diverse functional states of CD8⁺ T cells within the tumor microenvironment. Although single-cell RNA sequencing (scRNA-seq) has revolutionized cellular resolution, a systematic synthesis of this evidence to map CD8⁺ T cell heterogeneity and its clinical implications in DLBCL is currently lacking.

Preoperative neoadjuvant chemotherapy (NAC) is a commonly employed treatment strategy for triple-negative breast cancer (TNBC). Various clinical factors may influence the likelihood of achieving a pathological complete response (pCR) following NAC. This study conducted a meta-analysis to identify factors associated with pCR to inform clinical decision-making. EMBASE, PubMed, WOS, Scopus databases were selected as the information sources to identify studies published before July 1, 2025. Predefined inclusion and exclusion criteria were applied, and the quality of included studies was assessed. Commonly reported factors were subjected to meta-analysis. Thirteen studies published between 2011 and 2025 were included, with eight published before 2020 and five thereafter. Seven potential influencing factors were analyzed, including individual characteristics, pathological features, and serum biomarkers. The pooled results indicated that clinical tumor stage (OR (odds ratio) = 0.35, 95% CI: 0.21-0.59, p = 0.032), Ki-67 expression (OR = 2.91, 95% CI: 1.64-5.16, p < 0.001), BRCA1/2 mutation status (OR = 1.95, 95% CI: 1.04-3.66, p = 0.037), and neutrophil-to-lymphocyte ratio (NLR) (OR = 5.61, 95% CI: 2.05-15.34, p < 0.001) were significantly associated with pCR. In contrast, age at diagnosis, histological grade, and nodal status were not statistically significant predictors. The likelihood of achieving pCR in TNBC patients undergoing NAC is significantly associated with clinical stage, Ki-67 expression, BRCA1/2 mutation status, and NLR. These factors should be evaluated prior to chemotherapy to help tailor treatment strategies and optimize therapeutic outcomes.

Breast cancer (BC) is a highly heterogeneous malignancy originating from mammary epithelial cells and remains a leading cause of cancer-related mortality worldwide, with ∼2.3 million new cases and over 665,000-670,000 deaths annually. The disease is driven by complex molecular mechanisms, including hormone receptor signaling, genetic mutations (e.g., TP53, BRCA), and HER2 pathways. Advances in molecular classification have enabled the identification of distinct subtypes, including luminal A, luminal B, HER2-positive (HER2+) subtype, and triple-negative breast cancer (TNBC), each requiring tailored therapeutic strategies.

To systematically investigate the diagnostic performance of magnetic resonance imaging (MRI)-based radiomics and deep learning (DL) models for predicting p53 status in glioma and to generate pooled estimates for radiomics-based models.

Ovarian cancer (OC) remains a major global health issue, often diagnosed late and lacking effective screening.

Colorectal cancer (CRC) remains a major global health burden and a leading cause of cancer-related morbidity and mortality. Current blood-based biomarkers lack sufficient sensitivity and specificity, particularly for early detection. In this context, circulating immune-cell transcriptomic profiling has emerged as a promising minimally invasive approach. This systematic review was conducted following a PROSPERO-registered protocol (CRD42024604757) and PRISMA 2020 guidelines to evaluate the diagnostic and prognostic potential of circulating monocyte-related transcriptomic profiles in CRC. Of 295 records identified, six studies met the inclusion criteria. The available evidence consistently supports the diagnostic value of circulating transcriptomic profiles in distinguishing patients with CRC from healthy individuals and in reflecting tumour-associated immune alterations. Monocyte-related signatures, including CXCR2+ monocytes, were associated with disease stage and metastatic features. Epitranscriptomic modifications, such as m6A and m5C, further reinforced their diagnostic relevance, with some studies reporting higher diagnostic accuracy than classical biomarkers. In contrast, evidence for prognostic value remains limited, heterogeneous, and often indirect, largely due to small sample sizes, methodological variability, and reliance on public datasets. Overall, circulating immune-cell transcriptomic profiles are promising non-invasive biomarkers for CRC detection and characterization, although their prognostic utility remains unclear. Methodological heterogeneity limits clinical applicability, highlighting the need for standardized, CRC-specific studies with cell-type-resolved approaches.

To critically evaluate the evidence linking endometriosis to ovarian cancer, with particular focus on endometrioid and clear cell histologic subtypes, and to inform risk stratification and patient counseling.

Resectable melanoma remains associated with substantial relapse risk despite adjuvant therapy, and prognostic biomarkers for better risk stratification are urgently needed. We evaluated the prognostic and diagnostic performance of circulating tumor DNA (ctDNA) in patients with resectable melanoma.

Gastrointestinal (GI) tumours are one of the most prevalent cancers globally. Even with normal GI function, individuals may develop neoplasms, highlighting the need to better understand the underlying causes of tumorigenesis. The emergence of tumour drug resistance represents the main reason for the failure of drug treatment; thus, it is imperative to investigate all the potential mechanisms of this very complex phenomenon. It is significant that exosomes and noncoding RNAs, such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), originating from tumour cells, are linked to both GI drug resistance and the carcinogenesis and development of GI disease. Thus, we propose a systematic review of the literature to provide an overview of the current landscape concerning exosomal ncRNAs as diagnostic and prognostic biomarker resources in resistant GI cancer. We performed the current systematic review according to PRISMA guidelines and comprehensively explored PubMed, Web of Science, Scopus and Google Scholar databases to achieve the article search. Seventy-six studies were included in the investigation, comprising 50 cohort studies and 26 nested case-control studies (between 1994 and 2025). Among all systematically reviewed exosomal ncRNAs, we primarily found molecules with prognostic significance and predictive relevance, and those that serve both purposes have been identified. Furthermore, among all analysed ncRNAs isolated from exosomes, miRNAs, lncRNAs and circRNAs have emerged as the most extensively studied and are proposed as potential tools for predicting resistance or sensitivity to GI cancer treatments. Our analysis offers a comprehensive overview of the current landscape concerning exosomal ncRNAs as potential clinical biomarkers for resistant GI tumours. However, despite extensive research efforts, the application of exosomal biomarkers in GI cancers is still in its infancy. None of the identified exosomal biomarkers have advanced beyond preclinical studies, and their applicability in clinical settings remains limited, largely due to challenges in clinical validation, standardisation and biomarker specificity.

Uterine leiomyomas (ULs) are prevalent benign tumors in women of reproductive age characterized by cellular senescence. Cellular senescence is a state of stable, irreversible cell cycle arrest characterized by discrete changes in cellular morphology and gene expression. This systematic review, following PRIMSA guidelines, evaluated the molecular pathways contributing to senescence in ULs and the use of novel therapeutic agents to target senescence. Two investigators independently screened and identified relevant articles written in English involving human subjects. Sixty-nine articles were identified; 11 studies met criteria. Multiple studies recognized a range of biomarkers of senescence in ULs including senescence associated beta galactosidase (SA-β-gal), senescent associated proteins (p16, p21, p14ARF), and telomere shortening. Key pathways such as AKT and p14ARF-TP53-p21, and genes such as HMGA2 and MED12 have been implicated in regulating the balance between tumor proliferation and growth arrest and senescence. However, the specific genetic and epigenetic mechanisms that induce and maintain senescence in ULs are not fully understood. There is growing interest in investigating whether senescent cells can be therapeutically targeted in ULs by senolytic agents that induce apoptosis, and senomorphic agents that modulate the senescence-associated secretory phenotype (SASP) to reduce its pro-tumorigenic effects. While limited, non-clinical data suggests this approach may be promising, further investigation is needed to establish their clinical efficacy in patients with ULs.

ERBB2 (HER2)-mutant NSCLC, most commonly driven by exon 20 insertions, has historically shown limited benefit from early pan-ERBB inhibitors. Although multiple HER2-targeted agents have since emerged, the relationship between objective response, disease control, and durability remains incompletely defined across heterogeneous single-arm studies.

Ropeginterferon alfa-2b is an interferon used in the treatment of myeloproliferative neoplasms, particularly polycythemia vera. Its efficacy in achieving hematologic and molecular responses has been demonstrated in clinical trials, but pooled data on long-term outcomes and sustained response remain limited. This systematic review and meta-analysis aimed to evaluate the hematologic and molecular response over 36 months. PubMed, Scopus, Science Direct, and Google Scholar databases were searched to identify studies reporting hematologic and molecular responses to ropeginterferon alfa-2b. Studies were included if they provided data on complete hematologic response (CHR) and JAK2V617F variant allele frequency (VAF) reduction. Pooled proportions and mean reductions were calculated using random-effects models. The pooled proportion of CHR increased progressively from 0.19 (95% CI: 0.04-0.57) at 3 months to 0.73 (95% CI: 0.17-0.97) at 36 months. Molecular response, measured by VAF reduction, deepened over time from - 7.33 (95% CI: -9.85 to -4.81) at 3 months to -54.90 (95% CI: -65.61 to -43.99) at 36 months. Subgroup analyses revealed significant variability in response rates, particularly in early follow-up periods. Ropeginterferon alfa-2b achieves significant and sustained hematologic and molecular responses over 36 months. This makes it a promising treatment for polycythemia vera. While variability in early responses needs further investigation, the sustained long-term efficacy compared to hydroxyurea supports its use in clinical practice. Future studies should focus on identifying predictors of response and optimizing treatment protocols to maximize patient outcomes.

Type 2 diabetes mellitus (T2DM) and cancer are both major global public health concerns; however, their causal relationship remains unclear. This study aims to quantitatively investigate the potential causal associations between T2DM and 17 site-specific cancers through a systematic review and meta-analysis of Mendelian randomization (MR) studies.

Adenocarcinomas are rare histological subtypes of bladder cancer mainly presenting as primary bladder adenocarcinomas (PBACs), or urachal carcinomas (UrCs). The lack of standardized, evidence-based clinical recommendations for therapy results in individualized treatment decisions. These personalized treatments may be tailored based on molecular analyses to target driver mutations. The genetic background of UrC and PBAC has been increasingly explored through molecular analysis of relatively small case series. Similarly, experiences with targeted treatments are available from individual case reports and single institution case series. Consequently, currently available genetic and targeted treatment data are fragmented, hindering a comprehensive overview and firm conclusions. Therefore, we aimed to catalogue and interpret recent molecular genetic insights and targeted therapeutic experiences in UrC and PBAC in order to provide a basis for improved clinical decision-making. In this review, we screened online databases with search terms selective for genetic and targeted therapeutic data in UrC and PBAC. Utilizing the extracted data, we identified mutational frequencies, created OncoPrints, investigated signaling pathways, and evaluated treatment approaches guided by precision medicine. Our summary of genetic findings and targeted therapy strategies are intended to support off-label options for UrC and PBAC.

Microsatellite instability (MSI) has emerged as a key predictive biomarker for chemotherapy and immunotherapy response, and as a prognostic indicator in colorectal cancer (CRC). The current clinical standard for MSI detection relies on polymerase chain reaction (PCR) or immunohistochemical analysis of tumor biopsy specimens. CT, PET-CT, and MRI-based radiomics models present a promising non-invasive alternative for this purpose.