For centuries, Panax ginseng C.A. Meyer has been widely employed in traditional medicine, and its primary therapeutic constituents are a class of compounds known as ginsenosides. In particular, protopanaxadiol (PPD)-type ginsenosides exhibit potent anticancer properties, largely mediated through epigenetic mechanisms.

Oral leukoplakia (OL) represents the most common oral potentially malignant disorder globally, with highly variable reported malignant transformation (MT) rates creating challenges for evidence-based clinical management.

Twenty percent and 45.4% of high-grade ovarian carcinomas (OC) and endometrial carcinomas (EC) exhibit CCNE1 amplification (CCNE1-amp), respectively, which is related to poor prognosis, but could serve as predictive biomarker for response to innovative targeted therapies. However, there is no consensus regarding how to evaluate the CCNE1 status (at the DNA, RNA, and/or protein level). Therefore, we conducted a systematic review of CCNE1 status testing in tubo-ovarian neoplasms and EC, comparing their performance for clinical purposes and highlighting the test's interpretation criteria (CRD420250651291). Among the 734 records initially found on PubMed and Google Scholar, 48 reports were finally included. Molecular analyses and immunohistochemistry (IHC) were reported on 9774 tubo-ovarian neoplasms and 750 EC, and 6966 tubo-ovarian neoplasms and 856 EC, respectively. The most frequently morphological used method to detect CCNE1-amp was fluorescent in situ hybridization (13/16 studies, 81.3%), with quite consensual criteria to defined amplification (ie, CCNE1/chromosome 19 ratio ≥2, and/or >8/≥8 copies of CCNE1 per nucleus, and/or ≥4 CCNE1 copies in ≥40% of cells). The proportion of tubo-ovarian neoplasms with CCNE1 immunohistochemical overexpression varied from 13.5% to 96%, and 14.6% to 86.1% in EC. The sensitivity and specificity of CCNE1 IHC to detect/exclude CCNE1-amp varied from 54.5% to 100% and 59.3% to 90.1%, respectively. Given the reported data, CCNE1 overexpression should be considered either when an H-score is ≥100 or when the staining is >60% with >5% of cells strongly stained. Both CCNE1-amp and CCNE1 overexpressions were associated with poor prognosis and with response to Wee1 and CDK2 inhibitors in high-grade serous OC (overall response rate up to 53%, objective response rate of 32%-40%). In contrast, CCNE1 messenger RNA overexpression had no prognostic value. Thus, both CCNE1-amp detection by fluorescent in situ hybridization and CCNE1 protein levels quantification using IHC represent today the most validated tools to determine the CCNE1 status in OC/EC.

Variation in the prevalence and severity of late effects in similarly treated childhood cancer survivors suggests a role for genetic susceptibility. We aimed to provide an overview of genetic factors associated with selected late effects after childhood cancer, including metabolic syndrome, gonadal insufficiency, hearing impairment, and musculoskeletal impairment.

Cancer of unknown primary (CUP) represents a significant clinical challenge due to its heterogeneity and the poor prognosis often associated with the disease. Molecular profiling has emerged as a promising approach to address the challenges associated with CUP. This systematic review evaluates the existing evidence on the value of different types of molecular tools for CUP diagnosis and treatment.

Breast cancer is the most commonly diagnosed cancer in women in England. Breast cancer and chemotherapy treatment can impact upon patients' quality of life and survival. Tumour profiling tests can help to identify whether patients will benefit from chemotherapy.

To evaluate cysteine dioxygenase 1 (CDO1) gene promoter methylation in circulating tumor DNA as a biomarker for the early diagnosis of lung cancer.

Lung cancer remains the leading cause of cancer-related mortality worldwide, with a substantial risk of recurrence even in early-stage non-small cell lung cancer (NSCLC) after curative surgery. Circulating tumor DNA (ctDNA)-based detection of minimal residual disease (MRD) has emerged as a promising tool for identifying patients at increased risk of relapse. However, the predictive effectiveness of ctDNA remains uncertain because of variability in study designs, detection strategies, and statistical power.

There are meta-analyses about the correlation between non-coding RNA and the prognosis of gastric cancer, which are focus on a single or a particular type of non-coding RNA. This study aims to verify the correlation between various non-coding RNAs and the prognosis of gastric cancer through meta-analysis.

The BRAFV600E mutation is one of the most common genetic alterations in papillary thyroid cancer (PTC) and is widely recognized as a factor of poor prognosis. Radioactive iodine (RAI) therapy is recommended after thyroidectomy for patients with high-risk level PTC or distant metastatic PTC. However, the association between BRAFV600E mutation and RAI refractoriness remains controversial and requires additional investigation. This meta-analysis was conducted to evaluate the impact of BRAFV600E mutation on the curative effect of RAI therapy.

Klippel-Trénaunay syndrome (KTS) and Parkes Weber syndrome (PWS) are rare vascular disorders that share clinical features such as limb overgrowth and capillary malformations. However, they differ in the vascular flow dynamics. KTS is a low-flow malformation, while PWS is characterized by high-flow arteriovenous shunts.

Many women carry male cells of presumed fetal origin-so-called male-origin microchimerism (MOM) in their circulation and tissues. The association between MOM and cancer risk remains unclear. We aim to evaluate the effect of MOM on cancer risk among postpartum women.

Polycystic ovary syndrome (PCOS) is a common endocrinopathy affecting 5-20% of reproductive-age women. Besides genetic factors, environmental triggers are considered major underlying causes that play a role through epigenetic alterations. Since epigenetic studies can be a possible link to explain the complexity of multifactorial disorders, it is worthwhile to investigate differentially methylated regions (DMRs) associated with PCOS. Therefore, a systematic review was conducted to identify epigenetic modifications associated with PCOS and analyse their functional role in the pathogenesis of the syndrome. After following inclusion and exclusion criteria, various databases (PubMed, Google Scholar, Central Cochrane Library, and Science Direct) were searched with predetermined keywords up to 30th June 2025, and quality of the selected articles assessed through the Newcastle Ottawa scale (NOS). In-silico analysis was performed by STRING, and Shiny GO. A total of 46 eligible studies were included, were further sub-categorized based on the sample type. A total of one hundred eleven genes were identified with altered DMRs, out of which thirty seven genes were reported from the ovarian tissues alone. Their GO analysis shows a significant interaction with other PCOS-susceptible genes and their functions in female sex differentiation and gonadal development. However, in-silico analysis of thirty six genes identified in blood showed their functions were significantly involved in the insulin-like growth factor binding activity. Gene enrichment analysis of fifteen genes with altered methylation identified in adipose tissue shows the significant involvement of female sex differentiation and insulin-activated receptor functions. Further, alterations in methylation of which genes (INSR, AMHR2, YAP1, CYP19A1, LHCGR, CDKN1A, LINE-1, AMH and TOX3) have been reported by at least two separate studies, irrespective of sample type. Their in-silico analysis shows significant involvement of these genes in the female sex characters, and gonadal development The current study highlights tissue-specific epigenetic modifications in PCOS, summarizes DMRs of genes which are involved in reproductive and insulin-related pathways. DMRs of identified genes may have a role in the pathogenesis of PCOS, insight into which may provide novel therapeutic targets in the future.

Bladder cancer (BC) is a complex disease with patients showing widely variable responses to treatment. While immunotherapy has recently emerged as a promising alternative to the standard platinum-based chemotherapy, especially for platinum-resistant tumors, clinicians still lack reliable biomarkers to predict which patients will truly benefit from immunotherapy.

Immune checkpoint inhibitors targeting PD-L1 or PD-1 as monotherapy or combined with CTLA-4 inhibitors or chemotherapy (or both) are the standard of care for patients with advanced non-small-cell lung cancer (NSCLC). However, it remains unclear which patients benefit from the addition of CTLA-4 inhibitors. We aimed to evaluate whether dual checkpoint blockade with CTLA-4 and PD-L1 or PD-1 inhibitors provides similar efficacy to PD-L1 or PD-1 inhibitor monotherapy, or whether these strategies produce distinct outcomes across NSCLC subpopulations.

Adding cyclin-dependent kinase 4/6 inhibitors (CDK4/6i) to endocrine therapy (ET) is considered the first-line treatment of advanced HR-positive/HER2-negative breast cancer. However, with the recent approval of several additional targeted agents, the optimal treatment sequencing remains uncertain, and it is unclear whether the benefits of CDK4/6i extend beyond progression on first-line therapy.

No specific molecular profile endometrial cancer represents nearly half of the diagnoses, characterized by substantial molecular heterogeneity and intermediate recurrence and survival outcomes. Currently, no immunohistochemical or molecular markers are established in guidelines to improve prognosis estimation and personalize treatment in no specific molecular profile endometrial cancer. This systematic review and meta-analysis aimed to evaluate the prognostic significance of potential immunohistochemical and molecular surrogate markers in no specific molecular profile endometrial cancers.

Brain metastases (BMs) are the most common intracranial malignancy, often arising from lung, breast, and melanoma cancers. Receptor tyrosine kinases, such as EGFR and HER2, drive tumor progression and resistance to therapy. Noninvasive detection of these biomarkers, especially in brain metastases, is crucial due to challenges with traditional biopsy methods. This systematic review and meta-analysis assess machine learning (ML)-based models for detecting EGFR mutations and HER2 overexpression in metastatic brain adenocarcinoma using MRI-derived radiomic features.

Over the years, accumulating evidence has been associating interleukin-13 gene (IL-13) variants with a wide array of chronic inflammatory diseases. Also, recent findings have associated the potential role of a single nucleotide polymorphism (SNP) of IL-13, rs20541, to promote either anti- or pro-inflammatory responses in chronic inflammatory diseases. Although rs20541 has been widely associated with various immune-related and inflammatory conditions, its precise functional relevance in the pathogenesis of human diseases has yet to be fully clarified. Nonetheless, its consistent associations and known effects on IL-13 signalling underscore its potential biological importance. Hence, this meta-analysis aimed to investigate the associations between IL-13 SNP rs20541 with distinct groups of chronic inflammatory diseases. Eligible studies were selected from seven databases including PubMed, EBSCO Host (all databases), Medline, CINAHL Plus, Scopus, SNPedia and GWAS. In total, 45 case-control studies with 16,045 cases and 23,312 controls were categorised into four major groups: atopic, cardiopulmonary and autoimmune diseases as well as cancer and tumour. While no consistent associations emerged for asthma or overall atopic and cardiopulmonary groups, protective associations for psoriasis and glioma were observed across multiple genetic contrasts. The A allele of rs20541 was significantly associated with higher risk of chronic obstructive pulmonary diseases (COPDs) [1.17 (1.03-1.32)] but reduced risk of cardiovascular diseases (CVDs) [0.87 (0.75-1.00)], psoriasis [allele model: 0.71 (0.65-0.77); dominant model: 0.69 (0.62-0.76)], overall cancer [allele model: 0.82 (0.66-0.98); dominant model: 0.82 (0.67-0.98) and glioma [allele model: 0.82 (0.68-0.95); dominant model: 0.72 (0.57-0.87)]. In subgroup analysis and meta-regression, sources of between-study heterogeneity were associated with ethnicity, age, gender and sample size in respective disease groups (pz < 0.05, pres > 0.05). Overall, this meta-analysis demonstrates that IL-13 rs20541 is a key immunogenetic variant exerting context-dependent effects, either via direct lgE-dependent or indirect regulatory effects across chronic inflammatory diseases. These mechanistic differences help explain why rs20541 confers susceptibility in some diseases while providing protection in others, reflecting the pleiotropic and tissue-specific functions of IL-13. Future research should integrate transcriptional studies and eQTL analyses of rs20541 to clarify its downstream impact on inflammation-specific genes, ultimately informing cytokine-targeted therapies to more precisely manage and prevent chronic inflammatory disease.

To assess the available evidence on the expression of hallmarks of cancer and oral leukoplakia (OL) malignant transformation probability, with the goal of identifying the earliest oncogenic molecular events participating in oral cancer carcinogenesis.