This study aimed to investigate demographic and clinical factors associated with use of complementary and alternative medicine (CAM) and to compare CAM utilization patterns, including self-purchase behaviors and patient-reported satisfaction, between Korean women with female-specific and non-female-specific cancers. This exploratory subgroup analysis was conducted among female participants in a cross-sectional survey of Korean adults with solid tumors. Clinical and epidemiological characteristics were compared between CAM users and non-users. CAM use patterns-including reasons for use, initiation timing, duration, cost, self-purchase behavior, patient-reported satisfaction, and adverse effects-were compared between female-specific and non-female-specific cancers. Of the 150 female patients with solid tumors, 93 (62.0%) reported their use of CAM. The prevalence of CAM use was similar between patients with female-specific cancers (64.5%, 69/107) and those with non-female-specific cancers (55.8%, 24/43), with no statistically significant difference observed. However, patients with female-specific cancers were significantly more likely to self-purchase CAM than those with non-female-specific cancers (85.5% vs. 62.5%, P = 0.016). In addition, a higher proportion of patients with female-specific cancers reported high satisfaction with CAM use compared with patients with non-female-specific cancers (79.7% vs. 41.7%, P < 0.001). In multivariable analysis restricted to patients with female-specific cancers, high patient-reported satisfaction was independently associated with CAM use (OR, 5.96; 95% CI, 1.48-23.93; P = 0.012). Among patients with female-specific cancers, high patient-reported satisfaction was independently associated with CAM use, highlighting the psychosocial relevance of patient-initiated CAM behaviors beyond overall use prevalence.

The Adenomatous Polyposis Coli gene (APC) is a key tumor suppressor in colorectal cancer (CRC). While germline mutations in its Mutation Cluster Region (MCR) are implicated in familial CRC, the prognostic impact of specific mutation types within distinct populations remains poorly characterized. This study sequenced the APC-MCR in 96 Iranian familial CRC patients, 6 disease controls (gastritis/celiac), and 10 healthy controls. Variants were classified per ACMG guidelines. Patients were stratified into four genetic categories: Wild-Type (WT), Variant of Uncertain Significance (VUS) only, Truncating pathogenic/likely pathogenic (P/LP), and Missense P/LP. Associations with clinicopathological features were assessed using Chi-square, Fisher's exact tests, and independent t-tests. OR with 95% CI were calculated. Pathogenic mutations were identified in 39.6% (38/96) of patients and 0% of controls (P < 0.0001). A significant association existed between the mutation type and the tumor stage (P = 0.001). Advanced-stage (III/IV) disease was present in 22.2% of WT, 31.8% of VUS only, 61.3% of Truncating P/LP, and 71.4% of Missense P/LP patients. Truncating P/LP mutations conferred significantly higher odds of advanced-stage disease (OR = 5.54, 95% CI: 1.98-15.51, P = 0.001) versus WT. No significant association was found with age, sex, grade, or tumor location. The type of APC mutation, specifically truncating variants, is a powerful biomarker for advanced tumor stage in Iranian familial CRC, underscoring the critical need for genotype-driven risk stratification.

Nearly thirty years ago, T-lymphokine-activated killer (T-LAK) cell-originated protein kinase (TOPK), also known as PDZ-binding kinase, was first identified as a serine/threonine kinase with limited known functions. Over time, this molecule has gradually revealed a far more striking role in cancer biology. Initially detected mainly in proliferative tissues such as testes and activated lymphocytes, TOPK is now recognized as a protein that becomes aberrantly overexpressed in many human cancers, where it is consistently linked to aggressive tumor behavior and poor clinical outcomes. Research accumulated over the past three decades shows that TOPK governs a wide range of oncogenic processes, including proliferation, metastasis, cell cycle progression, DNA damage repair, resistance to apoptosis, autophagy regulation, inflammatory signaling, and immune modulation. Mechanistic studies reveal that TOPK communicates extensively with major signaling molecules such as extracellular signal-regulated kinase (ERK), β-catenin, the tyrosine-protein kinase Src/glycogen synthase kinase 3 beta/signal transducer and activator of transcription 3 (Src/GSK3β/STAT3), phosphoinositide 3-kinase/phosphatase and tensin homolog/protein kinase B (PI3K/PTEN/AKT), TGF-β/small mother against decapentaplegic (SMAD), NF-κB/Snail, and HIF-1α. Positive feedback interactions with ERK2, Src and other oncogenic regulators further intensify its tumor-promoting activity. TOPK also contributes to resistance to anti-cancer agents such as doxorubicin, gefitinib, oxaliplatin, and sorafenib through its influence on activator protein-1, phosphatase and tensin homolog, sirtuin 1 (SIRT1), p53, and additional downstream effectors. In the tumor immune microenvironment, TOPK enhances programmed cell death ligand 1 (PD-L1) expression and reduces CD8+ T-cell infiltration, promoting immune evasion. Although numerous natural and synthetic inhibitors of TOPK have been identified, their clinical application remains at an early stage. Overall, current evidence presents TOPK as a promising biomarker and therapeutic target with broad relevance across diverse cancer types.

Hepatocellular carcinoma (HCC) continues to impose a substantial global health burden, with the incidence and the mortality remaining closely aligned despite major advances in diagnostics and therapeutics. Over the past three decades, screening and treatment technologies have evolved from single-marker surveillance to risk-stratified, multimodal assessment, and from standalone local therapies to integrated radiologic and immunologic strategies. However, these innovations have not translated into proportional population-level benefits, as early detection rates remain persistently low across many regions. This review provides a comprehensive synthesis of the three-decade evolution in HCC surveillance and treatment, highlighting how biomarker innovation, imaging standardization, and emerging systemic therapies have reshaped clinical practice, while identifying key barriers that continue to limit real-world impact, including metabolic disease-related imaging challenges, inconsistent long-term surveillance adherence, and pronounced disparities in healthcare access. By integrating epidemiologic trends, clinical evidence, and technological advances, this review emphasizes a central principle: meaningful improvement in HCC outcomes depends less on the availability of sophisticated tools than on the timely identification and management of patients within the curative window. The insights presented aim to develop future precision-based, equitable, and multimodal strategies for HCC prevention and control.

Withaferin A (WA) is a small molecule present in Ashwagandha plant that prevents breast cancer progression in mice and rats. The mechanisms underlying breast cancer prevention by WA are not fully understood. Herein, we report effects of WA treatment on an immune landscape in C3(1)-TAg transgenic mice, which develop basal-like breast cancer. Oral administration of 12 mg/kg body weight of WA decreased the wet tumor weight by about 43%. Weight loss or any other adverse effects (e.g., impaired movement, hunched back, ruffled fur, etc.) were not observed. Tumors and splenocytes from WA-treated mice exhibited the increased proportion of CD4+ helper T cells when compared to control mice. The proportion of CD8α+ T cells and natural killer cells was not affected by WA treatment in either mammary tumor or splenocytes. Similarly, the proportions of lymphoid dendritic cells, myeloid dendritic cells, M2 macrophages, regulatory T cells, and myeloid-derived suppressor cells were comparable in mammary tumors and splenocytes of both control and WA-treated mice. Unlike the C3(1)-TAg mouse model, WA administration failed to increase the proportion of CD4+ T cells in mammary tumors of rats. The present study indicates that even though WA treatment increases the proportion of helper T cells in mammary tumors and spleen, attenuation of immune evasion may have a minimal role in its breast cancer prevention at least in rodent models of basal-like [C3(1)-TAg model] and luminal-type (rat model) breast cancer.

This study aimed to develop a non-invasive diagnostic model for gastric cancer (GC) by combining serum immune-inflammatory-nutrition indicators with traditional tumor markers to improve early diagnosis efficiency. Our retrospective analysis included 3,464 participants, comprising 833 GC patients and 2,631 chronic gastritis controls, recruited between January 2018 and July 2025. The dataset was split into training and validation sets at a 7 : 3 ratio, and least absolute shrinkage and selection operator (LASSO) regression was utilized to screen for characteristic variables. Of the candidate variables, seven key features-age, sex, body mass index, carcinoembryonic antigen, carbohydrate antigen 199, systemic immune-inflammation index/albumin (SII/ALB), and prognostic nutritional index (PNI)-were identified and integrated into a multivariate logistic regression model. The analysis indicated that advanced age (OR, 1.23; 95% CI, 1.20-1.26) and elevated SII/ALB ratios (OR, 2.63; 95% CI, 1.93-3.58) were significant risk factors, whereas higher PNI values (OR, 0.12; 95% CI, 0.09-0.17) were associated with a reduced risk. The model demonstrated excellent diagnostic performance, achieving an area under the curve of 0.93 (95% CI, 0.91-0.94) in the training set and 0.92 (95% CI, 0.90-0.94) in the validation set. Subgroup analysis further revealed that the seven key markers were significantly associated with Lauren classification, histological grade, and tumor-node-metastasis stage, progressively worsening with disease advancement. Our study underscores the high accuracy and clinical utility of this multimodal model, providing a reliable, non-invasive tool for the early screening and personalized pretreatment assessment of gastric cancer.

Colorectal cancer (CRC) is strongly associated with gut microbial dysbiosis, characterized by increases in Escherichia coli, Enterococcus faecalis, and Bacteroides spp., and reduction in short chain fatty acid producing taxa such as Akkermansia muciniphila, Faecalibacterium prausnitzii, and Roseburia.These shifts parallel metabolomic disturbances, including decreased butyrate and immune dysregulation.Several microbial and metabolic markers such as Akkermansia, Faecalibacterium, butyrate, tryptophan metabolites, and sarcosine have demonstrated strong diagnostic performance, with area under the receiver operating characteristic curve (AUC) values commonly ranging from 0.80 to 0.93 in CRC prediction models.This review integrates current evidence for microbes and metabolite interactions that drive CRC progression and summarizes biomarker studies employing high AUC microbial and metabolite signatures for early detection and patient stratification.We further highlight phytochemicals, including resveratrol, curcumin, and quercetin which mitigate CRC by modulating cyclooxygenase-2 activity, macrophage polarization, inflammatory cytokine signaling, metabolic pathways, and the restoration of beneficial gut microbial communities.These insights support the advancement of microbiome targeted and metabolite informed approaches for CRC risk assessment, diagnosis, and therapeutic development.

Ginseng has been widely consumed for its purported chemoprotective effects against various disease including cancer. However, the association between ginseng tea consumption and liver cancer (LC) risk remains unclear, particularly among individuals with underlying liver disease. We conducted a prospective cohort study using data from the Korean Multi-Center Cancer Cohort (KMCC), including 5,926 participants without cancer history who completed a baseline questionnaire on ginseng tea consumption between 2000 and 2005. Participants were followed for up to 14 years for incident LC through linkage with the national cancer registry. Multivariable adjusted Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% CIs. Stratified analyses were performed by liver disease status. During a median follow-up of 10.9 years, 61 incident LC cases were identified. Frequent ginseng tea consumption (≥ 2 cups/week) was significantly associated with an increased LC risk (adjusted HR = 2.15; 95% CI: 1.08-4.25), with the highest risk observed among daily consumers (HR = 3.35; 95% CI: 1.40-8.01). The association was notably stronger in individuals with pre-existing liver disease (HR = 3.57; 95% CI: 1.40-9.07; P for trend = 0.022), whereas no significant association was observed in those without liver disease. In conclusion, frequent consumption of ginseng tea among individuals with underlying liver disease was associated with the potentially increased risk of liver cancer.

This study aimed to determine the association between trajectories of obesity status and prediabetes reversion to normoglycemia or progression to diabetes. The study included 14,452 participants from the National Health Insurance Service-National Health Screening (NHIS-HEALS) cohort who continuously had prediabetes glycemic status during the index period (2002-2008), defined by their fasting plasma glucose. The exposure of the study was the trajectories of obesity (defined by body mass index ≥ 25 kg/m2) generated using latent class growth analysis. The outcomes were reversion to normoglycemia or progression to diabetes, whichever occurred first during the follow-up period (2009-2016). The association between trajectories and changes in prediabetes status were examined using cause-specific hazard regression by obtaining the hazard ratio (HR) with a 95% CI. We identified three distinct trajectories which were “Stable obese”, “Stable non-obese” and “Obese to non-obese”. After a median follow-up of 2 years, 51.99% of participants had their glycemic status back to normoglycemia and 32.17% developed diabetes. Compared with participants in the “Stable obese” group, those in “Stable non-obese” and “Obese to non-obese” groups were more likely to have reversion to normoglycemia (HR with a 95% CI = 1.30 [1.23-1.37] and 1.15 [1.07-1.24], respectively) and lower risk of developing diabetes (0.78 [0.73-0.84] and 0.90 [0.82-0.98], respectively). The findings suggest that maintaining or achieving a non-obese status is linked to higher reversion to normoglycemia as well as lower risks of developing diabetes.

This study aimed to examine differences in the association between reproductive factors and breast cancer (BC) risk across ethnic groups, particularly Asians and non-Asians, and to explore temporal trends through meta-analysis. The study focused on epidemiologic research published up to August 31, 2022, examining reproductive factors related to BC risk and family history. All effect sizes were calculated using a random-effect model. The protective effect of the higher number of childbirths against BC was stronger in Asians than in Europeans or Americans (childbirths ≥ 2 vs. 1; Asians, relative risk [RR]: 0.66, 95% CI: 0.59-0.74; Europeans, RR: 0.89, 95% CI: 0.86-0.92; Americans, RR: 0.91, 95% CI: 0.87-0.96). Similarly, the effect of high parity was more pronounced in Asians than in Americans and Europeans (Asians, RR: 0.72, 95% CI: 0.58-0.89; Europeans, RR: 0.81, 95% CI: 0.74-0.88; Americans, RR: 0.84, 95% CI: 0.76-0.92). In contrast, no significant differences among populations were found in BC risks associated with combined hormone replacement therapy use. While the association between family history and BC risk appeared to differ by ethnicity, no temporal change was observed (< 2010, RR: 1.58, 95% CI: 1.40-1.78; ≥ 2010, RR: 1.57, 95% CI: 1.46-1.67). These results suggest that some reproductive factors associated with BC differ across ethnicities and time trends, perhaps due to the prevalence of reproductive factors and the baseline hazard of BC.