搜索结果：Integrative cancer therapies

Aberrant regulation of autophagy and persistent activation of the phosphoinositide 3-kinase (PI3K)/mechanistic target of rapamycin (mTOR) signaling axis are recognized hallmarks of cancer progression, therapeutic resistance, and disease relapse. Coumarins, a chemically diverse class of natural and synthetic benzopyranone derivatives, have recently emerged as promising modulators of both autophagy and PI3K/mTOR signaling, positioning them as attractive candidates for next-generation anticancer strategies. This review critically examines current evidence on the ability of coumarin derivatives to regulate autophagy and PI3K/mTOR signaling in cancer, with emphasis on their mechanistic intersections, therapeutic implications, and translational potential. A structured and integrative analysis of preclinical studies was conducted using major scientific databases, including PubMed, Scopus, and Web of Science. Relevant articles were identified using combinations of keywords such as "coumarins", "autophagy", "PI3K/mTOR", and "cancer". Only peer-reviewed studies written in English and reporting data from cellular or animal cancer models were included. Mechanistic evidence related to autophagy induction or inhibition, modulation of the PI3K/mTOR pathway, pharmacokinetic properties, safety considerations, and combination therapy strategies was systematically evaluated. Accumulating evidence demonstrates that coumarins can either induce or inhibit autophagic flux in a context-dependent manner, often through direct or indirect modulation of PI3K/mTOR signaling. These dual actions influence cancer cell survival, apoptosis, senescence, and sensitivity to chemotherapy. Several coumarins exhibit multitarget activity, addressing therapy resistance while maintaining favorable safety profiles. Emerging data further support their use in rational combination strategies and patient-stratified therapeutic approaches. Coumarins represent versatile molecular scaffolds capable of fine-tuning autophagy and PI3K/mTOR signaling in cancer. A deeper mechanistic understanding, alongside optimization of pharmacokinetics and patient stratification, will be essential for translating coumarin-based modulators into clinically effective anticancer therapies.

Colorectal cancer (CRC) progression and metastasis are primarily driven by dynamic changes within the tumor microenvironment (TME). Cancer-associated fibroblasts (CAFs) exhibit significant heterogeneity within the TME and play a crucial role in regulating ferroptosis. Therefore, identifying novel ferroptosis-related biomarkers associated with CAFs could contribute to the development of personalized therapeutic strategies for cancer. This study integrates single-cell sequencing data from 64 CRC samples and uses hierarchical clustering to identify cancer-associated fibroblast (CAF) subpopulations. We then combined spatial transcriptomics, hdWGCNA, CellChat, and Monocle analyses to characterize CAF subgroups. Single-cell and spatial transcriptomic data were integrated with Seurat to build a comprehensive spatial atlas. Multiplex immunohistochemical staining was used to analyze the spatial relationships of key genes with CAFs. Functional validation of these genes was performed with molecular docking, qPCR, Western blot, and both cellular and animal experiments. Single-cell data analysis identified five distinct CAF subpopulations, among which inflammatory cancer-associated fibroblasts (iCAFs) were significantly associated with the ferroptosis pathway and closely correlated with the proliferation and metastasis of malignant epithelial cells (p = 0.87). WGCNA revealed that the iCAFs-M10 module exhibited the strongest correlation with the expression of ferroptosis-related genes (cor = 0.6796). Further investigation identified ATG13 as a key hub gene, highly expressed in tumor tissues and significantly associated with poor patient prognosis. Spatial transcriptomics and multiplex immunohistochemistry (mIHC) results demonstrated that ATG13 was highly expressed in CAFs and co-localized with CAFs markers, such as α-SMA and Vimentin. In vitro and in vivo functional assays confirmed that ATG13 knockdown effectively inhibited the proliferation, migration, and invasion of colorectal cancer cells. Additionally, ferroptosis was induced upon ATG13 silencing, as evidenced by increased levels of GPX4, SLC7A11, ACSL4, MDA, Fe2⁺, GSH, and lipid peroxidation. In conclusion, this study reveals that ATG13, highly expressed in iCAFs, is associated with ferroptosis suppression in CRC, suggesting a potential CAF-tumor cell crosstalk axis that warrants further mechanistic investigation, thereby promoting the malignant progression of colorectal cancer. These findings provide potential targets for therapeutic strategies aimed at targeting the CAFs-ferroptosis axis. This study identifies the iCAFs subpopulation as playing a key role in regulating ferroptosis in CRC, with ATG13 acting as a negative regulator of ferroptosis that promotes tumor progression. These findings provide new insights and potential targets for understanding the mechanisms of ferroptosis in CRC and for the development of targeted therapies.

Hematological malignancies are the fourth most common cancer type, with lymphoma as one of the most common hematological malignancies in this group. Radiation therapy plays a critical role in the treatment of hematological malignancies, particularly lymphoma, plasmacytoma, and leukemia. Radiation toxicities include side effects such as pain, dermatitis, mucositis, xerostomia, nausea, fatigue, anxiety, and pneumonitis. With emerging therapies in hematology, including chimeric antigen receptor T-cell therapy, bispecific antibodies, and transplant, patients are presented with unique side effects that may impact their ability to tolerate radiation. Integrative therapies, such as mindfulness-based interventions and yoga, have shown to have strong evidence in managing radiation-related fatigue, anxiety, and depression. Acupuncture has shown to be efficacious for radiation-related pain, xerostomia, and anxiety. As survival has continued to increase over the years, survivorship has become crucial. For patients who have undergone radiation, survivorship concerns such as increased cardiovascular risk, psycho-social concerns, secondary malignancy risk, and others may uniquely be addressed with integrative approaches. This review aims to give an overview of the current evidence for integrative therapies in managing toxicities secondary to radiation and improving the survivorship of patients who have received radiation therapy.

Prostate cancer is most common malignancy among men in the United States. As men are now living longer with prostate cancer due to advances in treatment, there exists a growing need to manage the long-term physical and psychological sequelae of this disease, which range from genitourinary dysfunction to cardiometabolic and psychosocial consequences. Over half of men with prostate cancer report unmet needs in symptom management. Integrative oncology, a patient-centered, evidence-informed field combining lifestyle, natural product, and mind-body interventions with conventional treatments, offers a promising approach to prostate cancer symptom management. This review summarizes the current landscape of integrative oncology research in prostate cancer and discusses the clinical implications.

Breast cancer remains one of the most commonly diagnosed cancers worldwide. Cancer treatments often cause a variety of physical and psychological symptoms that can last beyond the end of therapy. This article reviews the current evidence on integrative medicine approaches, including diet, exercise, and other modalities studied for managing symptoms often reported by breast cancer survivors. For each symptom, we highlight integrative medicine interventions with the strongest available evidence, including mind-body approaches (eg, mindfulness-based interventions, yoga, and hypnosis), acupuncture, massage therapy, and selected dietary supplements. This symptom-focused framework aims to help clinicians identify integrative interventions that, based on the existing evidence, may be suitable for addressing individual patient concerns.

The Society for Integrative Oncology (SIO) and the American Society of Clinical Oncology (ASCO) collaboratively developed evidence-based guidelines supporting selected integrative therapies for common cancer-related symptoms, specifically pain, cancer-related fatigue, depression, and anxiety. Despite growing evidence supporting their use, implementation in routine oncology practice remains limited. In this review, we summarize the SIO-ASCO guidelines and examine barriers to their implementation in clinical settings. We then explore strategies to improve guideline adherence using a "carrot and stick" framework that combines incentive-based approaches with accountability mechanisms. Finally, we present practical strategies to integrate the SIO-ASCO guidelines into routine clinical care. We conclude by discussing future directions for implementing integrative oncology in real-world clinical settings. These approaches aim to overcome the barriers associated with guideline adoption in clinical practice, supporting the widespread use of evidence-based integrative therapies across academic and community settings, improving patient symptom management and quality of life, and ensuring equitable access to integrative therapies for all patients. Together, these efforts will help to establish integrative oncology as a standard part of routine cancer care.

Colorectal cancer (CRC) remains a leading cause of cancer-related morbidity and mortality, with substantial heterogeneity that is not fully explained by genetic alterations alone. Emerging evidence positions metabolic reprogramming as a central driver of tumor behavior, integrating glycolysis, mitochondrial function, lipid and amino acid metabolism, and autophagy into coordinated networks that extend beyond cancer cells to the tumor microenvironment. Tumor-immune metabolic competition and metabolite-mediated signaling shape immune responses, often promoting immunosuppression and resistance to immunotherapy, particularly in microsatellite-stable (MSS) CRC. Systemic factors, including obesity, insulin resistance, and the diet-microbiota axis, further modulate tumor metabolism and immune function, reinforcing disease progression. Metabolic biomarkers reflecting these multi-level interactions, spanning tumor-intrinsic pathways, immune contexture, and host metabolism, offer promising opportunities for improved patient stratification and therapeutic targeting, although clinical validation remains limited. Current treatments, including chemotherapy, targeted agents, and immune checkpoint inhibitors, are effective in selected subgroups but are constrained by resistance mechanisms. In this review, we propose an integrative immunometabolic framework in which tumor, immune, and systemic metabolic processes co-evolve, defining CRC progression and treatment response. Targeting this interconnected network through combinatorial and metabolism-oriented strategies may enable precision therapies, particularly for immunotherapy-resistant MSS CRC.

Patients with early breast cancer frequently consider complementary therapies, yet structured, ethical discussions remain uncommon. Breast cancer is a particularly relevant context for such discussions because care pathways are prolonged, multimodal, and often associated with uncertainty, treatment-related symptoms, and high informational burden. We developed and pilot tested Kit-CAT, a serious-game-supported consultation to scaffold evidence-based, patient-centered conversations on complementary therapies. After developing Kit-CAT through an iterative process including clinicians, researchers, and patients, we conducted a monocentric before-and-after pilot (6-month periods). Women with non-metastatic breast cancer were included at diagnosis; the intervention added a 90-minute primary-care consultation. Feasibility was assessed across recruitment, delivery, and acceptability. No formal a priori threshold for feasibility success was specified. Outcomes included feasibility indicators, health literacy (HLQ), attitudes to CAT (CHBQ), CAT use, and satisfaction at baseline and 6 months. Of the 44 initially included participants, 41 were retained in the baseline analysis set and 38 provided at least one 6-month follow-up data point (25 in the control group and 13 in the intervention group). Recruitment to the intervention proved challenging: during the intervention phase, 49 eligible patients declined participation. Recruitment feasibility was therefore limited under the tested implementation conditions. Across several HLQ subscales, small descriptive trends in a favourable direction were observed in the intervention group, contrasting with modest declines in the control group; attitudes toward CAT were highly positive at baseline and remained stable. Satisfaction with the care pathway was high in both groups, with the intervention group numerically higher (92%vs 78% satisfied/very satisfied). No serious adverse events were reported; recorded adverse events were not considered related to Kit-CAT. Kit-CAT was deliverable and acceptable among consenting participants, but recruitment feasibility was limited, mainly because of early timing after diagnosis, off-site delivery, and scheduling burden. Descriptive health-literacy trends should be interpreted as exploratory. Future multicentre studies should first optimize implementation format before assessing effectiveness in an adequately powered design.

Ribociclib was recently approved for the treatment of hormone receptor-positive/human epidermal growth factor receptor 2-negative early breast cancer (EBC) at the starting dose of 400 mg orally once daily (3 weeks on/1 week off), following previous approval in hormone receptor-positive/human epidermal growth factor receptor 2-negative advanced breast cancer at the starting dose of 600 mg orally once daily (3 weeks on/1 week off). This study aims to characterize ribociclib pharmacokinetics and its relationship with QT interval corrected according to Fridericia's formula (QTcF) in patients with EBC and justify the dose in EBC. Data from several studies, including the pivotal phase III trial in patients with EBC and phase I-III trials in patients with advanced breast cancer and advanced cancer were analyzed. Ribociclib pharmacokinetics was characterized by non-compartmental or population pharmacokinetic analyses. The exposure-QTcF relationship was assessed by linear mixed-effects modeling. Neutropenia and QTcF data were compared by dose and population. At the 400-mg dose, ribociclib steady-state clearance was ~ 20% higher in patients with EBC than patients with advanced cancer, suggesting differences in pharmacokinetics between populations. Steady-state mean area under the plasma concentration-time curve and maximum (peak) plasma drug concentration were ~ 50% lower and steady-state clearance was ~ 50% higher in patients with EBC receiving 400 mg compared with patients with advanced cancer and advanced breast cancer receiving 600 mg, attributed to differences in both dose and population. The pharmacokinetic-QTcF analysis showed that the patient population was a significant covariate in QTcF response. The model-estimated mean change from baseline in QTcF at steady-state maximum (peak) plasma drug concentration was substantially lower in patients with EBC receiving 400 mg (10.0 ms) versus in patients with advanced breast cancer receiving 600 mg (20.7-23.7 ms), likely due to the dose and pharmacokinetic exposure effect and the population effect. Patients with EBC receiving 400 mg experienced lower rates and severity of both neutropenia and QTcF prolongation than patients with advanced breast cancer receiving 600 mg. This integrative analysis characterized the ribociclib pharmacokinetic and exposure-QTcF relationship, revealed the population effect on both pharmacokinetic and QTcF response, and justified the 400-mg dose in EBC. This work illustrates the utility and impact of quantitative pharmacology in justifying different doses across different patient populations for oncology therapies. NATALEE (NCT03701334, 2018-09-21); AMALEE (NCT03822468, 2019-01-28); MONALEESA-2 (NCT01958021, 2013-10-04); MONALEESA-3 (NCT02422615, 2015-04-01); MONALEESA-7 (NCT02278120, 2014-10-22); X1101 (NCT01898845, 2013-07-01); X2101 (NCT01237236, 2010-11-05); X2107 (NCT01872260, 2013-05-30).

Cisplatin is a widely used chemotherapy drug, but resistance mechanisms, including the role of SLFN11, pose significant challenges in colorectal cancer (CRC) treatment, with only 15-20% of patients showing objective responses. We conducted differential gene expression analysis using datasets GSE181094, GSE179896, and GSE231559, alongside TCGA-COAD and TCGA-READ datasets. DEGs were identified using DESeq2, Limma, and edgeR, followed by protein-protein interaction network analysis with STRING, and functional enrichment analysis via KEGG, GO, and GSEA. Mendelian randomization (MR) analysis was performed using the TwoSampleMR package with robust instrumental variable validation, and single-cell RNA sequencing data was analyzed using Seurat and SingleR to examine cell-type specific expression patterns. Our analysis identified several DEGs, including FOXL1 and GPC4, associated with cisplatin sensitivity in SLFN11 knockout cell lines. MR analysis revealed SLC46A3 as a significant gene related to CRC, showing a causal relationship (β=-0.2935, p = 0.0308). Single-cell RNA sequencing demonstrated high expression of SLFN11 in granulocyte-monocyte progenitor and common myeloid progenitor cells in adjacent normal tissues, with reduced expression in cancerous tissues. These findings highlight the significant impact of SLFN11 on gene expression and its potential as a biomarker for cisplatin sensitivity. SLFN11 plays a critical role in modulating cisplatin sensitivity in CRC, with implications for personalized cancer therapy. These findings establish SLFN11 as a potential biomarker for personalizing cisplatin-based therapies in CRC patients, potentially improving response rates and clinical outcomes.

With improving survival in breast cancer, supportive care has increasingly focused on long-term, treatment-related symptom clusters (e.g., pain, fatigue, vasomotor symptoms, insomnia, and anxiety) that impair quality of life and adherence. Within integrative oncology, non-pharmacological Traditional Chinese Medicine (TCM) therapies-especially acupuncture and mind-body exercises (Tai Chi/Qigong)-have attracted growing attention, yet the field's global structure, collaboration patterns, and evolving research priorities have not been comprehensively mapped. A bibliometric visualization study was conducted for English-language articles and reviews published from 2000 to 2025. Records were retrieved on January 8, 2026, from Web of Science Core Collection (WoSCC) and Scopus and deduplicated to form Dataset A for productivity, collaboration, and keyword analyses; Dataset B (WoSCC only) was used for co-citation analyses to ensure consistent cited-reference indexing. PubMed was used as an external source to validate annual publication trends. Analyses were performed using VOSviewer and R-bibliometrix (Biblioshiny). A total of 1,761 documents from 590 sources were included, showing rapid growth with acceleration after the mid-2010s (10 papers in 2000 and 171 in 2025), and trends were consistent with PubMed (Spearman's ρ = 0.982, p = 9.59×10-19 ). The field displayed a US-China bipolar pattern, with the United States leading in output, citations, and collaboration, and China showing fast recent growth but limited cross-regional institutional linkage. Integrative Cancer Therapies and Supportive Care in Cancer were the main outlets, and the knowledge base centered on RCTs and guidelines, particularly for acupuncture. Keywords revealed a shift from early treatment side-effect management to broader survivorship outcomes, and most recently toward evidence synthesis/implementation and targeted concerns such as sleep disturbance/insomnia, with emerging interest in mechanisms and subtype-related topics. Research on non-pharmacological TCM therapies for breast cancer has grown rapidly, shifting from "CAM" toward integrative supportive care. Acupuncture and mind-body exercises remain central, and emerging priorities include standardization, implementation, and mechanism-/subtype-informed approaches. Stronger international collaboration and harmonized outcomes are needed to support scalable clinical integration.

Triple-negative breast cancer (TNBC) is a major cause of mortality worldwide. Chinese herbal medicine (CHM) is often used as adjunctive therapy, but its long-term impact on TNBC remains unclear. This study analyzed a multi-institutional cohort from the Chang Gung Research Database, investigating long-term outcomes of integrative CHM use in TNBC patients newly diagnosed between January 1, 2011, and December 31, 2021. Patients were followed for up to 10 years or until death. Overall survival rate (OS) and disease-specific survival rates were assessed using Kaplan-Meier estimation with overlap weighting and landmark analysis to reduce bias. Core CHMs were identified through network pharmacology analysis on prescriptions made for TNBC patients. The analysis included 2174 TNBC patients, with 464 using CHM. CHM use was associated with a significantly higher 10-year OS compared to non-users (77.7% vs 70.2%, P = .007). In stages 1 to 3, the OS among CHM users was 6.6% higher (80.7% vs 74.1%, P = .018). After adjusting for demographic factors, CHM use reduced the risk of all-cause mortality (adjusted hazard ratio [aHR]: 0.71, P = .044). Lower disease-specific survival rates were observed among CHM users. Core CHMs, such as Hedyotis diffusa Willd., may have potential anti-cancer effects, while combinations like Jia-Wei-Xiao-Yao-San, Scutellaria barbata D. Don. and Suan-Zao-Ren-Tang may have a complementary role to standard treatments for TNBC. Use of CHM may improve 10-year OS in TNBC patients, and core CHMs provided crucial references for further studies.

Background: Sphingolipids are essential structural and signaling lipids that support membrane integrity and govern cell fate decisions. While the consequences of chronic sphingolipid inhibition have been extensively explored, the immediate cellular responses to acute suppression of sphingolipid synthesis remain poorly defined. Methods: We analyzed subcellular proteomic changes following an acute reduction in sphingolipid levels induced by myriocin, an inhibitor of de novo sphingolipid synthesis. We then evaluated the cytotoxicity of co-treatment with myriocin and inhibitors of the altered pathways in cancer cells. Results: We found that de novo sphingolipid synthesis is sensitive to myriocin, an inhibitor of serine palmitoyltransferase (SPT), and can be efficiently inhibited within 4 h of treatment. Cells respond to reduced sphingolipid levels by rapidly remodeling their proteome. Mass spectrometry analysis revealed changes in the abundance of hundreds of proteins across the membrane, cytosolic, and nuclear fractions. Gene set enrichment analysis revealed alterations in the proteome across several pathways involved in protein and lipid homeostasis and stress responses, including upregulation of cholesterol homeostasis and lysosome. Co-treatment with myriocin and cholesterol synthesis or lysosomal function inhibitors synergistically reduced cancer cell viability by promoting apoptosis rather than other forms of programmed cell death. Conclusions: Together, our work provides insights into how cells rapidly rewire the abundance of certain protein classes in response to reduced sphingolipid levels and identifies signaling and metabolic pathways that can be exploited for therapeutic intervention.

Radiation oncology has long paired precision with compassion, technical excellence with daily human connection. Integrative oncology extends that legacy, advancing a shift from reactive symptom management to proactive, coordinated care; from fragmented referrals to integrated pathways; and from isolated pilot efforts to implementation-ready science. In this volume of Seminars in Radiation Oncology international experts reflect on the collective toolbelt of integrative oncology, the maturation of the science, and the exciting opportunity before us in radiation oncology. By integrating complementary approaches alongside conventional treatment, integrative oncology seeks to improve symptom control, functional outcomes, treatment adherence, and quality of life, with emerging evidence supporting benefits in disease-free and overall survival in select settings. Integrative approaches include nutrition and the microbiome, physical activity, mind-body and nature-based interventions, acupuncture and East Asian medicine, Ayurveda, massage and manual therapy, yoga, tai chi, qi gong, music therapy, stress management, sleep medicine, herbs and supplements, psycho-oncology, and supportive care. Across this collection, three central themes emerge: (a) patient-centered care targeting symptoms that matter most to patients and caregivers; (b) data-driven practice grounded in clinical trials, guidelines, and mechanistic science; and (c) operational compatibility with radiation oncology workflows. We hope readers leave with two clear outcomes: practical integrative strategies applicable to patients beginning radiation therapy tomorrow, and a sharper understanding of the research and systems infrastructure required to make integrative oncology a standard and equitable component of care. The work presented here signals a structural evolution -aligning tumor control and survival with symptom science, biologic insight, and whole-person care. In doing so, radiation oncology is uniquely positioned not merely to participate in, but to lead the redefinition of integrative cancer care for the decades ahead.

Cancer progression is closely associated with dysregulation of apoptosis, enabling malignant cells to evade programmed cell death and develop resistance to therapy. Among the key regulators of this process, the tumor suppressor protein p53 and the Bcl-2 family of proteins play central and interconnected roles in controlling cell survival and mitochondrial integrity. In recent years, naturally occurring flavonoids have attracted considerable attention as potential modulators of these pathways due to their diverse biological activities and relatively low toxicity. This review provides a focused and integrative overview of how different subclasses of flavonoids modulate the p53-Bcl-2 signaling axis to regulate apoptosis in cancer cells. Particular emphasis is placed on the mechanistic interplay between p53 stabilization, transcriptional regulation of apoptotic targets, mitochondrial outer membrane permeabilization, and caspase activation. In contrast to previous general reviews on flavonoids and cancer, this work provides an integrated overview of evidence across multiple flavonoid subclasses and experimental cancer models, highlighting both shared and pathway-specific apoptotic responses. Experimental findings from in vitro and in vivo studies are discussed, including the effects of quercetin, kaempferol, myricetin, epigallocatechin gallate, and related compounds on cell-cycle arrest, oxidative stress, mitochondrial dysfunction, and intrinsic apoptotic signaling. Furthermore, the review examines the relationship between flavonoid chemical structure and biological activity, with particular attention to bioavailability, metabolic transformation, and strategies aimed at improving therapeutic efficacy, including structural modification and nanocarrier-based delivery systems. Despite promising preclinical findings, significant translational challenges remain, including poor pharmacokinetic properties, variability among experimental models, and limited clinical validation. Overall, flavonoids represent a promising class of bioactive compounds capable of targeting apoptosis through modulation of the p53-Bcl-2 network, and a deeper mechanistic understanding of their activity may support the development of novel targeted and combination anticancer therapies.

Neuroendocrine prostate cancer (NEPC) is an aggressive, treatment-refractory state that often emerges under androgen-receptor pathway inhibition. We hypothesized that dysregulated ubiquitination underpins NEPC lineage plasticity and that integrating bulk and single-cell transcriptomes would define a ubiquitination-centered signature and tumor microenvironment (TME) circuits of diagnostic and therapeutic relevance. Public bulk transcriptomic datasets were combined to compare NEPC with prostate adenocarcinoma, including a GEO discovery cohort of 49 tissue samples from GSE32967 and GSE104786, and intersected with a curated ubiquitination-related gene universe to derive ubiquitination-related differentially expressed genes (URDEGs). Co-expression networks, functional enrichment, and protein-protein interaction (PPI) network topology analyses were used to identify and prioritize candidate hub genes. An independent scRNA-seq cohort was integrated for biological contextualization to map cellular lineages, hub gene localization, and intercellular communication. We identified 317 URDEGs that clearly segregated NEPC from conventional prostate cancer and clustered into NEPC-associated modules enriched for cell-cycle and mitotic programs. Network integration yielded an 11-gene hub panel, including AURKA, CCNA2, EZH2, FGFR1, and TTK. In the single-cell dataset, 25,325 cells were retained after quality control, and UMAP resolved 17 clusters annotated into 8 major lineages. Single-cell mapping further revealed lineage-biased hub gene expression and highlighted a prominent stromal-vascular as well as immune MIF-CD74/CXCR4 signaling axis. This integrative analysis identifies a ubiquitination‑anchored transcriptomic signature and associated hub‑gene network that are consistently associated with NEPC in public bulk datasets and supported by cell‑type-resolved patterns in an independent scRNA‑seq cohort; these findings nominate candidate biomarkers and therapeutic hypotheses that warrant external validation in prospectively collected, clinically annotated cohorts with protein‑level assessment. Our analysis defines a ubiquitination-anchored gene signature that distinguishes treatment-induced NEPC from conventional prostate cancer, supporting more accurate classification of aggressive, therapy-resistant disease.Identified hub genes show strong diagnostic performance and are measurable in routine samples, providing realistic candidates for biomarker panels and companion diagnostics.Single-cell mapping of the tumor microenvironment highlights stromal–vascular crosstalk and a MIF–CD74/CXCR4 immune axis as potentially druggable communication hubs beyond tumor cells alone.These findings support integrating multi-omics profiling into care pathways and trials for advanced prostate cancer to detect NEPC early, guide treatment choice, and prioritize patients for targeted therapies.

BackgroundTraditional, complementary, and integrative medicine (TCIM) is an evolving field in oncology focused on managing cancer symptoms. Hydrogen water (HW) has gained attention for its antioxidant and anti-inflammatory properties, yet its clinical effectiveness needs further exploration. This randomized controlled trial aimed to assess the impact of gargling with HW on oral mucositis severity, pain levels, oral frailty, and quality of life in head and neck cancer patients undergoing radiotherapy or concurrent chemo-radiotherapy.MethodsIn this single-center, single-blind, parallel-group randomized controlled trial, patients were randomly assigned to receive either HW or distilled water (DW) for gargling. Oral mucositis (OM) severity, pain, oral frailty, and quality of life (QoL) were assessed using the World Health Organization Oral Mucositis Grading Criteria (WHO-OMGC), the Brief Pain Inventory-Taiwan (BPI-T), the Oral Frailty Checklist (OFC), and the EORTC QLQ-H&N35 questionnaire. Assessments were conducted at baseline (T0) and on Days 1 (T1), 3 (T2), 7 (T3), and 14 (T4) post-treatment.ResultsThe HW group showed significant OM improvement at Day 7 (p = 0.04) and Day 14 (p = 0.002). Pain decreased significantly in the HW group at Day 14 (p = 0.02). QoL improved in the HW group (p = 0.03), while OFC scores showed no significant difference between groups (p = 0.74).ConclusionHW gargling significantly alleviated OM severity and pain and improved QoL in head and neck cancer (HNC) patients undergoing radiotherapy or CCRT. HW gargling may serve as a simple, well-tolerated, and effective complementary and integrative therapy during cancer treatment.

The purpose of this review is to provide a practical and clinically relevant overview of the role of the microbiome in the development and treatment of digestive tract cancers. We describe the established associations between microbes and malignancy, such as Helicobacter pylori and Fusobacterium nucleatum, in gastric and colorectal cancer, respectively. We also review emerging evidence identifying additional microorganisms that may play a role in digestive tract cancer initiation and progression. We discuss the impact of microbial composition on the efficacy and toxicity of cancer-directed therapies, including radiation therapy and systemic chemotherapy. Beyond outlining gut microbial risk factors, we also highlight interventions on the oral and gut microbiome to prevent or alleviate symptoms associated with dysbiosis, along with proposed strategies to improve therapeutic outcomes in the future. Finally, we examine opportunities to support gut microbial health, including suggestions to reduce exposure to environmental toxins that may increase cancer risk.

This study aimed to assess the awareness, perception, and utilization of complementary and alternative medicine (CAM) among Korean patients with cancer and their caregivers. Furthermore, it evaluated CAM information sources, the reliability of these sources, communication patterns with clinicians, and the effect of caregiver beliefs on the use of CAM and patients' attitudes toward CAM. A nationwide cross-sectional survey was conducted from September 2021 to January 2022 across 19 hospitals in South Korea. Adult patients with cancer and their accompanying caregivers were recruited via convenience sampling from outpatient oncology clinics and inpatient settings and completed a structured questionnaire. Data from 1,804 patients and 768 family members were analyzed using descriptive statistics and appropriate comparative tests. Among patients, 47.2% had heard of CAM, and 41.0% expressed belief in it. Biologically based therapies were the most commonly used form of CAM among users (55.0%). The primary sources of CAM information were family/relatives (24.8%) and television (23.8%), whereas medical professionals accounted for only 5.4% of sources, although doctors and nurses were perceived as the most reliable (mean reliability: 3.43 on a 5-point scale). A significant communication gap was observed, with 71.7% of patients not discussing CAM with their medical professionals. Common reasons for non-disclosure included a lack of patient interest (39.4% of non-disclosers), the perception that CAM was irrelevant to their doctors (27.6%), and concerns about physician disapproval. Among patients who did consult their clinicians, 60.8% were advised against CAM use. Caregivers' CAM beliefs significantly influenced patients' beliefs (odds ratio [OR], 4.242; p<0.001), although this did not translate into a statistically significant direct effect on CAM use by patients (OR, 1.449; p=0.105). CAM awareness and use are substantial among Korean patients with cancer; however, a critical communication gap with healthcare providers persists. Family members are key information sources, and caregiver beliefs influence patient beliefs regarding CAM. Proactive, empathetic, and evidence-based communication about CAM is essential to promote shared decision-making and ensure safe, patient-centered integrative cancer care.