We hypothesized that a nursing navigator intervention with needs assessment, distress evaluation, and emotional support from diagnosis to follow-up would improve self-efficacy compared with standard care in colorectal cancer.

Patients with a physician-verified suspicion of colorectal cancer following colonoscopy were assessed for eligibility. Those who fulfilled inclusion criteria and consented were randomized to either intervention (nurse navigation) or standard care during the following cancer treatment trajectory. Five special educated nurse navigators delivered the intervention. Self-efficacy was assessed using the short form of the Cancer Behavior Inventory questionnaire (CBI-B) at baseline before randomization and at treatment completion or within 1 year at the latest. The group difference between CBI-B changes from baseline to follow-up was assessed in a population-averaged linear regression model employing generalized estimating equations.

Of 271 included participants, 222 were completed cases (115 in standard care, 107 in intervention). Based on 4888 observations, self-efficacy under standard care increased by a 2.06 score (CI -0.84; 4.97) and by 6.98 (CI 3.99; 9.97) under intervention. Estimated effect size was 4.92 (CI 0.75; 9.08), which was statistically significant (p = 0.021).

Tailored nurse navigation across the course of colorectal cancer treatment significantly increased patients' self-efficacy.

This study aimed to analyze the human papilloma virus (HPV) genotype distribution in vaginal intraepithelial neoplasia (VaIN) and its relationship with the anatomical location on the vaginal wall. A retrospective study was conducted on patients diagnosed with VaIN at the First Affiliated Hospital of Wenzhou Medical University between January 1, 2021, and December 31, 2024. A total of 1670 patients with low-grade VaIN and 259 patients with high-grade VaIN were included. Single HPV infection was the most prevalent type in VaIN cases. HPV52 was identified as the most common genotype in VaIN1 (25.0%), followed by HPV58 (15.7%), HPV53 (15.6%), and HPV16 (11.4%). In VaIN 2/3, the predominant genotypes were HPV16 (39.0%), HPV58 (22.4%), and HPV52 (15.1%). Multifocal lesions were observed in 34.7% of patients and were associated with both HPV co-infection and high-grade lesions. The diversity of HPV genotype was lower in the middle and lower segments of the vagina compared with the upper third and fornix. HPV16 was frequently and evenly detected across all vaginal segments in the specimen-level HSIL group (33.3%-47.2%). HPV52 was a leading genotype in the specimen-level LSIL group (17.6%-33.3%) and remained prevalent in the specimen-level HSIL group (10.3%-33.3%). HPV58 also accounted for a high proportion of infections. HPV exhibits distinct distribution patterns across different anatomical sites of the vaginal wall.

The development of immune checkpoint inhibitors (ICIs) targeting the programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) pathway has brought about a breakthrough in cancer treatment; nevertheless, therapeutic resistance remains a significant challenge. Recent research shows that mitochondrial metabolism plays an essential role in T-cell function and therapeutic efficacy. Activation of PD-1 inhibits glycolytic metabolism, mitochondrial biogenesis, and oxidative phosphorylation (OXPHOS), resulting in T-cell exhaustion and impaired function. Concurrently, metabolic reprogramming in tumor cells, characterized by increased glycolysis, glutaminolysis, and fatty acid oxidation (FAO), creates an immunosuppressive tumor microenvironment (TME) through nutrient deprivation and the accumulation of metabolites such as lactate and 2-hydroxyglutarate (2-HG). In this review, we analyze the bidirectional relationship between PD-1 signaling and mitochondrial dysfunction and discuss emerging therapeutic approaches that combine metabolic reprogramming with immune checkpoint blockade.

Robotic-assisted surgery has become an important modality in minimally invasive rectal cancer management because of its enhanced dexterity, three-dimensional visualization, and technical advantages in confined pelvic surgery. As the volume of research in this area continues to expand, a structured understanding of its scientific development is needed. This study aimed to map the global research landscape of robotic surgery in rectal tumor and rectal cancer through a bibliometric analysis of the published literature. A comprehensive search of Scopus, Web of Science Core Collection, and MEDLINE was performed, and records were screened using a PRISMA-guided selection process. The final dataset comprised 1,196 documents published between 2017 and 2026, including 1,168 journal articles and 28 conference/proceedings papers. Bibliometric performance indicators, citation analysis, and science-mapping approaches were applied using R (Bibliometrix/Biblioshiny) and VOSviewer to evaluate publication growth, influential sources, geographic and collaborative patterns, and thematic development. The results showed sustained growth over the study period, with the literature entering a more mature phase. The literature was concentrated in a limited number of core journals, led by Journal of Robotic Surgery, Surgical Endoscopy and Other Interventional Techniques, and Techniques in Coloproctology. The United States, Japan, and China were among the most productive countries, while thematic analyses showed a progression from early feasibility- and comparison-oriented research toward more specialized themes involving operative performance, postoperative outcomes, and oncologic quality. Overall, the field has developed into a mature and structured research domain with a strong clinical and outcome-driven focus. These findings provide a comprehensive overview of the intellectual, conceptual, and collaborative structure of robotic rectal surgery research and may help guide future investigation and international research cooperation.

Uterine corpus endometrial carcinoma (UCEC) ranks as the 6th most common malignancy among women. Emerging evidence indicates that the dysregulation of tRNA-derived fragments (tRFs) is involved in the pathogenesis of multiple cancer types, including UCEC; however, the molecular mechanisms underlying the roles of tRFs in UCEC remain poorly characterized. Desmocollin3 (DSC3), a transmembrane protein, is predominantly expressed in the basal and suprabasal layers of normal stratified epithelia. While accumulating evidence has implicated DSC3 in the pathogenesis of multiple disease entities, its functional role in UCEC remains elusive. The present study is designed to investigate the functional significance and underlying molecular mechanisms of tRF-19-79MP9PJZ in the progression of UCEC. In this study, tRF-19-79MP9PJZ was found to be significantly upregulated in UCEC tissues and cell lines, with its elevated expression correlating with unfavorable prognostic outcomes in UCEC patients. Furthermore, tRF-19-79MP9PJZ knockdown was observed to suppress the proliferative and migratory capacities of UCEC cells, while concurrently enhancing apoptotic processes. At the mechanistic level, tRF-19-79MP9PJZ was demonstrated to facilitate UCEC progression through targeted regulation of DSC3. Collectively, this study elucidates a previously uncharacterized mechanism whereby tRF-19-79MP9PJZ drives UCEC development, thereby highlighting the potential of the tRF-19-79MP9PJZ/DSC3 axis as a therapeutic target for UCEC intervention.

In acute myeloid leukemia (AML), therapeutic resistance is intimately linked to vascular microenvironment remodeling; however, the initiating molecular determinants remain elusive. Here, we identified exosomal pyruvate kinase M2 (PKM2) as a pivotal mediator of this pathogenic process. PKM2 was abundantly present in AML-derived exosomes and transferred to human umbilical vein endothelial cells (HUVECs), eliciting metabolic reprogramming characterized by enhanced glycolysis and angiogenic activation. Mechanistically, PKM2 knockdown in AML cells substantially attenuated exosome-induced endothelial migration and tube formation, whereas ectopic PKM2 overexpression in endothelial cells potentiated pro-angiogenic phenotypes. In NOD/SCID mouse xenograft, AML-derived exosomes promoted microvascular remodeling and accelerated disease progression, effects that were abrogated by the angiogenesis inhibitor endostatin. This vascular remodeling coincided with diminished cytarabine (Ara-C) sensitivity, indicative of a chemoprotective microenvironment. Consistently, in a systemic AML model, pharmacological PKM2 inhibition disrupted the vascular niche, suppressed angiogenesis, and restored Ara-C chemosensitivity. Clinically, PKM2 expression correlated positively with VEGFA and HIF-1α levels, and exosomes derived from AML patients with elevated PKM2 conferred enhanced tube-forming capacity upon endothelial cells. Collectively, these findings establish exosomal PKM2 as a critical regulator of the chemoprotective vascular niche in AML and underscore its translational potential as a therapeutic target.

Cervical cancer remains a leading cause of cancer related mortality in women worldwide. Cisplatin (CP) is a cornerstone chemotherapeutic agent; however, its clinical utility is constrained by dose-limiting toxicity and the emergence of drug resistance, necessitating novel combinatorial strategies. This study investigated the therapeutic potential of combining CP with Aloe vera extract (AVE) against HeLa cervical cancer cells and the normal human skin fibroblast cell line CCD-1072Sk. Cytotoxicity assays performed using the xCELLigence Real-Time Cell Analysis (RTCA) system determined IC₅₀ values of 18.45 µM for CP and 18.88 µg/mL for AVE in HeLa cells, compared with 53.31 µM and 19.09 µg/mL, respectively, in CCD-1072Sk cells. The CP + AVE combination exhibited markedly enhanced antiproliferative activity in HeLa cells compared with CP alone, while CCD-1072Sk cells exhibited continued but decelerated proliferation, suggesting a differential cellular response. Seahorse metabolic analysis revealed that AVE, both alone and in combination with CP, markedly increased mitochondrial oxygen consumption rate (OCR) and ATP-linked respiration in HeLa cells, indicating induction of sustained bioenergetic stress beyond the cells' adaptive capacity. Transcriptomic profiling of HeLa cells identified 453 differentially expressed genes (DEGs) upon combination treatment, with significant downregulation of oxidative phosphorylation (OXPHOS) components, mitochondrial electron transport chain subunits, and the fatty acid metabolism gene CPT1B, collectively indicating a severe disruption of cellular energy metabolism. DepMap database analysis confirmed that downregulated targets including CPT1B and CHN2 are functionally important for HeLa cell survival. Collectively, these data suggest that AVE drives HeLa cells into a hypermetabolic state that overloads mitochondrial capacity; in combination with CP, this converging bioenergetic stress produces enhanced cytotoxicity descriptively consistent with an additive interaction (a term used here in its dose-response sense, as no formal combination-index or Bliss/Loewe synergy analysis was performed) at the IC₅₀ doses employed. This study highlights the potential of AVE as a metabolically active combinatorial agent capable of potentiating CP efficacy by targeting cancer cell energy metabolism, and provides a mechanistic basis for further investigation.

Oxaliplatin resistance remains a major obstacle in the treatment of colorectal cancer (CRC). This study aimed to determine whether MYC contributes to oxaliplatin resistance by regulating ferroptosis and to clarify the downstream mechanisms involving FTH1 and GPX4.

Parental CRC cell lines, including HCT116, HT-29 and SW480, together with oxaliplatin-resistant HCT116-R cells, were used. MYC expression was manipulated by knockdown or overexpression. Oxaliplatin sensitivity was evaluated using CCK-8 assays and IC50 analysis. Intracellular Fe²⁺ and reactive oxygen species (ROS) levels were measured to assess ferroptosis-associated changes. RT-qPCR and western blotting were performed to examine gene and protein expression. Chromatin immunoprecipitation-qPCR and dual-luciferase reporter assays were used to investigate the transcriptional regulation of FTH1 and GPX4 by MYC. Rescue experiments with FTH1 or GPX4 overexpression and sorafenib treatment were also conducted.

MYC knockdown significantly increased oxaliplatin sensitivity in both parental and resistant CRC cells and elevated intracellular Fe²⁺ and ROS levels. MYC directly bound to the promoter regions of FTH1 and GPX4 and enhanced their transcriptional activity. Downregulation of MYC reduced FTH1 and GPX4 expression, whereas re-expression of either FTH1 or GPX4 partially restored oxaliplatin resistance. Sorafenib further enhanced oxaliplatin sensitivity in resistant cells.

MYC promotes oxaliplatin resistance in CRC cells, at least in part, by transcriptionally upregulating FTH1 and GPX4 and suppressing ferroptosis-associated cell death. The MYC-FTH1/GPX4-ferroptosis axis may represent a potential therapeutic target for overcoming oxaliplatin resistance in CRC.

Cancer patient-derived T cells often exhibit impaired activation and functional responsiveness due to chronic antigen exposure and therapy-induced immune dysregulation, limiting the efficacy of current immunotherapies. Mechanical forces, such as fluid shear stress (FSS), are emerging as critical regulators of immune cell activation, yet their role in modulating activation of patient-derived T cells remains largely unexplored. In this study, primary T cells isolated from patients with metastatic prostate cancer were exposed to FSS using a cone-and-plate viscometer during ex vivo activation in the presence and absence of bead-bound anti-CD3/CD28 monoclonal antibodies. FSS alone was sufficient to induce NF-κB phosphorylation and intracellular cytokine synthesis, demonstrating that mechanical stimulation can independently initiate T cell activation signaling. Moreover, FSS combined with anti-CD3/CD28 stimulation produced a synergistic increase in activation signaling, IL-2 and IFN-γ production, and CD25/CD69 expression. While trends were consistent across donors overall, inter-patient variability reflected differences in baseline T cell phenotype, with naïve-like cells displaying greater mechanosensitivity. These results indicate that cancer patient-derived T cells retain mechanotransduction capacity despite reduced antigen responsiveness. Incorporating FSS as a co-stimulatory signal during ex vivo expansion may be more effective at priming patient T cells for activation, enhancing effector function, and improving the efficacy of adoptive cell therapies.

The composition of the intestinal microbiome has been identified as a key factor influencing the efficacy of immune checkpoint inhibitors. This study aimed to systematically evaluate the potential associations among gut microbiota, metabolic profiles, and clinical outcomes in patients with MSI-H advanced colorectal cancer (CRC) treated with immunotherapy. Twenty advanced CRC patients receiving immunotherapy were enrolled and categorized into clinical benefit response (CBR) and non-benefit (NCB) groups based on treatment efficacy. Fecal samples were analyzed using metagenomic sequencing and untargeted metabolomics. The results revealed significant enrichments of s_Clostridium unclassified and metabolites such as guanosine, 3-carboxy-4-methyl-5-propyl-2-furanpropionic acid, and quercetin 3-(6"-malonyl-glucoside) in the CBR group, suggesting their potential positive predictive value for immunotherapy response. Conversely, the NCB group showed significant enrichments of s_Roseburia hominis, s_Marseilla massiliensis, and metabolites including pyrophosphate, riboflavin, and PC(22:5(4Z,7Z,10Z,13Z,16Z)/14:0), indicating a possible association with treatment resistance. By integrating fecal metagenomics and metabolomics, this study reveals distinctive "flora-metabolite" interactions linked to therapeutic response in advanced CRC patients undergoing immunotherapy. Specific microbial and metabolic profiles were positively or negatively correlated with immunotherapy outcomes, highlighting their potential not only as predictive biomarkers but also as a theoretical foundation for developing individualized immunotherapy strategies based on microecological modulation.