Renal collision tumors are rare neoplasms characterized by the coexistence of two histologically distinct tumor types within the same renal parenchyma, representing a diagnostic challenge due to their heterogeneous clinical and radiological features. We report a rare case of a renal collision tumor and discuss the diagnostic difficulties, pathological findings, and therapeutic management of this uncommon entity.

Immune checkpoint inhibitors (ICIs) have significantly prolonged patient survival in cancer therapy; however, overactivated immune responses can lead to endocrine immune-related adverse events (irAEs), primarily manifesting as thyroid dysfunction, hypophysitis, adrenal insufficiency, and insulin-dependent diabetes mellitus. Some of these endocrine injuries are irreversible and lack early warning indicators. This narrative review summarizes current evidence regarding the mechanisms underlying ICI-induced endocrine toxicities, including immune checkpoint pathways, organ-specific autoimmune responses, host-related factors, predictive biomarkers, and emerging precision management strategies. It summarizes potential predictive biomarkers, including thyroid autoantibodies, cytokine profiles, and single-cell sequencing, and discusses emerging approaches, including imaging-based assessment, liquid biopsy, and multidimensional prediction models, while emphasizing their current limitations and the need for prospective validation. Finally, by integrating organ-specific mechanistic evidence, biomarker-based prediction, and risk-stratified monitoring, this review frames these advances within the concept of "proactive endocrine protection," emphasizing the transition from passive toxicity management toward earlier identification and individualized surveillance.

Cancer immunotherapy has improved outcomes across many tumor types, but primary and acquired resistance, tumor heterogeneity and a shortage of safe targets remain unresolved. Part of this gap arises because tumor cells evade immune recognition not only through genomic mutation but also through post-transcriptional mRNA processing, a network comprising 5' capping, splicing, alternative polyadenylation (APA), RNA editing, epitranscriptomic modification, nonsense-mediated decay (NMD), RNA stability and translational control. These processes govern antigen presentation, transcript degradation, checkpoint expression and the suppression of innate immune sensing. Here we examine how mRNA processing can extend the target space of cancer immunotherapy. We consider alternative splicing as a source of tumor-specific isoforms, public neoantigens and chimeric antigen receptor (CAR) or T-cell receptor (TCR)-based targets; the effect of APA and 3'UTR remodeling on checkpoints such as PD-L1; the role of m6A, ac4C and other epitranscriptomic marks in antigen presentation, interferon signaling and the tumor microenvironment; the contribution of ADAR1-mediated editing to immunotherapy resistance through suppressed dsRNA and Z-RNA sensing; and the function of NMD as an antigen filter. We also review the discovery technologies that make these targets accessible, and assess the current state of clinical translation, including agent development, target specificity, patient selection, biomarkers and safety. mRNA processing-derived targets offer new sources of antigens, biomarkers and combination strategies in tumors with low mutational burden or refractory to checkpoint blockade. Realizing this will require validation of RNA-level candidates at the protein and HLA-peptide level, together with attention to tumor-normal specificity, HLA restriction, tumor heterogeneity and toxicity.

Psoralea corylifolia L. (PCL), a medicinal plant used in Traditional Chinese Medicine for the treatment of "Kidney-Yang deficiency" has long been applied within a multi-component therapeutic framework. This integrative approach aligns with emerging oncological paradigms that emphasize network-based pharmacology; however, a comprehensive correlation between its phytochemical composition and anti-tumor activity remains insufficiently defined.

This review aims to systematically evaluate the antineoplastic properties of PCL by integrating its phytochemical constituents with underlying pharmacological mechanisms and reported clinical relevance, thereby supporting its translational development.

A comprehensive narrative review was performed using PubMed, Google Scholar, Web of Science, and CNKI to identify studies published from 2010 to August 2026. Evidence from in vitro systems, in vivo models, and clinical observations concerning the antitumor mechanisms, immunomodulatory effects, and safety profile of PCL was critically evaluated according to the experimental model and categorized by mechanistic domain.

The principal bioactive constituents, including coumarins, flavonoids, and monoterpenoids, demonstrated several anticancer effects. These compounds exerted synergistic effects through multiple mechanisms, such as promoting apoptosis and cell cycle arrest, inhibiting metastatic progression, attenuating multidrug resistance, modulating the tumor immune microenvironment, and altering cellular metabolism. Additionally, the balance between therapeutic efficacy and potential toxicity, particularly hepatotoxicity, is critically discussed, alongside current strategies, including nanotechnology-based delivery systems and combinatorial herbal approaches, designed to improve therapeutic performance.

PCL represents a multi-target botanical candidate with potential utility in adjuvant cancer therapy. Future studies are required to clarify synergistic interactions, optimize delivery strategies, and support rigorous clinical translation.

Minimally invasive surgery (MIS) is increasingly used for gastric cancer surgery. MIS is expected to facilitate surgical precision because of its magnified view, and facilitating identification of anatomical dissection layers is expected to reduce postoperative complications. To our knowledge, there is no consensus on the most appropriate surgical approach for gastric cancer following chemotherapy.

This nationwide, observational study used data from the National Clinical Database. Patients who underwent total gastrectomy (TG) or distal gastrectomy (DG) for gastric cancer after receiving chemotherapy between January 2014 and December 2022 were included. The incidence of overall complications of Clavien-Dindo (CD) grade ≥ 1 was set as the primary outcome, and the risk ratio (RR) was estimated using inverse probability of treatment weighting based on propensity scores and G-computation, comparing MIS and open surgery. The incidence of each complication was considered the secondary outcome.

Overall, 18 100 patients were included in this study (TG, 9481; DG, 8619). MIS was associated with a lower incidence of overall complications of CD grade ≥ 1 in both TG (RR 0.91, 95% confidence interval [CI] 0.85-0.98) and DG (RR 0.78, 95% CI 0.72-0.84). MIS was also significantly associated with a lower incidence of superficial incisional surgical site infection (SSI), deep incisional SSI, and pancreatic fistulas in both gastrectomy groups.

MIS was associated with lower rates of overall postoperative complications of CD grade ≥ 1, and wound-related complications and pancreatic fistulas than open surgery in patients with gastric cancer who underwent TG and DG after chemotherapy.

Genomic alterations related to hematopoietic elements may be seen in solid tumour next-generation sequencing (NGS) panels. Here, we report the incidental finding of JAK2 V617F mutations in NGS performed on solid tumours.

Cases where JAK2 V617F mutation was detected on solid tumour NGS performed in-house between 2016 and 2021 were analysed.

12 cases (0.2%) of solid tumour NGS testing that identified JAK2 V617F were reviewed. The mean age of the patient population was 73.8 years (range: 53-87 years). The diagnosis included lung carcinoma ((n=9); adenocarcinoma (n=7), non-small cell carcinoma of the lung (n=1), metastatic adenocarcinoma, favour lung primary (n=1)), renal cell carcinoma-unclassified (1), undifferentiated malignant neoplasm (1) and metastatic poorly differentiated CK7 positive carcinoma (1).The variant allele frequency (VAF) for the JAK2 V617F mutation ranged from 2.4 to 18.4% (mean: 8.2%) and was consistently and statistically significantly different from the VAF observed for tumour-specific genomic variants based on Wilcoxon test. On further work-up, 8/12 patients had clinical history or laboratory evidence of an underlying clonal myeloid process, 6/12 patients had evidence of a JAK2 V617F positive myeloid neoplasm while 2/12 had evidence of pre-treatment thrombocytosis. The remaining two patients had no prior history of a myeloid neoplasm or documented abnormal blood counts.

A work-up for potential haematological disease should be undertaken when an alteration associated with haematological neoplasms is identified in solid tumour NGS panels, particularly when the VAF is different compared to the VAF of other tumour-associated variants.

To identify independent predictors of tetrafecta achievement after radical cystectomy (RC) and to assess its prognostic value for survival outcomes.

We queried a prospectively maintained single-center database of consecutive patients undergoing RC for nonmetastatic bladder cancer (2014-2025). Tetrafecta achievement was defined as: lymph node yield ≥16, negative soft tissue surgical margins, no intraoperative blood transfusion, and no 90-day major (Clavien-Dindo ≥III) complications. Predictors of tetrafecta achievement were analyzed using multivariable logistic regression. Time-to-event outcomes (overall survival [OS], cancer-specific survival [CSS], disease-free survival [DFS], local DFS [LDFS], metastasis-free survival [MFS]) were evaluated with Kaplan-Meier estimates and multivariable Cox regression adjusting for age, delayed RC (>90 days), locally advanced disease (≥pT3), nodal involvement, and neoadjuvant chemotherapy.

Of 330 eligible patients, 144 (43.6%) achieved tetrafecta. Compared with nonachievers, tetrafecta achievers were younger (median 67 vs. 72 years; P < .001), had lower age-adjusted Charlson Comorbidity Index (5 vs. 6; P = .02), more often had Eastern Cooperative Oncology Group 0 (70.8% vs. 59.1%; P = .028), and less frequently had preoperative hydronephrosis (23.6% vs. 38.7%; P = .004). They more commonly underwent robot-assisted RC (41.7% vs. 22.0%; P < .001) and orthotopic neobladder diversion (P < .001). On multivariable logistic regression, older age (odds ratio [OR] 0.96 [95% CI, 0.94-0.99]; P = .005), hydronephrosis (OR 0.55 [95% CI, 0.33-0.94]; P = .029), and cutaneous ureterostomy (OR 0.15 [95% CI, 0.04-0.53]; P = .003) independently reduced tetrafecta odds. With median follow-up of 34 months, OS was higher among tetrafecta achievers on Kaplan-Meier analysis (log-rank P = .012), whereas CSS, DFS, LDFS, and MFS did not differ (all P > .05). Tetrafecta achievement was not independently associated with any survival endpoint on multivariable Cox models.

Tetrafecta achievement after RC is primarily influenced by patient fitness and perioperative course and does not independently predict oncologic outcomes, which remain driven by pathological stage and nodal status.

Hyperthermia induces a multifactorial immune cascade reaction, potentially enhancing pharmacological effects of immune checkpoint inhibitors (ICIs) and overcoming limitations in their clinical application. This study aimed to clarify how hyperthermia affects tumor immunity and enhances the efficacy of ICIs.

Expression of phospho-signal transducer and activator of transcription 1 (p-STAT1), interferon regulatory factor-1 (IRF1), and programmed cell death 1 ligand 1 (PD-L1) was assessed on PD-L1-expressing MC-38 mouse colorectal cancer cells under hyperthermia or interferon gamma (IFN-γ) treatment. Effects of hyperthermia on p-STAT1, IRF1, CD8, and PD-L1 were also assessed in vivo. Antitumor effects and infiltrating CD8⁺ cells were evaluated in mice treated with PD-L1 antibody, hyperthermia, or a combination of the two. Immunohistochemistry was performed to assess PD-L1 expression and CD8+ cell infiltration in samples from a patient after treatment with hyperthermia for breast cancer and a patient after hyperthermia and ICI treatment for Lynch syndrome-related colorectal cancer.

Expression of p-STAT1, IRF1, and PD-L1 was enhanced in vitro by IFN-γ treatment but not by hyperthermia. Hyperthermia enhanced the expression of p-STAT1, IRF1, CD8, and PD-L1 in vivo. The combination therapy of hyperthermia and PD-L1 antibody demonstrated a greater antitumor effect than either therapy alone. Infiltration of CD8⁺ T-cells was significantly increased by hyperthermia compared to the control and was even more strongly increased by treatment using hyperthermia combined with PD-L1 antibody. PD-L1 expression was mildly elevated in the sample from the patient with breast cancer and strongly elevated in that from the patient with colorectal cancer; CD8⁺ cell infiltration was also elevated significantly in both.

Hyperthermia potentially enhances PD-L1 expression by increasing the efficiency of CD8⁺ cell infiltration into tumors and induces a strong antitumor effect in combination with an ICI.

Head and neck squamous cell carcinoma (HNSCC) is the seventh most common cancer globally and has demonstrated an etiological shift over recent decades. Human papillomavirus (HPV) infection is a key risk factor for HNSCC, and its incidence has been rising since 1980. HPV-associated HNSCC display a unique tumorigenesis process and respond differently to traditional HNSCC treatment. Triptolide, a natural derivative, has shown promise as a chemosensitizer against HPV-positive HNSCC. The aim of this study was to investigate activity of triptolide in HNSCC in addition to in silico analysis of triptolide gene targets.

Effects of triptolide on proliferation of HPV-positive and HPV-negative HNSCC cells were evaluated using an MTT assay in vitro. Effects of triptolide on TP53 promoter activity and phosphorylation of TP53 protein were measured by reporter gene assay and western blot respectively. Next, enrichment of triptolide gene targets was evaluated through cBioPortal and The Cancer Genome Atlas (TCGA) with a subsequent STRING analysis.

Triptolide acts as a chemosensitizer in combination with low-dose cisplatin. This effect is most pronounced in HPV-positive cells. HPV-positive cells also show increased TP53 promoter activity and TP53 protein phosphorylation. STRING analysis shows involvement of JAK-STAT signaling, interleukin-23 signaling, and apoptosis pathways in HPV-positive samples. In HPV-negative samples, enriched triptolide targets are implicated in RUNX3 regulation of CDKN1A transcription and interleukin-4, interleukin-13, and interleukin-17 signaling.

Triptolide acts as an in vitro chemosensitizer in HPV-positive HNSCC, likely through reactivation of wild-type TP53 and restoration of apoptotic control. Inflammatory cytokine signaling blockade may provide an additional mechanism contributing to this chemosensitizing effect.

Hepatic resection is the standard of care for colorectal and neuroendocrine liver metastases, but its role for metachronous liver metastases from non-colorectal non-neuroendocrine (NCRNNE) gastrointestinal cancers remains controversial, with limited evidence and no established guidelines. The aim of this study was to evaluate whether surgical treatment of metachronous liver metastases is associated with improved overall survival compared with non-surgical management in patients with primary non-colorectal non-neuroendocrine gastrointestinal cancers.

A systematic review and meta-analysis was conducted to compare surgical treatment versus non-surgical management in patients with non-colorectal non-neuroendocrine gastrointestinal cancers and metachronous liver metastases. PubMed/MEDLINE, Scopus, and the Cochrane Library were searched for comparative studies published in English from 1 January 2005 to 8 December 2025. Studies reporting overall survival outcomes were included. Overall survival at 1, 3, 5 years was analyzed using relative risks (RR) with 95% confidence intervals (CI), and pooled estimates were calculated using a random-effects model. Between-study heterogeneity was assessed using the I² statistic.

Ten comparative studies were included. Surgically treated patients showed longer median overall survival. When survival was analyzed at fixed time points, surgical treatment was associated with significantly higher overall survival at 1 year compared with non-surgical management (RR=1.93, 95% CI=1.26-2.98), with a similar, though not statistically significant, trend favoring surgery at 3 years (RR=2.45, 95% CI=0.99-6.11) and 5 years (RR=2.26, 95% CI=0.97-5.29). Analyses showed substantial heterogeneity (I²=67-86%), reflecting important clinical and methodological variability across studies and the likely influence of patient selection in the surgical cohorts.

Surgical treatment of metachronous liver metastases from non-colorectal non-neuroendocrine gastrointestinal cancers was associated with longer median overall survival and significantly higher overall survival at 1 year compared with non-surgical management, with a favorable but not statistically significant trend at 3 and 5 years.