Primary myelofibrosis (PMF) is a myeloproliferative neoplasm frequently treated with the Janus kinase (JAK) inhibitor Ruxolitinib. Perioperative management of Ruxolitinib presents a clinical dilemma. Continued therapy may increase the risk of infection, cytopenia, and impaired wound healing during major surgery, whereas abrupt discontinuation can precipitate Ruxolitinib Discontinuation Syndrome (RDS), an inflammatory rebound syndrome that may be life-threatening. Currently, there are no established perioperative guidelines for the management of Ruxolitinib. We report a case of a 65-year-old patient with PMF undergoing elective coronary artery bypass graft (CABG) surgery. Following multidisciplinary discussion with haematology, Ruxolitinib was withheld for 48 hours perioperatively and prophylactic corticosteroids were administered. The patient underwent uncomplicated surgery and recovery without evidence of infection, thrombocytopenia, or RDS. This case highlights the challenges associated with perioperative Ruxolitinib management and emphasises the importance of multidisciplinary decision-making and individualised risk assessment. Reporting such cases contributes to the limited literature guiding perioperative management of JAK inhibitor therapy in patients undergoing major surgery.

To critically evaluate oligoprogression in advanced gastric and gastroesophageal junction (GEJ) cancer and propose a practical multidisciplinary framework integrating local therapy, systemic treatment decisions, and biomarker reassessment.

We reviewed direct gastric/GEJ evidence and clearly distinguished it from evidence extrapolated from oligometastatic disease and other tumor types.

No prospective comparative study has demonstrated that local treatment with continuation of systemic therapy improves survival specifically in gastric/GEJ oligoprogression. In carefully selected patients, local treatment may be considered to delay the next systemic therapy, prevent or relieve symptoms, maintain local control, or preserve quality of life. Tissue rebiopsy or circulating tumor DNA analysis may be useful when technically obtainable and likely to change management. HER2 reassessment has established clinical relevance after HER2-directed treatment, whereas repeat assessment of CLDN18.2, PD-L1, FGFR2b, and other emerging targets remains exploratory. A negative plasma circulating tumor DNA result does not exclude resistant disease, particularly in low-volume, peritoneal, or central nervous system progression.

Management should remain individualized and multidisciplinary, with explicit recognition that the proposed framework is provisional and that a survival benefit from local therapy with systemic treatment continuation remains unproven.

Monensin, a polyether ionophore widely used in veterinary medicine, has recently emerged as a multimodal anticancer candidate. This review provides a comprehensive overview of preclinical studies showing that monensin exerts selective cytotoxic and anti-progression effects across a wide range of malignancies. Its activity spans breast cancer to leukemia, reflecting both versatility and significant therapeutic potential. In breast cancer, monensin reduces proliferation, induces apoptosis, and enhances chemosensitivity, suggesting a role in combination therapies. In prostate cancer, it disrupts androgen receptor signaling, induces oxidative stress, and triggers mitochondria-dependent apoptosis. In pancreatic cancer, it suppresses EGFR signaling and promotes programmed cell death, while in ovarian and cervical cancers, it inhibits proliferation, migration, and invasion by modulating EGFR and MEK/ERK pathways and enhancing SUMOylation. In renal carcinoma, monensin induces cell-cycle arrest, autophagy, and apoptosis, whereas in bladder and squamous cell carcinoma, it interferes with EGFR-related signaling and lectin-mediated interactions. It selectively kills liver cancer cells through intracellular Na⁺ overload and mitochondrial damage, and in thyroid cancer, it disrupts cellular respiration and AMPK/mTOR signaling. In glioblastoma, it exhibits both anti-tumor and anti-angiogenic effects, while in hematologic malignancies such as leukemia and lymphoma, it induces apoptosis, cell-cycle arrest, and glycosylation alterations. Collectively, these findings highlight monensin as a highly promising, broad-spectrum anticancer candidate. Its multifaceted mechanisms of action and consistent efficacy across diverse tumor types provide a compelling rationale for continued preclinical evaluation and potential clinical translation. These insights position monensin as an innovative therapeutic avenue, offering new hope for the development of versatile and effective cancer treatments.

Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide, with tumor-associated macrophages (TAMs), predominantly M2-polarized, shaping a tumor-promoting microenvironment. ETS proto-oncogene 2 (ETS2) is aberrantly upregulated in CRC, but its role in exosome-mediated intercellular communication and TAM polarization remains unclear. Here, public datasets and single-cell RNA sequencing were analyzed to characterize ETS2 expression and cellular distribution in CRC. Co-culture of THP-1-derived M0 macrophages with CRC cells (LoVo and HCT-116), combined with isolation of tumor-derived exosomes, was used to assess exosome-mediated ETS2 transfer and macrophage M2 polarization. CRC cell proliferation, migration, apoptosis, CD8⁺ T cell apoptosis, and macrophage M2 polarization were evaluated by CCK-8, EdU incorporation, flow cytometry, RT-qPCR, and Transwell assays. Chromatin immunoprecipitation and dual-luciferase reporter assays confirmed transcriptional activation of pre-mRNA processing factor 4 (PRPF4) by ETS2, and a xenograft mouse model was used to assess in vivo effects. ETS2 expression was elevated in CRC tissues and TAMs and correlated positively with M2 polarization. Silencing ETS2 inhibited CRC cell proliferation and migration, promoted apoptosis, reduced macrophage M2 polarization, and decreased CD8⁺ T cell apoptosis. Mechanistically, ETS2 activated PRPF4 transcription, and PRPF4 overexpression reversed the inhibitory effects of ETS2 knockdown. CRC-derived exosomes mediated ETS2 transfer to macrophages, promoting M2 polarization, and in vivo PRPF4 overexpression significantly rescued tumor growth suppressed by ETS2 knockdown. These findings indicate that exosomal ETS2 promotes CRC progression and M2 macrophage polarization via PRPF4, highlighting the ETS2/PRPF4 axis as a potential therapeutic target.

Fibroadenoma is the most common benign fibroepithelial lesion of the breast; it occurs most frequently in adolescents and women of reproductive age. While fibroadenoma is considered a non-invasive lesion with a good prognosis, some fibroadenomas may show rapid growth, recurrence, stromal hypercellularity, epithelial proliferative changes and even show radiological overlap with phyllodes tumour and breast carcinoma resulting in significant diagnostic dilemmas. In recent years, molecular pathology and biomarker studies have led to better understanding of the biology of fibroadenomas, and their ability to differentiate between fibroadenomas and malignant breast lesions. This review will provide a comprehensive overview of biomarkers involved in the diagnosis, prognosis, prediction, molecular, genetic, epigenetic, functional, circulating and imaging of breast fibroadenoma and breast cancer. The key biomarkers such as MED12 mutation, Ki-67, p53, Bcl-2, ER/PR, HER2, VEGF, MMPs, γ-H2AX, ctDNA, circulating tumour cells and transcriptomic classifiers are discussed in the context of tumour proliferation, apoptosis, angiogenesis, invasion, genomic instability and malignant transformation risk. The retrieved relevant literature was from 2000 to 2025 from the databases of PubMed, Scopus, Web of Science, and Google Scholar. The review further emphasizes the growing significance of liquid biopsy, radiomics, artificial intelligence, digital pathology, and the integration of multi-omics techniques for enhancing lesion classification, diagnostic accuracy, and personalized risk assessment. Many challenges still exist such as a lack of standardised cut off values for biomarkers, overlap between fibroadenoma and phyllodes tumour, a lack of molecular panels specifically designed for fibroadenoma and a lack of long-term validation studies. Further incorporation of molecular profiling, imaging biomarkers, computational pathology, and precision oncology approaches into the future could greatly enhance the risk stratification and handling of benign and malignant fibroepithelial breast lesions.

Spatial patterns of glioblastoma (GBM) progression inform focal salvage eligibility, but interpretation across studies is limited by heterogeneous spatial definitions, high between-study heterogeneity, and incomplete reporting of non-enhancing/FLAIR-dominant progression. We synthesized reported progression-location involvement after upfront radiotherapy/temozolomide (RT/TMZ) and salvage therapy.

We systematically searched PubMed and Scopus from January 1, 2000, to February 1, 2026, and performed arm-level random-effects meta-analysis of logit-transformed proportions. Enhancing progression was harmonized as non-mutually exclusive local/in-field, marginal/field-edge, and distant/out-of-field involvement among evaluable cases, using each study's spatial framework. The supplementary broad escape-pattern construct was defined as reported progression beyond purely local/in-field enhancing failure.

We included 107 studies (122 arms; 10,529 patients). At first progression after upfront RT/TMZ ± TTF, reported local/in-field enhancing involvement among evaluable cases was 79.2% (95% CI 75.7-82.3; k = 94; n = 6,989; I²=84.8%), and distant/out-of-field involvement was 16.9% (95% CI 14.3-19.9; k = 89; n = 6,493; I²=85.2%). After salvage therapy, local/in-field involvement remained the majority pattern reported among evaluable cases (59.8%, 95% CI 52.8-66.4; k = 27; n = 1,572; I²=80.5%), with distant/out-of-field involvement of 17.5% (95% CI 12.9-23.3; k = 21; n = 1,307; I²=75.5%) and a supplementary broad escape-pattern estimate of 38.6% (95% CI 31.9-45.9; k = 27; n = 1,572; I²=80.1%). Non-enhancing/FLAIR-dominant progression was sparsely and likely selectively reported; only six recurrent/salvage arms contributed data, yielding an exploratory pooled estimate of 27.8% (95% CI 12.8-50.3; n = 216; I²=75.7%).

Published GBM cohorts show predominantly local/in-field enhancing progression after upfront therapy (~ 80%) and persistent majority local/in-field involvement after salvage therapy (~ 60%). Standardized reporting of enhancing, non-enhancing/FLAIR-dominant, disseminated, posterior fossa, and brainstem progression is needed.

Poly(ADP-ribose) polymerase inhibitors (PARPi) have shown limited efficacy in gastric cancer, primarily due to the rarity of inherent homologous recombination (HR) deficiency. The nuclear Arp2/3 complex was recently implicated in DNA double-strand break repair via HR. Here, we investigate whether pharmacological inhibition of Arp2/3 can induce a functional HR-deficient state to synergize with PARPi in gastric cancer cells.

HR repair efficiency was assessed using a direct repeat green fluorescent protein (DR-GFP) reporter assay in HEK-293T cells following Arp2/3 inhibition with CK666, siRNA-mediated knockdown, or CRISPR/Cas9-mediated knockout of ACTR2/ACTR3. HGC-27 and AGS gastric cancer cells were treated with CK666 alone and in combination with olaparib or niraparib. Cell viability and synergy were evaluated by Cell Counting Kit-8 (CCK-8) and clonogenic assays (n = 3 independent experiments). DNA damage and apoptosis were assessed by immunofluorescence for gamma H2A histone family member X (γH2AX) foci (≥100 cells per condition) and Western blot analysis for cleaved PARP.

Arp2/3 inhibition with CK666 significantly impaired HR repair efficiency in the DR-GFP assay (p < 0.01). This effect was recapitulated by genetic knockdown or knockout of ACTR2/ACTR3. CK666 alone exerted minimal cytotoxicity, but synergized with both olaparib and niraparib to suppress proliferation (Combination Index <1), reducing the half-maximal inhibitory concentration (IC₅₀) of PARPi by approximately threefold. Combination treatment markedly enhanced γH2AX foci formation (p < 0.0001) and increased the level of cleaved PARP compared with either monotherapy.

Inhibition of Arp2/3 compromises HR repair capacity, thereby creating a synthetic lethal interaction with PARP inhibition in gastric cancer cells. This combination strategy represents a promising therapeutic approach to broaden the clinical utility of PARPi in HR-proficient tumors and may also enable dose reduction to mitigate associated toxicities.

This review examines recent advances in the use of probiotics combined with immune modulation for the prevention and treatment of gastric cancer. It highlights the interactions between gastrointestinal probiotics, including Lactobacillus, and Helicobacter pylori infection, emphasizing their roles in gastric cancer initiation and progression. The article evaluates how probiotics exert anticancer effects by restoring intestinal microecological balance, enhancing mucosal immunity, and suppressing H. pylori. It also discusses preliminary findings on Lactobacillus in colorectal cancer and their potential relevance to gastric cancer research. Finally, the clinical potential of combining probiotics with immunotherapy for gastric cancer is assessed, and future research directions in this rapidly evolving field are proposed.

Cervical cancer (CC) is a prevalent malignancy in women. RNA-binding motif single-stranded interacting protein 3 (RBMS3) acts as a tumor suppressor in many cancer types, but its role and underlying regulatory mechanisms in CC remain unclear.

The expression levels of RBMS3 and heat shock protein family A member 6 (HSPA6) were evaluated in clinical CC tissues. Gain- and loss-of-function assays, transcriptome sequencing, and rescue experiments were performed in CC cell lines and nude mouse xenograft models.

RBMS3 expression was notably lower in CC tissues (n = 306) than in normal cervical tissues (n = 22), with reduced levels linked to shorter overall patient survival (p < 0.05). Overexpression of RBMS3 reduced cell proliferation, migration, and invasion in vitro, as well as tumor growth in vivo (p < 0.001). HSPA6 was identified as a key target of RBMS3 and was also downregulated in CC tissues. RBMS3 potentially binds to HSPA6 mRNA and enhances its stability. Knockdown of HSPA6 reversed the tumor-suppressive effects of RBMS3 (p < 0.001).

RBMS3 inhibits CC progression by stabilizing HSPA6 mRNA. The RBMS3-HSPA6 axis may represent a prognostic biomarker and therapeutic target in CC.

Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine-metabolic disorder characterized by dysregulated ovarian signaling, metabolic inflammation, insulin resistance, and aberrant angiogenesis, for which effective disease-modifying therapies remain limited. Resveratrol (RES), a pleiotropic polyphenol, has attracted increasing attention for its ability to modulate multiple molecular and cellular pathways implicated in PCOS pathophysiology. In this review, we synthesize current evidence to clarify how RES regulates key pathological signaling networks in PCOS, including ovarian follicular dysfunction, impaired insulin signaling, hyperandrogenism, oxidative stress, and vascular remodeling. Rather than merely cataloguing isolated mechanisms, we integrate findings from experimental models to highlight major convergent nodes-such as phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mechanistic target of rapamycin (mTOR), sirtuin 1 (SIRT1)/AMP-activated protein kinase (AMPK), nuclear factor kappa-B (NF-κB), and vascular endothelial growth factor (VEGF)-related pathways-through which RES may exert coordinated regulatory effects at the cellular and tissue levels. We further examine the available clinical studies to assess the translational relevance of these mechanistic insights, with particular emphasis on phenotypic heterogeneity, dose dependence, and the treatment window. Although clinical outcomes remain modest and variable, the available evidence suggests that RES may provide context-dependent benefits in selected PCOS subtypes. Collectively, this review offers a network-based framework linking the molecular actions of RES to the complex pathophysiology of PCOS and identifies key knowledge gaps that must be addressed to improve translational precision and therapeutic applicability.