To examine the perceived need, acceptability and anticipated feasibility of the nurse-led telephone follow-up care (NLTFC) approach as an adjunct to specialist-led breast cancer follow-up in India from the perspectives of survivors and healthcare professionals.

A convergent, qualitatively driven mixed methods study (QUAL + quan). Semi-structured interviews were conducted with 21 survivors and 27 healthcare professionals (19 nurses, 8 doctors). Surveys were completed by 120 survivors and 112 healthcare professionals (96 nurses, 16 doctors). Qualitative data were analysed using reflexive thematic analysis, and quantitative data were summarised using descriptive statistics and exploratory Fisher's exact tests. Findings were integrated and reported through narrative weaving and a joint display.

NLTFC received high survey-based support from survivors (99%), nurses (98%) and doctors (94%), with no statistically significant differences between nurses and doctors across the six perception statements. Participants perceived that NLTFC could improve accessibility, care coordination, psychosocial support and survivor empowerment while reducing travel, waiting times and financial burden. Despite the strong support, interviews identified concerns about clinical safety, nurses' preparedness and professional role boundaries. Structured follow-up plans, specialised oncology training, clearly delineated roles and multidisciplinary oversight were considered necessary for implementation.

NLTFC was perceived as an acceptable adjunct to specialist-led follow-up with potential to strengthen supportive care and redistribute specialist workload. The findings demonstrate anticipated rather than operational feasibility. Safe delivery would require formal clinical governance and investment in advanced oncology nursing roles. Prospective evaluation is required to assess feasibility, clinical safety, effectiveness and sustainability in India.

Nanomedicine has broad prospects in tumor diagnosis and treatment, but its clinical translation has long been limited by targeted delivery efficiency. The heterogeneity of the tumor microenvironment is like a "sea fog" that hinders precision medicine. This makes it difficult for traditional active targeting that relies on natural targets to achieve precise delivery. For this difficulty, this review summarizes the constraints of tumor microenvironment heterogeneity on nanomaterials in terms of time and space. Pre-targeting strategies enhance delivery efficiency by constructing an "artificial lighthouse." According to the source of the target and the mode of specific binding, this review divides pre-targeting strategies into two categories: biomolecular recognition-mediated and bioorthogonal click chemistry-mediated. On this basis, this review comprehensively introduces recent progress in pre-targeting-enabled nanomedicine in body fluid-based detection, in vivo imaging, and multi-therapies. Furthermore, this review is the first to summarize the synergistic mechanisms of pre-targeting with prodrugs, insitu self-assembly, and dual-targeting strategies. This review systematically summarizes the complete framework of pre-targeting strategies, from mechanisms and classifications to applications and expansions. It aims to provide inspiration for the development of nanomedicine in the field of oncology for effective cancer diagnosis and treatment.

Colorectal cancer (CRC) exhibits intrinsic resistance to conventional therapeutic regimens. By integrating single-cell and bulk transcriptomic data from CRC cohorts, we demonstrate that proliferative capacity alone constitutes an inadequate prognostic predictor. Instead, an immunosuppressive tumor microenvironment (TME) emerges as the dominant driver of disease progression. Galectin-1 (LGALS1), highly upregulated in metastatic CRC, correlates with robust infiltration of regulatory T cells (Tregs) and M2 macrophages to facilitate immune evasion and poor clinical outcomes, thereby serving as a promising therapeutic target for anti-tumor immunotherapy. The stromal barrier mediated by cancer-associated fibroblasts (CAFs) restricts intratumoral penetration of antitumor agents and diminishes therapeutic efficacy. To overcome this physical barrier, we constructed a CAF extracellular vesicle-based co-delivery platform termed CEV@Comb, encapsulating the LGALS1 inhibitor OTX008 and 5-fluorouracil (5-FU). CEV@Comb selectively accumulates in tumors, suppresses growth in vitro and in vivo, and remodels the immunosuppressive TME by boosting M1 macrophages and cytotoxic CD8⁺ T cells while reducing intratumoral Tregs. Combination therapy with CEV@Comb and anti‑programmed death‑1 antibody (αPD-1) further amplifies anti-tumor immunity in the Apc^-/-, Kras^G12D, Trp53^-/-, Smad4^-/-(AKPS) CRC mouse model. This study identifies LGALS1 as a core immunosuppressive mediator and provides an innovative chemoimmunotherapeutic strategy to improve clinical outcomes for patients with advanced CRC.

Oncogenic viral pathogens, such as human papillomavirus (HPV), Epstein-Barr virus (EBV), hepatitis B and C viruses (HBV, HCV), and Kaposi's sarcoma-associated herpesvirus (KSHV), are involved in a significant proportion of human cancers worldwide. While genetic and epigenetic mechanisms underlying viral oncogenesis have been thoroughly investigated, emerging evidence underscores a critical role for epitranscriptomic regulation in virus-host interactions and their clinical consequences. RNA modifications such as N6-methyladenosine (m6A), 5-methylcytosine (m5C), and pseudouridine (Ψ) dynamically modulate RNA stability, translation, and immune recognition, thereby regulating viral replication and persistence. The present review describes current knowledge on the epitranscriptomic landscape of oncogenic viral pathogens and its functional implications. This review discusses how viral and host transcripts are selectively modified by cellular writers, erasers, and readers, shaping key stages of the viral life cycle, including replication, latency, and reactivation. Particular emphasis is placed on the role of RNA modifications in maintaining chronic infection and promoting tumourigenesis through the regulation of oncogenic pathways, cell proliferation, and apoptosis. Additionally, the present review examines how epitranscriptomic marks contribute to immune evasion by altering innate immune sensing and interferon responses. Finally, it explores the therapeutic potential of targeting epitranscriptomic machinery, highlighting recent advances in small-molecule inhibitors and the challenges associated with specificity and off-target effects. A deeper understanding of epitranscriptomic regulation in oncogenic viruses may reveal novel biomarkers and therapeutic strategies for virus-linked malignancies.

Circulating plasmablasts and plasma cells are characteristic but underrecognized features of acute dengue virus (DENV) infection because of their transient nature. Their presence on peripheral blood smears may erroneously suggest a plasma cell dyscrasia.

We report a case of secondary acute DENV serotype 3 infection in a 57-year-old traveler returning from the Caribbean that had morphologically suspected circulating plasma cells and thrombocytopenia, documented by peripheral blood smear and serial hematology analyzer scattergrams. Immunophenotypic confirmation was unavailable. We also performed a narrative review of published reports of plasmablast/plasma cell kinetics in DENV.

An abnormal reactive lymphocyte scattergram with an increased very high-fluorescence cell signal prompted smear review, which revealed the abrupt appearance of reactive (activated) lymphocytes (25%) and suspected plasma cells (5%) on day 6 after symptom onset, coinciding with the platelet nadir, despite clinical improvement. Published reports have described circulating plasmablasts/plasma cells from day 2, peaking around day 6, and disappearing by day 12, mirroring thrombocytopenia.

Increased very high-fluorescence cell signal on the lymphocyte scattergram should prompt peripheral blood smear review to assess suspected plasmacytosis because high-fluorescence gating, although sensitive, is not definitive. In the appropriate context, circulating plasma cells with thrombocytopenia should raise suspicion of DENV rather than a plasma cell neoplasm. These cells' kinetics may represent a potential adjunctive, phase-related laboratory clue that requires prospective validation.

Head and neck squamous cell carcinomas (HNSCCs) remain a significant clinical challenge due to treatment resistance and therapy-associated toxicity. Here, we evaluate the therapeutic potential and mechanism of action of AOH1996, a first-in-class small molecule that targets a cancer-associated isoform of proliferating cell nuclear antigen (caPCNA). Across HPV-positive and HPV-negative HNSCC models, AOH1996 induces robust cytotoxicity associated with mitotic arrest, multipolar mitosis, failed cytokinesis, cell-cell fusion, and DNA damage. Live-cell imaging reveals widespread mitotic catastrophe with limited successful mitotic progression. Notably, AOH1996 sensitivity correlates with c-Myc abundance, suggesting a potential biomarker of response. In vivo, AOH1996 suppresses tumor growth with minimal toxicity in xenograft models. Together, these findings establish AOH1996 as a promising therapeutic candidate that disrupts mitotic fidelity and induces cancer-selective cytotoxicity in HNSCC.

To determine whether prototype integrated slice-specific shimming (iShim) diffusion-weighted imaging (DWI) combined with Boost diffusion sampling improves image quality and diagnostic performance for focal liver lesions compared with conventional DWI and alternative iShim sampling schemes.

Eighty-five patients with focal liver lesions underwent 3T MRI with conventional DWI and iShim-DWI using Boost, flow-compensated (FC), monopolar (Mono), FC with five lobes (FC5), and stimulated echo acquisition mode (Steam) sampling at b-values of 0 and 1000 s/mm². Two radiologists independently scored six image-quality features. Signal-to-noise ratio (SNR), contrast-to-noise ratio (CNR), and apparent diffusion coefficient (ADC) were measured. Interreader agreement, between-sequence differences, ADC correlations and agreement, and diagnostic performance for differentiating benign from malignant lesions were assessed.

Boost iShim-DWI yielded significantly better artifact, diagnostic-confidence, and total-image-quality scores than all other sequences (p < 0.05) and achieved the highest lesion SNR, liver SNR, and CNR (p < 0.05). Interreader agreement was excellent (ICC = 0.839-0.953). ADC values correlated strongly across sequences (rₛ = 0.812-0.961, p < 0.001). Boost iShim-DWI achieved the highest diagnostic performance (AUC = 0.942; 95% CI 0.897-0.988). Discussion: Boost iShim-DWI improves liver DWI image quality while preserving ADC comparability and may enhance differentiation of benign and malignant focal liver lesions.

Gastrointestinal stromal tumors (GISTs), the most common mesenchymal neoplasms of the gastrointestinal tract, are molecularly heterogeneous diseases rather than a single entity. Activating mutations in KIT and PDGFRA define the dominant biological dependencies and establish tyrosine kinase inhibition as a therapeutic backbone. Imatinib, followed by later-line tyrosine kinase inhibitors, including sunitinib, regorafenib, ripretinib, and genotype-selected avapritinib, have substantially prolonged survival. However, durable disease control remains limited by clonal evolution, most notably, polyclonal secondary KIT mutations and lesion-to-lesion molecular heterogeneity. Molecular profiling using serial tissue and circulating tumor DNA analyses may improve precision care by identifying spatially and temporally evolving resistance mechanisms and guiding mutation-matched treatment selection. In this review, we summarize the biological and molecular landscape of advanced GIST, as well as the current therapeutic strategies and major mechanisms of resistance. Finally, we highlight promising therapeutic strategies supported by preclinical and clinical evidence that may advance subtype-informed precision medicine.

NTRK-rearranged spindle cell neoplasm is a rare lesion in the uterus (including the cervix), with more than 60 tumors reported in the literature so far. Most of them are characterized by fascicles of spindle cells in herringbone pattern with entrapment of endocervical glands. We report an additional tumor occurring in the uterine cervix of a 43-year-old Chinese woman, which demonstrated unusual morphologic features in addition to the conventional fibrosarcoma-like spindle cell proliferation. These included areas of neural-like whorls, as well as nuclear palisading that resembled a schwannoma. Focal myxoid stroma with loose clusters of rhabdoid cells was also identified. The nuclear grade was intermediate to severe and geographic necrosis was identified. Immunohistochemistry showed diffuse positivity for pan-TRK with patchy CD34 and focal S100 expression. Molecular analysis revealed the presence of TPM3::NTRK1 fusion with CDKN2A/B homozygous deletion and low mutational burden. Our case report and literature review highlight the diverse morphological appearance of this tumor. Specifically, nuclear palisading and rhabdoid cells are rarely reported in uterine NTRK-rearranged spindle cell neoplasm. As more clinical and molecular data become available, the clinicopathological features of this entity can be further characterized.

Primary large cell neuroendocrine carcinoma (LCNEC) of the bladder is an extremely rare and highly aggressive malignancy with a poor prognosis, bringing major challenges to clinical diagnosis and treatment. We report the case of a 77-year-old man who presented with recurrent gross hematuria for more than 8 months, accompanied by urinary frequency, urinary urgency, and lumbosacral pain. Imaging revealed a large soft-tissue mass on the posterior bladder wall without pathognomonic imaging findings. Urine exfoliative cytology revealed atypical tumor cells with large cellular size, high nucleocytoplasmic ratio, scant cytoplasm, and marked nuclear atypia. Given the advanced age and multiple underlying comorbidities, the patient underwent transurethral resection of the bladder tumor. Histopathologically, the tumor was arranged in diffuse sheets with organoid architecture, composed of large polygonal cells with prominent atypia, active mitosis, focal necrosis, and intravascular tumor thrombi. Immunohistochemically, CK-Pan showed a paranuclear punctate expression pattern; neuroendocrine markers INSM1, Syn, and CD56 were diffusely positive; Ki-67 showed a high proliferation index; and P53 displayed diffuse strong expression. The final diagnosis of primary bladder LCNEC was confirmed by integrated morphological and immunohistochemical findings, with preoperative contrast-enhanced CT defining an advanced clinical stage of cT3N0M0 (American Joint Committee on Cancer, AJCC 8th edition). The patient received postoperative adjuvant chemotherapy, and tumor recurrence was identified at the 3-month follow-up with a stable general condition during the observational period. This case indicates that bladder LCNEC lacks specific clinical and imaging manifestations. Urine exfoliative cytology is a valuable non-invasive ancillary tool for detecting high-grade malignant cells in the urinary tract, whereas combining histopathology and immunohistochemistry remains the gold standard for definitive diagnosis. Surgical resection combined with individualized chemotherapy constitutes the main therapeutic regimen, and close long-term follow-up is indispensable for this highly aggressive tumor. Further clinical studies are required to optimize therapeutic strategies and improve patient prognosis.