The tumor microenvironment (TME) is essential for the regulation of tumor progression, immune responses, and therapeutic outcomes. The importance of the tumor microbiome, a complex ecosystem of microorganisms that reside within the TME, in shaping tumor dynamics and modulating treatment responses has been underscored by recent advancements in cancer research. Oncolytic viruses (OVs) have been recognized as promising treatment options in cancer immunotherapy due to their ability to selectively target and eliminate tumor cells while protecting normal tissue. Recent preclinical studies suggest a bidirectional relationship between OVs and the microbiome, although direct evidence that OVs remodel tumor-resident microbial communities remains limited. Most available data concern the gut microbiome, where OV treatment has been associated with changes in microbial composition, while baseline or experimentally manipulated microbiota can, in turn, influence virotherapy efficacy. This review examines these emerging interactions, distinguishes direct experimental evidence from proposed mechanisms, and discusses how microbiome-informed strategies may complement OV-based immunotherapy. We also highlight the scarcity of longitudinal intratumoral and clinical microbiome data and identify the experimental steps required to establish causality.

Bone metastasis remains a major determinant of disability, treatment failure, and poor survival in solid tumors. It is no longer adequately explained as a late consequence of tumor spread or as a process driven only by osteoclast-mediated bone destruction. Current evidence supports a broader view in which bone metastasis emerges through progressive remodeling of a receptive niche, followed by selective tumor cell seeding, adaptive persistence, and eventual outgrowth under continued pressure from both local and systemic cues. In this framework, bone is not merely a target organ but an active biological system in which remodeling, hematopoiesis, immunity, and stromal signaling jointly shape metastatic fate. This perspective also helps explain why conventional management, although effective in reducing skeletal complications and relieving symptoms, rarely changes the long-term course of disease. In this review, we discuss how recent advances have redefined the biology of bone metastasis, from early niche conditioning to overt lesion progression, and examine how these insights are reshaping diagnosis and therapy. We further highlight the translational shift from lesion detection and antiresorptive treatment toward risk prediction, biological stratification, and mechanism-guided combination strategies. A more integrated understanding of tumor evolution within bone may provide the basis for earlier intervention and more durable disease control.

Abiraterone is a first-line therapy for metastatic castrate-resistant prostate cancer. In vitro, abiraterone metabolites inhibit OATP1B1, the primary hepatic uptake transporter for several substrates, including statins. We describe the case of a 70-year-old man taking rosuvastatin who commenced treatment with abiraterone for metastatic castrate-resistant prostate cancer. Two months later, he presented to hospital with nonspecific symptoms including fatigue and diffuse myalgias with laboratory evidence of rhabdomyolysis and associated acute kidney injury. Plasma rosuvastatin concentrations were more than 40-fold higher than expected for the dose. Subsequent pharmacogenetic testing showed the patient was heterozygous for SLCO1B1*15, a variant of the SLCO1B1 gene encoding OATP1B1, which results in moderately reduced OATP1B1 transport activity. Considering the high frequency of statin prescribing, clinicians should be aware of the possible drug-drug interactions between statins and abiraterone and the associated risk of rhabdomyolysis, which is also affected by genetic differences.

Natural killer (NK) cells constitute the first line of human immune defense. They have attracted extensive research in the field of tumor immunity owing to their potent cytotoxicity, robust cytokine secretion, and immunomodulatory capacity. However, chronic tumor antigen exposure would induce exhaustion in NK cells (NK-ex). This study leverages public single-cell RNA sequencing datasets of NK cells to identify NK-ex subsets and map a transcriptional continuum derived from computational trajectory ordering. Our investigation revealed that NK3 exhibited more exhaustion features compared to other NK subsets in tumor patients. lymphocyte-activation gene 3 (LAG-3) expression is relatively specific enriched in the NK-ex subpopulation. Clinical analyses infer that functionally dominant NK-ex subsets are strongly correlated with responses to immune checkpoint blockade (ICB) therapy, and phenotypic shifts toward exhaustion can be observed post-treatment. This study preliminarily characterizes NK-ex subpopulations and suggests that LAG-3 may participate in regulating the progression of NK cell exhaustion, which could offer potential theoretical references for developing immunotherapeutic strategies targeting NK-ex cells.

Effective oncology communication depends on both patients' and clinicians' capacity to recognize and convey emotional information. Alexithymia has predominantly been studied as an individual trait. This Letter proposes dual alexithymia - an emergent interactional state arising when emotional awareness is constrained on both sides of the clinical encounter - and argues that it may disrupt the compensatory scaffolding available in single-sided dyads, producing a communication breakdown that neither party readily registers. The construct is distinguished from burnout, empathy deficits and other competing explanations, situated against existing dyadic alexithymia research, and translated into falsifiable predictions, a concise measurement strategy, and a hypothesized structural role for a third detecting node such as oncology nursing.

SPIB (Spi-B transcription factor), an ETS family transcription factor predominantly expressed in immune cells, plays a critical role in regulating tumor cell proliferation, apoptosis, migration, and invasion. Aberrant SPIB expression has been reported across diverse cancers; in some contexts, elevated SPIB promotes tumor progression and drug resistance, whereas in others, reduced SPIB expression is associated with poor patient survival. This review synthesizes current evidence on the dual role of SPIB as both a tumor promoter and suppressor, highlighting its underlying molecular mechanisms and signaling pathways across cancer types. By systematically evaluating SPIB expression patterns and functional roles across different cancer types, this review provides a conceptual framework for future studies exploring the potential clinical relevance of SPIB and may facilitate future translational research.

In recent years, the mechanisms of abnormal metabolite accumulation in tumor development have become an emerging research field. Cells within the tumor microenvironment (TME) sustain tumor proliferation via metaboalic reprogramming. Such metabolic remodeling triggers aberrant oncometabolite accumulation, which drives tumor progression, distant metastasis and therapeutic resistance through the modulation of tumor cell proliferation, angiogenesis and immune evasion. Notably, fumarate and itaconate, originating from different subcellular localizations, modulate protein function primarily covalent or non-covalent interactions. Functionally, the modified target proteins can be roughly divided into four categories that drive tumor progression: key metabolic enzymes, epigenetic regulators, immune-related molecules and resistance-associated proteins, which respectively modulate metabolic rewiring, epigenetic reprogramming, the immunosuppressive microenvironment and therapeutic resistance. Herein, we systematically summarize the oncogenic mechanisms of these two oncometabolites, propose viable strategies to address technical hurdles in studying non-enzymatic protein modifications and offer new directions for the clinical treatment of tumors through targeted inhibition of fumarate and itaconate.

Tumour immunotherapy has reshaped the landscape of oncology by translating fundamental insights from immunosurveillance, immunoediting, and checkpoint biology into effective clinical strategies. This review traces the historical trajectory of tumour immunotherapy, from the early observations of William Coley to the development of modern immune checkpoint inhibitors (ICIs) targeting cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) and programmed cell death protein 1/ligand 1 (PD-1/PD-L1). Moreover, a comprehensive analysis of the progress of immunotherapy across different tumour types is provided. In solid tumours, significant benefits have been achieved in ``inflamed'' or ``hot'' cancers like melanoma, non-small-cell lung cancer, and renal cell carcinoma. However, formidable hurdles remain in ``non-inflamed'' or ``cold'' tumours such as pancreatic ductal adenocarcinoma, glioblastoma, and microsatellite-stable colorectal cancer. In hematologic malignancies, living drugs and redirecting immunotherapies have demonstrated profound efficacy: CAR-T therapy has achieved durable remissions in B-cell acute lymphoblastic leukemia (B-ALL) and diffuse large B-cell lymphoma (DLBCL), while T-cell engagers offer a rapid, ``off-the-shelf'' option for multiple myeloma. Collectively, this review synthesizes these developments into a practical framework based on tumour immune context, offering a guide for optimizing current treatments and directing future research to overcome resistance and benefit more patients.

Single-cell sequencing (SCS) technologies have revolutionized cancer research by overcoming the critical limitations of bulk sequencing, enabling unprecedented resolution in deciphering intratumoral heterogeneity and the tumor microenvironment (TME). Unlike bulk approaches that average molecular signals across cell populations, SCS resolves rare subpopulations-such as pre-existing therapy-resistant clones and cancer stem cells-and reconstructs clonal evolutionary trajectories driving metastasis and treatment resistance. By profiling individual cells, SCS reveals dynamic cellular interactions, functional states, and spatial architectures within the TME, including immune-stromal crosstalk and transcriptional plasticity. Applied pan-cancer, SCS uncovers conserved molecular programs that transcend tissue origin, such as universal T-cell exhaustion signatures, recurrent stromal reprogramming, and fundamental pathways like epithelial-mesenchymal transition and angiogenesis. Technological advancements in scalability, cost-effectiveness, and spatial multi-omics integration now enable high-resolution mapping of tumor ecosystems. Large-scale initiatives like the Human Cell Atlas and CancerSCEM harmonize datasets, revealing both universal mechanisms and tissue-specific adaptations. Clinically, SCS enhances diagnostic sensitivity and enables precision prognostication through cellular biomarkers. It informs novel therapeutic strategies, such as targeting specific TME components or optimizing immunotherapy response. Emerging artificial intelligence (AI) tools further amplify SCS's impact by integrating multi-omic data to predict drug responses and resistance mechanisms. Despite challenges in standardization and cost, the future convergence of SCS, spatial technologies, and AI-driven modeling positions SCS as a cornerstone of precision oncology. This review systematically summarizes the advances of SCS technologies and their transformative applications in pan-cancer research and clinical translation.

Small cell carcinoma (SCC) of the anal canal is a rare and highly aggressive neuroendocrine malignancy, and its infrequency has limited the development of evidence-based treatment approaches. As a result, management of extrapulmonary SCC (EPSCC) is often extrapolated from small cell lung cancer (SCLC), given the similar disease biology and the lack of formal approval for many SCLC-directed agents. We report the case of a 60-year-old woman who presented with metastatic SCC of the anal canal and whose disease course illustrates both the challenges and therapeutic uncertainties inherent in treating this diagnosis. Given the absence of established standards, she was treated with SCLC-based regimens and achieved a partial radiographic and clinical response to platinum-based chemotherapy in combination with the immune checkpoint inhibitor atezolizumab. Upon subsequent progression, she was treated with lurbinectedin and tarlatamab, a bispecific T-cell engager targeting delta-like ligand 3 (DLL3), reflecting evolving treatment paradigms in SCLC. Her response suggests that novel therapies developed for pulmonary small cell disease may offer benefit in select extrapulmonary cases. This case highlights the need for continued reporting of clinical experiences and prospective investigation to better define the role of emerging therapies in rare and aggressive extrapulmonary neuroendocrine malignancies.