To synthesize current evidence on ketamine for cancer-related pain and its intersecting psychiatric, anti-tumor, and immunomodulatory actions, emphasizing mechanisms, clinical relevance, and uncertainties relevant to oncology. Ketamine provides analgesia primarily through non-competitive antagonism of N-methyl-D-aspartate receptors and additional effects on excitatory, inhibitory, and opioid-related signaling. In patients with refractory cancer pain, it may be a useful adjunct to opioid-based multimodal analgesia and may reduce opioid requirements; however, clinical evidence remains limited and heterogeneous. Its rapid antidepressant effects may be relevant to the reciprocal burden of pain and depressive symptoms in cancer. Preclinical studies report antiproliferative, pro-apoptotic, and ferroptosis-associated effects across several tumor models, involving phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin, extracellular signal-regulated kinase, and non-coding RNA-associated pathways. These findings are not uniform: breast cancer models have suggested potentially pro-metastatic effects. Immune effects are likewise dose-, context-, and perioperative-setting dependent, with reports of anti-inflammatory, immunosuppressive, and neutral effects. Ketamine is a potentially valuable opioid-sparing adjunct for selected patients with cancer-related pain and may also address comorbid depressive symptoms. Its putative direct anti-tumor and immunomodulatory actions remain predominantly preclinical and context dependent and should not currently guide oncologic treatment decisions. Appropriately powered clinical studies should define patient selection, dose and route, duration, safety, immune consequences, and long-term oncologic outcomes. Ketamine alleviates both cancer pain and cancer pain-related depression (CPD). NMDAR antagonism and neuroplasticity drive rapid analgesic and antidepressant effects. Ketamine provides a substantial opioid-sparing effect for advanced cancer patients. Ketamine modulates oncogenic signaling pathways, including PI3K/Akt and MAPK/ERK. Ketamine acts on multiple targets involved in pain, mood, immunity, and cancer.
Glioblastoma is the most aggressive and fatal primary malignant brain tumour in adults, characterised by extensive intra-tumour heterogeneity, diffuse infiltration into surrounding brain tissue. Despite advances in surgery, radiotherapy, and chemotherapy, patient prognosis remains poor, underscoring the critical need for improved biological insight to guide precision medicine potential strategies. Although traditional bulk genomic and transcriptomic analyses have made a substantial contribution to understanding glioblastoma pathophysiology, such average molecular signals across cell populations obscures tumour microenvironment influence and clinically significant cellular states. Recent advances in single-cell and spatial omics technologies have revolutionised glioblastoma research by enabling high-resolution analysis of tumour composition, cellular plasticity, and spatial organisation. These modalities have revealed that glioblastoma is composed of dynamic and plastic cellular states as opposed to fixed molecular subtypes, including stem-like and therapy-resistant populations that contribute to recurrence. The tumour architecture is preserved by spatially resolved transcriptomic and proteomic approaches, which reveal regional transcriptional programmes influenced by the tumour ecosystem. The findings provide a more resolved view of glioblastoma evolution and treatment resistance, challenging current classification systems. However, significant challenges remain in integrating these high-dimensional datasets, managing technical and computational demands, and translating these approaches into clinically scalable workflows which collectively hinder their translational adoption. This review aims to synthesise recent advances in glioblastoma single-cell and spatial omics, critically evaluating both advantages and limitations in understanding tumour heterogeneity and tumour microenvironmental interactions. Furthermore, it assesses the current challenges of glioblastoma precision medicine and evaluates the potential of these technologies to advance such approaches.
This review evaluates the evolving landscape of cardiovascular toxicities associated with two pillars of modern cancer treatment: immune checkpoint inhibitors (ICIs) and chimeric antigen receptor T-cell (CAR-T) therapy. It examines their distinct immune-mediated pathophysiologies, clinical manifestations, and management frameworks. While ICIs carry a clinical trial incidence for cardiotoxicity of approximately 1
Biliary tract cancer (BTC) is a heterogeneous group of malignancies with limited systemic treatment options and poor prognosis. While immunochemotherapy has become the first-line standard, second-line therapy remains inadequate. Antibody–drug conjugates (ADCs) have emerged as a promising therapeutic modality leveraging antigen-specific targeting to deliver potent cytotoxic payloads. This review provides a comprehensive, multi-target appraisal of the ADC landscape in BTC. Trastuzumab deruxtecan (T-DXd), supported by DESTINY-PanTumor02 (ORR 22
