Immuno-Oncology and Tumour Metabolism
Anti-tumour immunity depends on antigen generation, presentation, immune-cell access and effective killing. Tumour metabolism intersects with every stage by shaping oxygen, nutrients and suppressive metabolites in the microenvironment.
Quick answer
No single immune or metabolic biomarker describes the whole tumour ecosystem. A useful interpretation connects tumour-intrinsic changes, immune-cell state, spatial context and the exact assay rather than treating one score as a universal answer.
How the cluster fits together
Key gene profiles
Immuno-oncology and metabolism library
Trace the path from tumour antigens to immune escape, microenvironmental suppression and metabolic vulnerabilities.
Neoantigens and Tumour Immunogenicity
How tumour mutations create new peptides the immune system can recognise, why only a fraction become effective targets, and how this links to mutational burden and treatment response.
3 min readB2M and MHC Class I Loss: Hiding From T Cells
How loss of beta-2-microglobulin or other antigen-presentation components lets tumours evade CD8 T cells, and why it is a recognised mechanism of checkpoint-inhibitor resistance.
3 min readJAK1/JAK2 Loss and Interferon-Signalling Resistance to Immunotherapy
How loss-of-function mutations in JAK1 or JAK2 make tumour cells unresponsive to interferon gamma, and why this is a mechanism of primary and acquired checkpoint-inhibitor resistance.
3 min readHLA Loss of Heterozygosity: Losing Half the Presentation Repertoire
How tumours delete one parental copy of the HLA locus to narrow which antigens they can present, how it is detected, and why it matters for immunotherapy and neoantigen prediction.
3 min readHot Versus Cold Tumours: What T-Cell Infiltration Means
What makes a tumour immunologically hot or cold, how infiltration patterns relate to checkpoint-inhibitor response, and why the label is a simplification of a spectrum.
3 min readLAG-3, TIM-3 and TIGIT: Checkpoints Beyond PD-1 and CTLA-4
How the next-generation inhibitory receptors LAG-3, TIM-3 and TIGIT contribute to T-cell exhaustion, and where blocking them has and has not shown benefit.
3 min readCTLA-4 Versus PD-1 Blockade: Different Brakes, Different Effects
How CTLA-4 and PD-1 inhibitors act at different stages of the T-cell response, why the combination is more active and more toxic, and what that means clinically.
3 min readTumour-Infiltrating Lymphocytes: Prognosis and Prediction
What tumour-infiltrating lymphocytes are, how they are scored in pathology, why they carry prognostic weight in several cancers, and the difference between prognostic and predictive value.
3 min readImmune-Related Adverse Events: When the Immune System Overshoots
Why checkpoint inhibitors cause inflammatory side effects in healthy organs, which organs are most often affected, and the general principles of recognition and management.
3 min readCAR T-Cell Therapy: Targets, Response Markers and Escape
How chimeric antigen receptor T cells are engineered to recognise a surface target, what predicts response and toxicity, and how tumours escape through antigen loss.
3 min readThe Warburg Effect: Why Cancer Cells Ferment Glucose
Why many tumours take up large amounts of glucose and produce lactate even with oxygen available, what this supports biosynthetically, and how it underlies FDG-PET imaging.
3 min readGlutamine Metabolism in Cancer
Why many tumours consume large amounts of glutamine, how it feeds the TCA cycle and biosynthesis, and the status of glutaminase inhibitors.
3 min readMTAP Deletion and PRMT5: A Metabolic Synthetic Lethality
How co-deletion of MTAP with CDKN2A creates a targetable dependence on the arginine methyltransferase PRMT5, and how MTA-cooperative inhibitors exploit it.
3 min readThe Adenosine Pathway: CD39, CD73 and A2A Receptors
How tumours convert ATP into immunosuppressive adenosine through CD39 and CD73, how the A2A receptor dampens T and NK cells, and where inhibitors stand.
3 min readThe Tumour Microenvironment: More Than Cancer Cells
An overview of the non-cancer cells and structures that surround a tumour, how they support or restrain growth, and why they influence treatment response.
3 min readFrequently asked questions
Does a high neoantigen burden guarantee immunotherapy response?
No. Antigen presentation, T-cell access, checkpoint state and other tumour and host factors can still limit an immune response.
What makes a tumour hot or cold?
The terms summarise immune context, especially T-cell infiltration and inflammatory signalling, but definitions and assays vary across studies and tumour types.
Why is metabolism relevant to tumour immunity?
Cancer and immune cells compete for nutrients, while hypoxia and metabolites such as adenosine can reshape immune-cell function in the tumour microenvironment.