Immunotherapy Strategies in Advanced Melanoma
Summary
In recent years, immunotherapy has transformed the management of advanced melanoma by harnessing the patient’s own immune system to recognise and eliminate malignant cells. Key strategies include blockade of inhibitory receptors such as CTLA-4 and PD-1/PD-L1 to restore T-cell effector functions, as well as novel approaches involving cytokine therapy, oncolytic viruses and adoptive cell transfer. Combination regimens, notably dual immune checkpoint inhibitors, have delivered unprecedented response rates and durable remissions but carry an increased risk of immune-related adverse events. Concurrent development of biomarkers – for example, tumour mutational burden and inflammatory gene signatures – has improved patient stratification and informed personalised treatment selection. Ongoing research is refining the integration of immunotherapies into adjuvant and neoadjuvant settings, exploring resistance mechanisms within the tumour microenvironment, and investigating emerging targets such as LAG-3 and STING agonists. Globally, these advances are elevating survival benchmarks and expanding therapeutic options, while highlighting the importance of balancing efficacy with safety in order to optimise long-term outcomes.
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Immunotherapy Strategies in Advanced Melanoma publication trend
The graph below shows the total number of articles in immunotherapy strategies in advanced melanoma across all publications each year (not limited to Nature Index journals).
Technical terms
Immune checkpoint inhibitor: A monoclonal antibody that blocks inhibitory pathways (such as CTLA-4 or PD-1) to enhance T-cell mediated antitumour activity.
CTLA-4: Cytotoxic T-lymphocyte-associated protein 4, an inhibitory receptor on T cells that down-regulates immune responses.
PD-1: Programmed cell death 1, an inhibitory receptor on T cells that limits immune activation upon binding its ligand.
PD-L1: Programmed death-ligand 1, a protein expressed on tumour or immune cells that binds PD-1 to suppress T-cell function.
Tumour mutational burden (TMB): The total number of somatic mutations per coding area of a tumour genome, used as a biomarker of response to immune checkpoint blockade.
Oncolytic virus: A genetically engineered or naturally occurring virus that selectively infects and kills cancer cells, also promoting antitumour immunity.
References
- Long-Term Outcomes With Nivolumab Plus Ipilimumab or Nivolumab Alone Versus Ipilimumab in Patients With Advanced Melanoma. Journal of Clinical Oncology (2021).
- Potential Immune-Related Adverse Events Associated With Monotherapy and Combination Therapy of Ipilimumab, Nivolumab, and Pembrolizumab for Advanced Melanoma: A Systematic Review and Meta-Analysis. Frontiers in Oncology (2020).
- TMB and Inflammatory Gene Expression Associated with Clinical Outcomes following Immunotherapy in Advanced Melanoma. Cancer Immunology Research (2021).
- Immunotherapy in Melanoma: Recent Advances and Future Directions. Cancers (2023).
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