In cancer immunology, tumors are often classified as ´hot´ or ´cold´, reflecting their immune landscape.  
 
Hot tumors are inflamed, characterized by high levels of cytotoxic T cell infiltration, presence of pro-inflammatory cytokines, and expression of immune checkpoints such as PD-L1. These tumors tend to respond better to immunotherapies like checkpoint inhibitors, CAR-T cells, or BiTEs [1]. 
 
Cold tumors are immune-excluded. They exhibit low T cell infiltration, dense stromal barriers, immunosuppressive myeloid populations, and metabolic conditions that inhibit immune cell function. Because of these they are resistant to many standard immunotherapies, being challenging for treatment in clinical oncology [2]. 
 
Practical application of this terminology is complex. The molecular and cellular determinants that define a tumor as hot or cold are often heterogeneous even within the same patient. For example, one lesion may be inflamed while another remains immune-excluded, complicating treatment strategies. 
 
Strategies to Heat up Cold Tumors
Oncolytic viruses are one promising approach, since they can induce local inflammation, attract T cells, and reshape the tumor microenvironment to make it more permissive for immune attack. Combination therapies using checkpoint inhibitors, CAR-T cells, BiTEs, or targeted therapies are also being explored to overcome immune exclusion [3]. 
 
Speculative Hypothesis:
Could spatially controlled delivery of immunostimulatory agents or engineered CAR-T cells equipped with biosensors selectively ´ignite´ cold tumor regions? 
 
Question for the Audience: Have you ever tried converting cold into hot tumor? 
 
Stay tuned for 𝗗𝗮𝘆 𝟴𝟰: 𝗩𝗶𝗿𝘂𝘀𝗲𝘀 𝗮𝘀 𝗩𝗲𝗰𝘁𝗼𝗿𝘀: Harnessing Viral Platforms for Gene Delivery in Immunology 
 
References:
1. DOI: 10.1016/j.immuni.2013.07.012 
2. DOI: 10.1038/s41591-018-0014-x 
3. DOI: 10.1038/nbt.2287 
 
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