Cancer immunotherapy is a group of treatments that help the immune system recognize and attack cancer. Rather than constituting a single drug or procedure, it includes therapies that remove inhibitory immune signals, supply cancer-fighting immune cells, direct immune activity toward tumors, or stimulate responses to tumor-associated targets. These approaches differ substantially in their mechanisms, clinical uses, and adverse effects. Immunotherapy can produce lasting responses in some patients, but effectiveness varies between cancers and between individuals. (cancer.gov)
Biological basis
Immune cells can detect and destroy abnormal cells, yet cancers can develop ways to escape this activity. Tumor-associated antigens provide targets for immune recognition. Cancer cells may become less visible through genetic changes, display inhibitory proteins on their surfaces, or alter surrounding cells so that they suppress immune responses. The presence of immune cells within a tumor therefore does not necessarily mean that those cells can control its growth. (cancer.gov)
Many immunotherapies act through T cells, which can attack cancer cells. Treatment may strengthen existing T-cell activity or introduce cells selected or modified outside the body. Other approaches use antibodies or immune signaling molecules. These mechanisms explain why immunotherapy is more specific than the general idea of “boosting immunity”: different treatments intervene in particular recognition, signaling, or cell-killing processes. (cancer.gov)
Immune checkpoint inhibitors
An immune checkpoint is a regulatory mechanism that limits immune activity and helps prevent excessive responses. Tumors can exploit inhibitory checkpoint pathways to evade attack. Checkpoint inhibitors block selected components of these pathways, allowing immune cells to respond more strongly against cancer. Important targets include CTLA-4, PD-1, and PD-L1, a protein that interacts with PD-1. These drugs generally act by modifying immune regulation rather than directly poisoning cancer cells. (cancer.gov)
Checkpoint inhibitors are used in defined treatment settings across numerous cancers, including melanoma, lung cancer, bladder cancer, and Hodgkin lymphoma. Their use depends on the particular drug, cancer characteristics, and clinical setting; approval for one indication does not establish effectiveness for every cancer. Blocking immune inhibition can also permit immune responses against healthy tissues, accounting for characteristic inflammatory toxicities. (cancer.gov)
Cellular therapies
Adoptive cell therapy involves collecting immune cells, expanding or modifying them in a laboratory, and administering them to a patient. Tumor-infiltrating lymphocyte therapy uses immune cells recovered from a tumor. Cells with antitumor activity are expanded into larger numbers before infusion. Treatment commonly includes preparatory therapy, and some protocols also administer immune-stimulating agents. (cancer.gov)
CAR T-cell therapy genetically modifies T cells to express chimeric antigen receptors that recognize selected targets on cancer cells. Approved applications include particular forms of leukemia, lymphoma, and multiple myeloma. These treatments are individualized cellular products rather than conventional drugs manufactured identically for every recipient. Their production requires cell collection, laboratory processing, and subsequent infusion. (cancer.gov)
Cellular immunotherapy also has applications beyond blood cancers. On February 16, 2024, the United States Food and Drug Administration granted accelerated approval to lifileucel, a tumor-derived T-cell therapy, for specified adults with previously treated unresectable or metastatic melanoma. That approval was based on tumor response evidence and required confirmation of clinical benefit. (fda.gov)
Antibodies, vaccines, and immune modulators
Monoclonal antibodies are laboratory-produced antibodies designed to bind particular molecular targets. Some mark cancer cells for immune destruction. Antibody-based treatments have varied mechanisms, however, and not every therapeutic antibody is classified as immunotherapy simply because it is an antibody. The relevant distinction is whether its anticancer action involves an immune response. (cancer.gov)
Therapeutic cancer vaccines stimulate immune recognition of an existing cancer, unlike preventive vaccines directed against cancer-causing infections. Sipuleucel-T is a cellular treatment vaccine used for certain patients with advanced prostate cancer. Oncolytic virus therapy uses viruses that replicate within and destroy cancer cells while also promoting immune responses. Talimogene laherparepvec, or T-VEC, is injected into tumors and is used in specified melanoma settings. (cancer.gov)
Immune modulators include cytokines such as interleukin-2 and interferon alfa. These signaling molecules can increase the activity or number of immune cells involved in antitumor responses. BCG, a preparation of weakened bacteria, is another form of immunotherapy: administration directly into the bladder stimulates an immune response against bladder cancer cells. (cancer.gov)
Response, biomarkers, and resistance
Immunotherapy does not benefit all patients. Some tumors fail to respond initially, while others progress after an earlier response. Resistance can involve poor immune recognition, inhibitory signals, or suppressive conditions around the tumor. Research evaluates combinations of immunotherapies and their integration with other treatment approaches to address these barriers. (cancer.gov)
A biomarker can help characterize a cancer and inform the use of particular treatments. Relevant checkpoint-inhibitor biomarkers include PD-L1 expression, tumor mutational burden—the number of genetic changes in tumor DNA—and deficiency in DNA mismatch repair. Their predictive value is incomplete: a favorable marker does not guarantee response, and its significance depends on the cancer and treatment being considered. (cancer.gov)
Adverse effects
Checkpoint inhibitors can cause inflammation in healthy organs, including the skin, bowel, liver, lungs, and endocrine glands. Immune-related adverse effects may begin during treatment or after it has ended and can occasionally be severe or fatal. Their frequency and severity vary by treatment and patient. (cancer.gov)
Cellular therapies have a different toxicity profile. Cytokine release syndrome results from rapid immune signaling and can produce fever, low blood pressure, and other systemic symptoms. CAR T-cell treatment can also cause neurological effects, including confusion and difficulty communicating. Treatment vaccines and immune modulators may cause flu-like symptoms, infusion reactions, or treatment-specific complications; immunotherapy is therefore not inherently free of serious toxicity. (cancer.gov)