Germline variants alter immune surveillance

• 成果类型: Editorial Material
• 署名作者: Waddell, Nicola; Addala, Venkateswar
• 署名单位: QIMR Berghofer Medical Research Institute
• 刊物名称: SCIENCE
• ISSN/ISSBN: 0036-13244
• DOI: 10.1126/science.adp7370
• 发表日期: 2024-05-31
• 页码: 961-962
• 关键词: mutational processes; association; landscape; diversity; cancers; RISK

摘要

The formation of tumors is complex and multifaceted, involving cancer cell-intrinsic and -extrinsic factors. An important influence on tumorigenesis is the immune system, by which immune surveillance (and subsequent elimination) provides a selective pressure that causes the evolution of tumor cells to evade detection (immunoediting). Cancer immunoediting involves three phases: immunosurveillance to eliminate tumor cells; the coexistence of tumor and immune cells through equilibrium; and immune evasion, in which tumor cells escape immune control ( 1 ). Tumor-specific neoantigens, formed as a result of somatic mutations that arise in cancer cells ( 2 ), are an important component of immunosurveillance because they can determine the immunogenicity of a cell and thus whether it is recognized by T cells to elicit an immune response. On page 975 of this issue, Houlahan et al. ( 3 ) report that epitopes derived from germline variants contribute to human breast cancer formation by modulating immunoediting.