Oncolysis

Oncolysis refers to the destruction or lysis of cancer cells. In oncology, the term can describe cell death that occurs as a direct result of therapy, or spontaneous tumor cell death driven by immune responses or intrinsic tumor vulnerability. Lysis of tumor cells can occur through necrosis, apoptosis, autophagy, or other forms of programmed cell death, and may lead to tumor shrinkage or local control of disease. Oncolysis can be facilitated by a range of agents and strategies, including oncolytic virotherapy, targeted drugs, immune-mediated cytotoxicity, and combinations thereof.

A central area within oncolysis is oncolytic virotherapy, which uses replication-competent viruses designed to preferentially infect and lyse cancer cells. These viruses exploit defects in antiviral defenses that are common in tumor cells, leading to selective replication, cell rupture, and release of tumor antigens. The resulting local inflammation can stimulate systemic anti-tumor immunity, potentially addressing untreated tumor sites. Some oncolytic viruses are engineered to express immune-stimulating or anti-tumor molecules to enhance this effect. Oncolytic viruses can be used alone or in combination with other therapies, such as immune checkpoint inhibitors, to bolster anti-tumor responses.

Clinical development of oncolysis includes several virotherapy candidates and related approaches. The most widely known approved agent is talimogene laherparepvec (T-VEC), an engineered herpes simplex virus approved for melanoma. Other candidates have reached various stages of clinical testing and carry potential for use against multiple cancer types. Limitations of oncolysis include host antiviral immunity reducing efficacy, uneven distribution within solid tumors, and safety considerations for viral therapies. Research continues to optimize selectivity, delivery, and combination strategies.