In this study, the induction of apoptosis and necrosis was examined in terms of temporal dose responses, comparing a malignant and nonmalignant breast cell line.

Key driver of cancer cell death pathway that activates immune cells uncovered and may fine-tune immunotherapies for cancer.

Tumor necrosis factor α-induced protein 3-interacting protein 1 (TNIP1) is a ubiquitin-binding protein that is widely expressed, but its function in breast cancer cells remains unknown.

When an individual suffers from cancer, the process of programmed cell death called apoptosis does not occur normally, permitting abnormal cells to thrive.

Cancer cells do not exist in the body for everyone. The human body is constantly in a cycle where new cells grow, divide, and die in a controlled manner, a process known as apoptosis.

The latest findings on the interaction between cell death and cellular senescence in cancer and their pathophysiological significance have been reviewed.

A University of Pennsylvania research team has shown that it can kill tumor cells in mice by necrosis, rather than by inducing apoptosis, by giving them alkylating agents that block their energy ...

Chemotherapy drugs can kill cancer cells by halting DNA replication, but a glucose-depleted environment can help cancer cells overcome this effect and resist death.

In this particular case, it turned on the apoptosis gene that BCL6 normally keeps turned off. By turning it back on, the researchers found that they could self-destruct cancer cells.

Scientists discovered a class of molecules that use endogenous proteins to modulate genetic pathways involved in cell death.

Cancer treatments aim to kill tumor cells, and the immune system is tasked with getting rid of the resulting cellular corpses.

Scientists have demonstrated a creative new way to kill cancer cells effectively, with few side effects. Gluing two particular proteins together tricks the tumors into destroying themselves.