Apoptosis is a physiological response in development and homeostasis of metazoans. Apoptosis is triggered during pathological events as a means to renew affected tissues and eliminate cancer cells. The immune system regulates the extrinsic pathway of apoptosis, where signals such as TNFα or displayed ligands on the surface of immune cells trigger signal cascades by death receptors present on targeted cells.

In the last 10 years, the marker “Human Epididymis protein 4 (HE4)” for the management of gynecological tumors has entered powerfully in the world literature. At the moment, carrying out an accurate research in the main scientific portals such as PubMed, we can find more than 2,000 works concerning Cancer antigen-125 (Ca125), but those concerning HE4 are less than 400.

Botulinum toxin (BT) is a potent poisonous neurotoxin produced by the bacterium Clostridium botulinum and related species [1]. Its action consists of inhibiting neuromuscular junctions by blocking the release of acetylcholine and desensitizing sensory nerves.

NOXA is a critical mediator of stress responses to anticancer drugs. This BH3-only protein sets the apoptotic threshold in cancer cells in response to chemotherapies by counteracting the prosurvival BCL-2 family protein MCL-1. A complex and dynamic network relying on both highly controlled gene transcription activity and protein degradation by proteasome, regulates cellular NOXA levels from low in steady state to rapidly enhanced upon stressful condition.

Neuropilins (NRPs) are a class of transmembrane glycoprotein co-receptors including Neuropilin 1 (NRP1) and Neuropilin 2 (NRP2). They are the co-receptors of different families of receptors, thus they are involved in many hallmarks of cancer.