Tumor cell radiosensitivity enhancement

“Tumor cell radiosensitivity enhancement” refers to a therapeutic strategy or pharmacological process rather than a specific molecular entity. The goal is to make tumor cells more susceptible to the damaging effects of ionizing radiation during cancer radiotherapy. This can be achieved by pharmacologically targeting various cellular pathways that repair radiation-induced DNA damage, control cell cycle progression, regulate cellular stress responses, or modulate apoptotic thresholds. Drugs used to enhance radiosensitivity may inhibit DNA repair proteins, abrogate cell cycle checkpoints, alter hypoxic stress responses, or block oncogenic survival pathways. No unique “tumor cell radiosensitivity enhancer” molecule or receptor exists; rather, the term describes a class of agents and interventions that modulate existing molecular targets to potentiate the effect of radiotherapy[1][2][5][6].

Abrogation of cell cycle checkpoints (G2 and S phase); Inhibition of DNA repair mechanisms (e.g., NHEJ, HR, Rad51); Induction of endoplasmic reticulum stress under hypoxic conditions; Modulation of oxidative stress pathways (e.g., glutathione synthesis); Targeted inhibition of pro-survival pathways (e.g., Hsp90 client proteins like ErbB2)