Enhancing radiosensitisation of BRCA2-proficient and BRCA2-deficient cell lines with hyperthermia and PARP1-i.

Poly(ADP-ribose)polymerase1 (PARP1) is an important enzyme in regulating DNA replication. Inhibition of PARP1 can lead to collapsed DNA forks which subsequently causes genomic instability, making DNA more susceptible in developing fatal DNA double strand breaks. PARP1-induced DNA damage is generally repaired by homologous recombination (HR), in which BRCA2 proteins are essential.

Enhancing synthetic lethality of PARP-inhibitor and cisplatin in BRCA-proficient tumour cells with hyperthermia.

Background: Poly-(ADP-ribose)-polymerase1 (PARP1) is involved in repair of DNA single strand breaks. PARP1-inhibitors (PARP1-i) cause an accumulation of DNA double strand breaks, which are generally repaired by homologous recombination (HR). Therefore, cancer cells harboring HR deficiencies are exceptionally sensitive to PARP1-i.

Augmentation of radiation-induced apoptosis by ellagic acid.

This study evaluates the potential of ellagic acid (EA) as an enhancer of radiation-induced apoptosis in cancer cells. HeLa cells treated with EA and gamma radiation showed increased superoxide generation, upregulated p53 protein expression, and decreased antioxidant enzymes. We also found that EA and radiation enhance capase-3 activity via oxidative stress, increased intracellular calcium levels, and phospholipase C and cause a drop in mitochondrial potential.