Synthetic Lethality and Its Use in Cancer Treatment: Parp Inhibitors (Essay Sample)

SYNTHETIC LETHALITY AND ITS USE IN CANCER TREATMENT: PARP INHIBITORS
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The different types and the overwhelming number of cancer cases across the globe have prompted scholars to pursue more effective therapies than traditional treatments. One approach that has demonstrated considerable progress is related to the use of PARP inhibitors. Essentially, PARP inhibitors such as Talazoparib, Olaparib and Rucaparib use a concept of synthetic lethality to kill tumour cells. According to Sebastian(2011) synthetic lethality occurs when a deficiency in one gene expression does not cause cell death while a collection of two or more deficiencies in gene expression leads to cell death. PARP inhibitors exploit this concept to eradicate tumour cells.
In detail, normal and cancer cells undergo constant DNA damage due to environmental hazards and other molecular toxics. Normal cells repair DNA damage through two pathways; (1)PARP which is primed for repairing single strands and ; (2) BCRA1/2 that repairs double strands  (Sebastian, 2011; Litton, et al., 2018). By contrast, a cancer cell with deficiencies in BCRA1 and BCRA2 gene expression only has the PARP pathway to repair DNA damage (Sebastian, 2011). Therefore, introducing PARP inhibitors such Talazoparib, Olaparib and Rucaparib make it impossible to repair DNA damage in tumour cells thus, leading to further damage ending in cell death  (Sebastian, 2011; Litton, et al., 2018). PARP inhibitors do not kill normal cells as they still have the BCRA1/2 pathways to repair DNA (Litton, et al., 2018).
One of the most common cancer therapies based on PARP inhibitors is