The Impact Of Traditional Chemotherapeutic Agents On Patients

In contrast to a decade ago, we’ve seen an explosion of new drugs and virtually all of these drugs are targeted therapies. The substantial increase in the transition of FDA approvals from standard chemotherapeutics to targeted therapies is also equally astounding (Martino et al., 2015). The traditional chemotherapeutic agents are simply not being developed with the same frequency by drug companies any more. While chemotherapeutics have had a real impact and in some diseases a dramatic impact, for most common solid tumours, these impacts have been minimal. Moreover, standard chemotherapy often results in collateral damage to healthy cells causing unwanted side effects while targeted therapies are associated with fewer and less toxic side†¦show more content†¦This chromosome abnormality involved the exchange of genetic information between ABL gene on chromosome 9 and BCR gene on chromosome 22. What was remarkable about this was that 95% of patients with CML had this chr omosomal abnormality (ROWLEY, 1973). Subsequent research showed that in a CML cancer cell, the fusion protein BRC-ABL functions as a constitutively activated intracellular tyrosine kinase that binds to ATP and transfers a phosphate group to its target substrate protein. The target substrate protein then becomes phosphorylated and progresses to stimulate cell growth of the leukaemia cells (Lugo et al., 1990). The drug, Gleevac mimics ATP so it binds to the site within the BRC-ABL that’s normally bound by ATP, preventing it from binding. It thereby prevents phosphorylation of the substrate target protein and prevents cancer cell growth (Deininger, Buchdunger and Druker, 2005). Based on the 1998-2000 clinical studies, Imatinib yielded high response rates with minimal toxicity in all phases of CML and consequently received FDA approval in 2001 (Druker et al., 2001) (O Brien et al., 2003) (Druker et al., 2001) (Hahn, 2003). This was actually the fastest drug approval in FDA history as within three years the drug went from being an experimental drug to an FDA-approved drug. However, just after Imatinib came into clinical practice, reports of resistance against the drug started emerging with most