Molecular Basis of Drug Interactions of Methotrexate, Cyclophosphamide and 5-Fluorouracil as Chemotherapeutic Agents in Cancer

Abstract

Abstract-At present, chemotherapy is one of the principal methods of treatment of cancer. For many years, chemotherapy is possibly the only way to control cancers that do not respond to either surgery or radiation. To date a good number of chemotherapeutic drugs have been developed which are effective in the treatment of human cancers. But, A few drugs have been known to be safe and promising. The most widely used chemotherapeutic drugs include methotrexate, cyclophosphamide, 5-fluorouracil etc. In this review, the molecular basis of drug interaction of methotrexate, cyclophosphamide and 5-fluorouracil has been studied. Understanding of the molecular basis of drug interaction of the chemotherapeutic agents is fundamental in order to enhance the clinical effectiveness of chemotherapy as well as to increase our knowledge of the cytotoxic effects of chemotherapeutic drugs. Increased understanding of the pharmacokinetics and the mechanism of action also help to develop biomodulating strategies. The boundary between the efficacy and toxicity of chemotherapeutic drugs is very narrow. So, novel approaches are needed to be formulated in order to enhance the efficacy and to minimize the toxic effects of the chemotherapeutic agents. Though a lot of information is needed to be learned and a lot of task is needed to be accomplished, chemotherapy can be the ultimate and feasible way for controlling cancers if the toxic effects of chemotherapy can be reduced or minimized.

Bone marrow and adipose mesenchymal stem cells attenuate cardiac fibrosis induced by methotrexate in rats

“…On the other hand, MTX induces apoptosis by activation of caspase‐3 . Contrary, stem cells are capable of reducing apoptosis as compared with the MTX group.…”

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“…The rationale of such different therapeutic approach might reside in the complex interactions between TP53 mutations, BRAF mutations and sensitivity to MTX. MTX inhibits the synthesis of DNA, RNA, thymidylates and proteins because it is a potent inhibitor of the dihydrofolate reductase (DHFR) enzyme, which converts dihydrofolate to tetrahydrofolate (THF) [ 62 ]. TP53 mutations induce an increase of E2F1 and are associated with DHFR gene amplification to start the invasion and metastasis process [ 63 ].…”

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“…One major pathway of classical apoptosis is the receptormediated pathway or the extrinsic pathway. Another major pathway for the initiation of apoptosis is the mitochondrial pathway or the intrinsic pathway [25,26]. Both of these pathways are linked and involve caspases.…”