Can anyone tell me what is the actual mechanism involved in targeting a cancer cell form an anticancer drug?
How will an anticancer drug target specifically on cancer cells (Which is nothing but a normal cell which has started to divide uncontrollably)?
How is a cancer cell (at the molecular level) different from a normal cell that makes an anticancer drug target specific?
Cancer is fundamentally about uncontrolled replication. So many cancer drugs directly or indirectly target replication. Many cancer drugs stall replication, including those that limit nucleotide incorporation into DNA (e.g., gemcitabine) and those that block replication fork progression (e.g., camptothecin and platinum drugs). Similarly, radiation therapy works because the DNA damage from ionizing radiation causes cells with unregulated replication to die by mitotic catastrophe because cancer cells initiate replication without completing DNA repair, often this is due either to defective DNA repair or to defective cell cycle checkpoints. So a cancer cell is different from a normal cell from decreased controls over replication - hence its uncontrolled replication as you describe in your question. This is an Achilles' heel for many cancer cells and improved therapeutics may better target the replication-repair interface.
Cancer cell however is an abnormal cell which is regarded as immortal, the cell that has forgotten to die. How this extraordinary ability is acquired by a cancer cell would be a very pertinent question to ask and seek the answer in order to prevent, control and if possible cure cancer.
For more details You can refer following article
http://www.apocpcontrol.org/page/apjcp_issues_view.php?sid=Entrez:PubMed&id=pmid:23886219&key=2013.14.6.3987
To follow up on John Tainer's excellent summary, current cytotoxic drugs have specificity for replicating cells however the specificity is not always as complete as desired. Thus while Top1 poisons such as camptothecin are largely S-phase specific drugs they can also cause DNA damage in cells undergoing transcription which can contribute to systemic toxicities. A drug I am developing F10 is highly specific for DNA replication and thus has very low systemic toxicity.
Thank you for attaching your paper sir....Wish you all the best for your drug development study
Regards
Sujay
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