Topic: About Targeted Therapy(an easier way to understand)
Below is part of the lecture by Dr. David Gerber at Southwestern medical Center through RAN(Research Advocate Nework ) about targeted therapy that may be of interest to you.
There are two kinds of them
1. Monoclonal antibody(MoAB)--like Avastin, Cetuximab and Panitumumab;they are big in size,therefore can only work out side of the cancer cells(ie: avastin works outside the cancer cells and blocks the formation of tiny blood vessels to attach to the cancer cell to supply blood and nutrients to the cancer .); the MoAB are more target SPECIFIC compare to small molecule targeted agents like Tarceva(ie;MoAB goes to attack just one specific cancer cells and therefore produces less overall side effects like traditional chemo agents like 5FU.),In general the effects of MoAB last longer(ie:for days)
2. Small molecule inhibitors(SMI)--like Erlotinib(Tarcevar),gleevec,Sorafenib (Nexavar); are small in sizes and therefore can get thru the membrane of the cancer cells and work inside to kill either by blocking the complex cancer cell growth pathways or destroy the cancer inside.But unlike MoAB, small molecule targeted agents are LESS target specific than MoAB(ie;SMI can act on MORE than one type of cancer cells(ie:Naxavar works on different cell pathways-EGFR,KIT,PDGFR etc.) thus there side effects are more than the MoAB. In general the effects of the drug will last shorter.(ie:in hours)
3. MoAB usually are given via Iv infusion and Small molecule targeted agents are by mouth.
4.Because of each patient is different in medical status(ie; older age, have other chronic disease like diabetes or high blood pressure etc already;and also disease state (ie: stage of the cancer) and other issues can affect the overall treatment .
The response of the targeted treatment will be different among patients on the same dose of the same drug due to difference in GI absorption and liver processing of the drug(most of the SMI are taken by mouth).
The amount ofFREE drug particles(both by route of IV or oral) available in the blood stream without binding to other protein can be different too (ie; that will mean some patients will have more drug available to destroy,either by drug attachment on the surfaces(MoAB) or like (SMI) go inside the cancer cells to disrupt the cancer cell growth pathways ; other patients will have less drug to work with.( called the protein binding effect of the drug).
Even for the SAME patient,depend on the location of the tumor or the type of cancer, the amount of free drug available to treat the patient will be different too. In short, the effectiveness of the targeted therapy and chemotherapy are also related to each patient's health and biological status.
(this section #4.,due to the added explanation to make it easy to understand this section; this section may not be completely identical to Dr.Gerber's lecture.)
5. with regard to the current time requirement to develop a targeted agent.
this is the comparison He gives.
Target research of EGFR discovered in 1978;not until 36 years later(2004) the drug called Erlotinib(Tarcevar) was developed into a targeted agent for use in cancer.
Compare to Crizotinib (ie; an agent targeted the ALK pathway),it only take 3 years,(ie: from identify the cancer target pathway to the production of an useful drug to fight cancer).
What a difference it makes in cancer research ; so everyone(patients and cargivers) please hang in there,the dream of finding drugs that are less toxic and more effective is not just talk or hope ,but it will be reality pretty soon.
And for finding a "cure', it may still be possible if you look into the cancer called CML;now it is 100% treatable.