• monoclonal Ab against VEGF for colon cancer (along with 5-FU)
  • causes regression of tumor vasculature
  • reduces intratumoral pressure, thus improving the delivery of cytotoxic agents to the tumor (synergy with combo therapy drug)
  • inhibit new blood vessel formation restricting tumor growth

First anti-angiogenic agent with demonstrated anticancer benifit in phase III trials

• amplification of BCR/ABL gene
• mutation of BCR/ABL gene
• activation of compensatory survival signaling pathways
• MDR (P glycoprotein mediated resistance)

1. insert in ATP binding pocket
2. prevent kinase activity (can't transfer Tyr moiety to substrate)
3. this leads to stopping cell division
4. after a prolonged time of not undergoing cell division, tumor cell intiates apoptotic pathway

• most prevelant in blastic phase
• second most prevelant in accelerated phase
• chronic phase is least prevelant

1. when a tumor cell grows to a certain size, the center tumor cells get hypoxic
2. this leads to the induction of angiogenesis by secreting VEGF (tell bv's multiply and come to me)
   • also downregulates antiangiogenic factors
3. leads to new blood supply

• monoclonal Ab against Her2 (target extracellular domain)
  • remember, in some breast cancers, you have amplification or overexpression of the HER2 gene
  • blocks EGF (epidermal growth factor) from binding to HER2
  • this will slow growth

In order to find out who has the HER2 type breast cancer, use Ab test or chromosomal FISH test

• block EGFR (is used in combo with other drugs)
  • competitive reversible inhibitor of ATP
  • inhibits ligand induced cell growth
  • delaying tumor growth and induce tumor regression

• target HER/EGFR protein
• indication: non small cell lung cancer
• work among females who have never smoked, and especially Asian women with an adenocarcinoma cell type