- Rutgers University - New Brunswick/Piscataway
- Genetics 245
- Rational Treatment
Last Modified: 2011-07-17
• Extracted patient cellular mRNA copied into cDNA (more stable), labeled with
• Microarray (cDNAs) is incubated with labeled sample and hybridization occurs.
• Array washed to remove unbound molecules, and positions of labeled fragments are measured and compared to controls
- during oncogenesis- cancer cells can defective differentiation
- cancer cells also enter post-mitotic state, prolonging metastases
- evidence in vitro/vivo targeting early and late oncogene and tumor suppressor gene sequences and their proteins are important as part of treatment – therefore k-ras and Her2/neu gene silencing early to stop proliferation
- 'drugable' proteins must have identifiable enzyme or catalytic cleft for drug to bind to
- for low MW to form non-covalent bonds allowing drug to bind to its target
- drugs should target known proteins malfunctioning in cell
- kinases are evolutionary similar so difficult to target
- molecular structure of protein should provide design for chemical structure of drug
- measurements of pharmacodynamics (what drug does to organs, pervasiveness, effectiveness) and pharmacokinetics (what body does to drug-absorption, metabolism) and toxicity
- efficacy and toxicity in which drug should be administered to work
- treatment for pancreatic cancer
- w/drug live slightly longer than treated with 5-flurouracil
- both agents are pyrimidine derivatives- prevent DNA synthesis
- FDA approved even though only marginal increase in survival rates because pancreatic cancer is so invasive
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