Combination Therapies
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a look into the current state of combination therapies
![Combination Therapies: the promise to cure… everything ? By I&C President Ryan Witt [email_address]](https://image.slidesharecdn.com/combinationtherapies-100404200933-phpapp01/85/Combination-Therapies-1-320.jpg)
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Combination Therapies
- 1. Combination Therapies: the promise to cure… everything ? By I&C President Ryan Witt [email_address]
- 16. FUS1 , MDM2 , & P53 therapy Tested in clinical trials separately.
Notas del editor
- Need to not only find different molecular patterns, but you have to be able to know the signaling patterns to properly predict and devise a therapeutic regiment!! For instance, an inhibitor to an oncogene may be under-expressed .. Hence attacking the over-expressed oncogene wont matter.
- Source: http://en.wikipedia.org/wiki/File:Signal_transduction_pathways.png Molecular differences even within the same person in the case of cancer!!
- Sources: http://www.medscape.com/viewarticle/704990; http://news.bbc.co.uk/2/hi/health/8256494.stm; http://breastcancer.about.com/od/targetedbiologictherapies/p/parp_basics.htm
- Cancer refers to the uncontrollable growth of cells. This arises from an over-expression of what are called oncogenes, and an under-expression of what are called tumor suppressors. You can think of oncogenes as a GREEN light for cells to grow (their definition is any protein/enzyme that, when normally expressed, promotes cell growth), and tumor suppressors as a RED light (they are any enzyme/protein that, when normally expressed, suppresses or stops cell growth). There are many, many oncogenes and tumor suppressors in the cell, very often working at the same time. “ EGFR” is a growth receptor / oncoprotein (remember genes code for proteins) that is often over-expressed in tumors. There is a therapy known as Tarceva that inhibits EGFR proteins from functioning by binding to that protein’s energy source – it’s ATP binding site. However, an over-expression of “MET” – another oncoprotein, is associated with RESISTANCE to Tarceva. This means that if you have an over-expression of MET and EGFR, then Tarceva will NOT be beneficial to you. http://awurl.com/7urUWKWlv This dynamic concept illustrates why it is important to know the molecular profile of the diseased cells in the body to see if they express MET and EGFR or if they just over-express EGFR when deciding treatment options. Another Example: Xeloda + TP overexpression = good, but Xeloda + thymidylate synthase overexpression = bad. http://www.biomedcentral.com/1471-2407/8/386; http://awurl.com/xODVcukKl
- Source: http://www.medicalnewstoday.com/articles/176486.php?nfid=79262
- FUS1, MDM2, P53 Therapy : This is going to get very tough to follow so be careful. P53 is a “stopper” of cell growth. It is a very often knocked out (inactive or missing) in tumor cells. MDM2 is an inhibitory protein of p53 (so it’s a promoter of cell growth – an oncoprotein). FUS1 is an inhibitor of MDM2, which inhibits p53, thus FUS1 is a stopper of cell growth (tumor suppressor). Application Let’s say, you took a sample of someone’s tumor and it showed an overexpression of MDM2; however, you didn’t test for other mutations/expression levels. You then gave that person MDM2 antibodies / inactivators as a treatment. The problem here with this is, if this tumor cell also has a mutated, inactive p53 gene, then blocking the action of this inhibitory protein makes no difference because p53 will still be inactive. This illustrates the need to test for various proteins in these known signaling pathways to realize the most effective benefits of a therapy. It is important to note here that every protein has another promoter/inhibitor molecule regulating it. Each of these regulating proteins are coded by a cell’s DNA. The signaling pathways within cells has taken decades to understand and is still far from fully being understood. However, there are known signaling pathways that we can test patients for particular discrepancies in – enhancing the effectiveness and safety of therapeutic effects on patients. As well, if a database were to be collected and everyone were to undergo this “sequencing” and testing of proteins/genes, then we could isolate the causes of rare side effects.
- Sources: http://www.medscape.com/viewarticle/704990; http://news.bbc.co.uk/2/hi/health/8256494.stm; http://breastcancer.about.com/od/targetedbiologictherapies/p/parp_basics.htm
- Source: http://www.drugresearcher.com/Emerging-targets/A-drug-cocktail-to-bust-brain-tumours
- Source: http://www.cancer.ucla.edu/Index.aspx?page=644&recordid=148
- Source: wiki, clinical trials