Derek Lowe, an Arkansan by birth, got his BA from Hendrix College and his PhD in organic chemistry from Duke before spending time in Germany on a Humboldt Fellowship on his post-doc. He's worked for several major pharmaceutical companies since 1989 on drug discovery projects against schizophrenia, Alzheimer's, diabetes, osteoporosis and other diseases.
To contact Derek email him directly: derekb.lowe@gmail.com
Twitter: Dereklowe
For those of you interested in the recent work on the diversity of different cancer cell genotypes inside single tumors, there's a review out that covers the field well. The authors also go into some of the major unanswered questions: does having a tumor cell population with a lot of genetic diversity correlate with a poor prognosis for treatment? Can small populations of potentially troublesome cells be identified ahead treatments that might give them too free a field to work in? Can the huge genetic diversity be reduced to a more manageable set of practical phenotypes, to make therapeutic recommendations? This will keep everyone busy for a long time to come.
Although, it is interesting to find genetic heterogeneity as a basis of poor prognosis, I still have some reservations and wonder how it effects our approach to tumor targeting. Not all mutations/chromosome alterarions are of significance. A famous Harvard Professor, Judah Folkman, who died a few years ago, discovered that we (humans) by the time we die have a huge burden of micro-tumors in our tissues. Fortunately, these never acquire the cancer phenotype (here, neoangiogenic potential) and grow to be a problem. Ultimately, among all the "genotypes" described in current papers there will a just a handful that will need to be targeted. Now, the question is how we get to those few.
A couple of months ago I saw Bert Vogelstein give an interesting talk where he pointed out that, despite all the various different mutations we see in tumors, all cancers involve at least one of 12 pathways, so presumably if we have agents that can act on each one of those 12, we ought to be able to find some combinations of treatment for most patients.
1. Chris Swain on May 18, 2012 10:38 AM writes...
Really interesting, thanks for flagging this.
Permalink to Comment2. Ajay K Malik on May 20, 2012 2:38 PM writes...
Although, it is interesting to find genetic heterogeneity as a basis of poor prognosis, I still have some reservations and wonder how it effects our approach to tumor targeting. Not all mutations/chromosome alterarions are of significance. A famous Harvard Professor, Judah Folkman, who died a few years ago, discovered that we (humans) by the time we die have a huge burden of micro-tumors in our tissues. Fortunately, these never acquire the cancer phenotype (here, neoangiogenic potential) and grow to be a problem. Ultimately, among all the "genotypes" described in current papers there will a just a handful that will need to be targeted. Now, the question is how we get to those few.
Permalink to Comment3. Jonathan on May 21, 2012 12:33 PM writes...
A couple of months ago I saw Bert Vogelstein give an interesting talk where he pointed out that, despite all the various different mutations we see in tumors, all cancers involve at least one of 12 pathways, so presumably if we have agents that can act on each one of those 12, we ought to be able to find some combinations of treatment for most patients.
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