Optimism and despair at the cutting edge of cancer genomics.
| 1 Comment |


New York Times reporter Gina Kolata has written three moving articles on the slow but inexorable (thanks to increasingly powerful "omics" technologies and plummeting prices) journey of whole genome sequencing and proteomics from academic laboratories into the frontlines of cancer treatment.

In her first article, Kolata writes about a young cancer researcher, Dr. Lukas Wartman, struck by one of the very diseases that he had hoped to spend his career researching, adult acute lymphoblastic leukemia.

Fortunately, Wartman happened to work at a cutting edge genomics institute at the Washington University of St. Louis, and his colleagues pooled their talents and tools to try and unravel the driving force of his cancer and find a way to halt it before it killed him.

Wartman also turns out to be "lucky" in one other key respect - his cancer is driven by the "upregulation" of a normal gene (FTL3), which was "wildly active" in his leukemia cells. He gets even luckier when his colleagues realize that there is already a drug approved to inhibit FTL3, Sutent. This particular story has a happy ending, with Wartman's cancer going into remission for a second time.

In her second article, Kolata chronicles a sadder outcome - the story of 69 year old Beth McDaniel, afflicted with a rare type of lymphoma. In McDaniel's case, whole genome sequencing of her cancer leads to only a brief reprieve, as her cancer rapidly develops resistance to another promising drug, Yervoy.

In her third, and final article in the series, Kolata, examines how emerging genetic tests can help predict cancer outcomes (in this case, for a type of ocular melanoma) but not necessarily help patients identify treatments that will change their prognosis.

Writing about emerging treatments at the cutting edge of medicine is a challenging affair. Those who benefit from new treatments and protocols may have better access to new technologies and treatments, whether by dint of employment, friendship, wealth, or connections. It seems like an arbitrary process, and it is.

But this is certainly no more or less arbitrary than the genetic "lottery" of cancer itself, which strikes the wealthy and affluent - like Steve Jobs and Christopher Hitchens - as well as the poor and indigent. And although Jobs and Hitchens were "early adopters" of genomic technologies they may not have benefitted from them and certainly weren't cured by them. And future patients undoubtedly benefit from the efforts of the wealthy afflicted to find cures for their own diseases (through, for instance, intiatives like the Michael J. Fox Foundation).

Cancer may be the most complex human disease, and the effort required to battle it - let alone defeat it - is staggering. And Kolata's series gives a real sense of that: even when we have the technology to identify the molecular drivers of cancer growth, we may not have any drugs that block those targets, or the cancer may rapidly grow resistant to targeted therapies.

But the underlying trends favor cancer patients and their doctors, not cancer. The cost of sequencing technologies is dropping, and dropping rapidly. The analysis of the reams of data generated by sequencing is the current bottleneck, but increasingly powerful computers and information technologies will eventually crack that problem as well. And as more patients have their tumors sequenced, researchers will develop much better "roadmaps" for use in developing cocktail therapies to control metastatic cancers.

The remaining challenges, like the enormous cost of drug development and the speed with which we can validate and test drugs against new targets, are real and serious problems. It may take years, or even decades, to overcome them. But overcome them we will.

In this case, a picture is really worth a thousand words.

cost_per_genome-1024x768.jpg

1 Comment

Paul-
Elegant work to be sure, but I'm not so optimistic. While tyrosine kinase inhibitors (probably the mot common targeted therapy) have had some successes, cancer cells have turned out to be more clever than we thought. First, when a specific growth pathway is blocked there are other redundant pathways that can take over (resistance). But more disturbing is a recent study that showed that there is a great deal of genetic variation between a primary tumor and the metastasis derived from it. Still worse--the primary tumor itself is far from genetically homogenous, making it likely that other mutated cancer cells can take over even if the primary tumor is successfully targeted. This is worse than resistance--it is innate genetic diversity. Someone may figure out a way to deal with this, but it ain't gonna be easy.

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