The cancer research establishment seeks - as a near-term goal - to develop the means to turn almost all cancers into managed conditions. Possibly costly and inconvenient, but not fatal, just as researchers have accomplished for class after class of medical conditions over the past century - and they were hard tasks all. As suggested by a recent Technology Review piece, however, we might ask ourselves what sort of hard task this is in the case of cancer - easy hard or hard hard:

The largest study yet of genetic changes across a broad range of cancers has turned up some unexpected results. Mutations thought to cause one kind of cancer also seem to be important in others, suggesting that the same drugs might be useful for patients with very different kinds of cancer. But all the mutations in the study--even those shared among cancers--occurred at low frequencies, suggesting that the search for cancer genes may be more difficult than researchers had hoped.

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But Chanock says the study also provides "a good reality check." Thirty percent of the tumors in the study had none of the mutations Garraway's group looked for. Chanock says this study forces researchers to address the question, "What's it going to take to make sense of [the genetic changes behind cancer]?" The answer, he says, is even larger genotyping studies, on the order of 10,000 tumors. And, as those tumors with no known mutations in this study suggest, many of the genetic changes that drive cancer remain to be discovered.

Genes are keys to cancer, because they are a starting point from which to decode biochemical mechanisms, and thus move onto the development of ways to intervene. There are other possible forms of key too, buried in process, and more subtle than single gene mutations:

When the teams compared patterns of gene activity in stem cells from healthy and cancerous tissue they found that those from cancers were often locked in a state in which they carry on multiplying as primitive stem cells, instead of maturing into specific tissues. ... When they're in this state they divide more, and in the process may accumulate additional mutations which ultimately turn them cancerous ... supporting a stem cell origin of cancer in which reversible gene repression is replaced by permanent silencing, locking the cell into a perpetual state of self-renewal and thereby predisposing to subsequent malignant transformation.

Easy hard means that there is a key within reach - or at least only a few keys - for almost all cancers; some small group of unifying or common mechanisms that could be addressed with the biotechnology we have today, or will have in the 2010s. The easy hard problem is finding the keys - or perhaps the real easy hard problem is determining that the keys are likely to exist, and thus devoting effort to finding them.

Hard hard means that we'll have to undertake 300, 3000 or some other unfeasibly large number of different projects in biochemistry, with little common ground between them, to tame cancer with the tools we have now or will develop over the next decade or so. The bottom line in that case is that we'll need much better tools, which means more time to slip the leash upon cancer.

If we ignore the limitations of today and look at the blue sky future of biotechnology, it seems that we may be able to engineer out cancer by modifying our biochemistry in some fundamental way - a better type of key impossible to verify or make use of now, but quite possibly an easy hard task for the medical science of 2040. Aubrey de Grey includes one suggested methodology as a present component of SENS, the Strategies for Engineered Negligible Senescence, a proposed plan for repairing the damage caused by aging - though I can imagine there will be others:

we don't actually need to fix chromosomal mutations at all in order to stop them from killing us: all we need to do is develop a really really good cure for cancer. The one that I favour (which was the topic of the third SENS roundtable, a roundtable meeting I convened in Cambridge in 2002) is called WILT, for Whole-body Interdiction of Lengthening of Telomeres.

You can download a PDF explaining WILT from the SENS website; it makes for interesting reading against the backdrop of present day cutting edge cancer research.

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Posted by Reason at February 18, 2007 6:09 PM | TrackBack (0)