FIGURE 33.7 Twenty-four-color chromosome painting identifies multiple translocations and other signs of aneuploidy in a breast cancer tumor cell line. (Courtesy of Joanne Davidson.)

tumor cells. If specificity of treatment spared the cells of the immune system, might we also find ourselves able to fine-tune the immune system response to tumor cells to help eliminate any cells missed by the drugs?

We also see great gains to be made in diagnostics. If we can arrive at knowing not just what kind of cancer it is, but also which biochemical pathways have become involved in the tumor's progression, it may streamline targeting just the right treatment not just for that cancer but for that stage of that cancer. Of great importance, we anticipate better diagnostics arising from molecular genetics that will reduce the problem of people being diagnosed "too late." Imagine home monitoring systems akin to home pregnancy tests or the blood-sugar monitoring systems used by a diabetic patient, allowing those with especially high risk levels to watch for recurrence of a banished tumor, or appearance of an expected tumor that has not yet manifested itself.

Will the magic bullets yet to come provide a simple outright cure for cancer the way we cure an infection with an antibiotic? Perhaps. For sporadic cases who did not inherit a cancer gene, we expect that cures will be achievable and that curing their cancer once will mostly take care of the problem. Perhaps for individuals who inherited that first hit, a cure will really involve three different stages. First, as for the nonhereditary cases, there will be the problem of how to shoot just the right magic bullets early enough to end the

FIGURE 33.6 Use of an Affymetrix Cancer Array gene chip to examine gene expression in cancer. This image shows that certain genes show higher levels of mRNA (in red) in metastatic tumors than in tumors that have not metastasized. Other genes show the opposite pattern. Different kinds of cancers will show a different profile of gene expression levels that can point to where critical biochemical events in the cell are taking place, and eventually assays of changes of this kind will be important in distinguishing different stages of cancer. In this case the RNA samples came from medul-loblastoma tumors, and analysis of images like this one allowed the authors to identify genes that play a role in medulloblastoma metastasis. Some gene chips and microarrays can display thousands or tens of thousands of genes, but use of specialized chips that do not contain the full array of human genes lets researchers focus in on where the critical differences are. (Modified from T.J. MacDonald et al, Nature Genetics 29:143-1 52, 2001. Used by permission.)

initial cancer. The second stage will involve ongoing diagnostics to detect any new tumors at the earliest possible stage. Third, there will be ongoing medical management to suppress development of subsequent tumors. However, if we identify key proteins produced by tumor cells, key changes in gene expression events, can we in fact also concoct a surveillance system that can knock out any cell that turns on the particular cancer pathways characteristic of that individual's hereditary tumors before the tumor ever gets large enough for anyone to know it is there? We expect that eventually harnessing key features of our own immune systems along with the magic bullets from the pharmacy may allow for many cancers to become a chronic disease, treated over a long lifetime through your local pharmacy. How much of an advance would that be? Of course, we would hope that answers will arise that will offer simple, clean cures, but twenty years from now, if cancer has moved out of the acute life-threatening category into a chronic management category, we will feel as if a dream has come true.

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