In what they’re calling one of the most exciting cancer research developments in years, scientists are developing ways to make computers churn out new cancer remedies—with no need for anyone to even know how they work.

Called chemical genomic screening, the technique is designed to bypass the hard, sometimes futile work of trying to learn precisely what goes wrong in a specific cancer in order to fix it.

The technique exploits the fact that an organism’s state at any time depends not only on its genes, but on which genes are active, since a gene can also lie dormant, unused. Partial activation is also possible.

Within a cell, the activation situation at a given time results in a distinct profile, which existing technologies can record.

In the new technique, researchers feed into a computer an activation profile linked to a particular form of cancer. The machine then checks this against a database of known drugs, which contains previously known information on how each drug changes gene activation patterns.

Finally, the computer lists which of these compounds tend most strongly to convert the “sick” profile, which had been fed into it, into a profile known to be associated with a healthier state. By fixing the profile, scientists reason, the drug may help remedy the underlying problem. All this can occur with little or no knowledge of the malady’s causes.

Researchers stress that they’re not giving up on learning causes—indeed, this could enhance the results—but in the meantime, shortcuts to new treatments could bring desperately needed relief to millions.

The technique “promises to significantly enhance the drug discovery process,” wrote Harvard Medical School’s Scott A. Armstrong and colleagues in a paper describing some of the new findings, in the Sept. 28 online issue of the research journal Cancer Cell.

But researchers also cautioned that the technology, still at an early stage, isn’t clearly capable of providing cures. For now, it’s geared toward helping to convert particularly virulent forms of cancer into more manageable ones, making them better treatable by existing remedies. These could be administered alongside the newly found treatment.

In their paper, Armstrong and colleagues described work with victims of childhood acute lymphoblastic leukemia, a cancer of the blood and bone marrow. Scientists had previously found that a subset of these children have a particularly poor prognosis. This is associated with a weak response to a common first-line treatment, the hormone glucocorticoid.

Armstrong’s team found that in this “glucocorticoid-resistant” group, cancerous cells tend to have a specific profile of gene activation, or gene expression, as it’s technically called. In the other victims, the profile is different.

The researchers applied the new technology toward converting the glucocorticoid-resistant cells into non-resistant cells. They fed the expression profiles of both types into a database of 453 known, genome-wide expression profiles resulting from treatment of various cell types with different drugs.

The database, called The Connectivity Map, revealed that an existing drug called rapamycin should reverse the bad profile, researchers said.

Investigating further, they found that rapamycin affects molecules linked to a process that leads to a form of cellular “suicide.” This would be a logical point for a cancer drug to work at, because this “suicide” is implicated in the ailment. Naturally, healthy cells kill themselves when they start to become malignant, protecting the body against cancer. Full-blown disease occurs when this suicide system, called apoptosis, fails.

In sum, rapamycin and glucocorticoid together may be a useful treatment, the researchers said. Rapamycin is currently used to prevent the body from rejecting organ transplants.

In a separate paper published in the same issue of the journal, the medical school’s Todd R. Golub and colleagues took an analogous approach to prostate cancer.

Hormone treatments often provide initial success in fighting this illness. The medicines work by blocking a molecule, called a receptor, that allows hormones called androgens to circulate. But the drugs tend to stop working eventually because tumor cells evolve a resistance to them, and androgen circulation revives.

How this happens is unclear; but one helpful fact is that the high- and low-androgen states have different expression profiles, the researchers said. Again using the Connectivity Map, they identified two plant-derived products—celastrol and gedunin—as powerful androgen “inhibitors” that can switch the profile.

The profiles are obtained using microarrays, tiny arrays of DNA sequences corresponding to different genes.

When a gene in the body is active, it produces a molecule called RNA that is chemically related to the gene’s own DNA. Greater activation means more RNAs. These can also be converted into a form that will link chemically with the DNA for that gene. To obtain the profile, researchers extract a cell’s RNA, convert it and dump it onto the microarray. Then each RNA molecule sticks to a chemical “partner” on the array. The result is a pattern of attachments that reflects the gene activation profile.

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