Poised to test whether new drugs can work against a wide range of cancers independently of where they originated - breast, prostate, liver, lung for the first time ever are three pharmaceutical companies.
The drugs go after an aberration involving a cancer gene fundamental to tumour growth, the New York Times reported.
Many scientists see this as the beginning of a new genetic age in cancer research.
Even though great uncertainties remain, such drugs could mean new treatments for rare, neglected cancers, as well as common ones.
Merck, Roche and Sanofi are racing to develop their own versions of a drug they hope will restore a mechanism that normally makes badly damaged cells self-destruct and could potentially be used against half of all cancers.
Researchers and federal regulators say that no pharmaceutical company has ever conducted a major clinical trial of a drug in patients who have many different kinds of cancer.
Experts say that this has major implications for cancer philanthropy.
Advocacy groups should shift from fund-raising for particular cancers to pushing for research aimed at many kinds of cancer at once, Dr. Brawley said.
At the heart of this search for new cancer drugs are patients like Joe Bellino, who was a post office clerk until his cancer made him too sick to work. Seven years ago, he went into the hospital for hernia surgery, only to learn he had liposarcoma, a rare cancer of fat cells.
A large tumour was wrapped around a cord that connects the testicle to the abdomen.
Companies have long ignored liposarcoma, seeing no market for drugs to treat a cancer that strikes so few. But it is ideal for testing Sanofi's drug because the tumours nearly always have the exact genetic problem the drug was meant to attack - a fusion of two large proteins.
If the drug works, it should bring these raging cancers to a halt. Then Sanofi would test the drug on a broad range of cancers with a similar genetic alteration. But if the drug fails against liposarcoma, Sanofi will reluctantly admit defeat.
The genetic alteration the drug targets, has tantalized researchers for decades. Normal healthy cells have a mechanism that tells them to die if their DNA is too badly damaged to repair.
Cancer cells have grotesquely damaged DNA, so ordinarily they would self-destruct. A protein known as p53 that Dr. Gary Gilliland of Merck calls the cell's angel of death normally sets things in motion.
But cancer cells disable p53, either directly, with a mutation, or indirectly, by attaching the p53 protein to another cellular protein that blocks it. The dream of cancer researchers has long been to reanimate p53 in cancer cells so they will die on their own.