Health sciences - how cancerous tumors develop

An alternative explanation for the origin of tumors could lead to improved cancer treatment

 On a steamy August evening in 2009, marketing consultant Pat Elliott noticed her legs were swelling. She was not surprised by this because that day she was on her feet for long hours during a workshop she gave in Phoenix, Arizona. "I thought it was the heat," she says. But Elliot also felt pain in her feet, so she decided to play it safe and go to her doctor who recommended some tests. A few days later it was discovered that she had developed a rare type of blood cancer known as chronic myeloid leukemia (CML).

Elliott's cancer is the result of a genetic mutation that occurred in some stem cells in her bone marrow (which normally produce the various blood cells in our body). The defect caused the stem cells and their descendants to produce an abnormal enzyme known as Bcr-Abl. The enzyme signals the bone marrow to produce too many immature white blood cells and also allows them to survive too long. These proliferating cells crowd out healthy blood cells, damage the bone marrow and allow infections to develop. Once these damaged cells enter the bloodstream, they can also cause the spleen to swell and damage other organs. The pain and swelling in Elliott's feet were likely due to kidney problems caused by her illness. In the beginning, CML is usually not a harmful disease, especially if it is treated. But without treatment it may develop into an aggressive and even fatal condition.
To curb the disease, Elliott takes one bright yellow pill every day. The drug, known as imatinib (and sold as Gleevec), binds to the defective enzyme and stops the signaling that causes cells to multiply. Without this enzyme, the excess white blood cells mature and die normally. Indeed, recent research suggests that CML patients who survive at least two years after starting imatinib can expect a normal life expectancy. But the pill does not cure the disease. A small number of cancer cells continue to exist in Elliott's body. If you stop taking the medicine, the cancer will come back.

Although imatinib is keeping Elliot alive and healthy, and 22,000 other CML patients in the US, the drug's failure to eradicate the cancer suggests that there is some kind of failure in the accepted model describing how cancerous tumors develop, and in the drugs that have resulted from this model. If the alternative hypothesis turns out to be more accurate, doctors will have to change the therapeutic approaches and direct the treatments to destroy a specific subset of cells within the tumor.