When basketball great Kareem Abdul-Jabbar found out he had leukemia, he feared the worst. To his surprise, though, modern-day drugs have turned his disease into a long-term, manageable condition.

Ravi Bhatia aims to block leukemia at its stem-cell source.

His recent public disclosure about the diagnosis drew widespread attention to the disease, bringing a spotlight to a cancer once tough to beat. Abdul-Jabbar was diagnosed with chronic myeloid leukemia, or CML, a cancer with answers.

And City of Hope researchers are working to make those answers even better over the coming years.

For decades, CML remained difficult to control and nearly impossible to cure. In the late 1980s and the 1990s, blood stem cell transplants using marrow or stem cells from healthy donors remained the only hope of long-term control or cure for most patients.

That all changed when a drug called Gleevec hit the scene and began clinical trials in 1998. Nearly every CML patient who tried it responded.

Gleevec, also called imatinib, targets an abnormal protein that sparks CML growth. Blocking the protein stunts CML cell growth. Treatment is simple: Patients take a small pill.

Most patients can remain on Gleevec and keep their CML under control for years.

But, there are risks involved. Gleevec doesn’t actually cure CML for most patients. Sometimes CML becomes resistant to the drug and the disease returns.

The chief culprit behind this recurrence may be leukemia stem cells, according to scientists.

These early, immature cells lurk, dormant, in the patient’s marrow, waiting to generate adult, disease-causing cancer cells. Current cancer therapies — even Gleevec — can’t target these cells. They escape treatment.

Even more ominous, while the leukemia stem cells lie in wait, some of them can become resistant to Gleevec. When the cancer stem cells finally divide and generate mature cells, the patient develops leukemia again.

Ravi Bhatia, M.D., director of the Division of Stem Cell and Leukemia Research, is studying leukemia stem cells and searching for their weaknesses. He hopes to find a way to finish the job Gleevec starts.

One of the main options under study are drugs called histone deacetylases inhibitors. These drugs, more commonly called HDAC inhibitors, appear to make cancer stem cells self-destruct. They also may help other drugs better do their cancer cell-killing work.

Bhatia is testing an HDAC inhibitor that might knock out the stem cells behind Gleevec-resistant CML. If he’s right, combining the HDAC inhibitor and Gleevec could provide the one-two punch that finishes the CML cells for good.