“I haven’t experienced anything bad. No symptoms. No side effects, nothing,” she says. “I tell my granddaughter that my blood is sick, but I’m not sick.”
Whittington’s experience reflects a shift in the treatment for the disease known as CLL, from traditional chemotherapy to newer targeted therapies that attack cancer cells without harming normal cells — an area in which MD Anderson is leading the way.
“With these new targeted drugs, CLL patients are doing very well, maintaining normal lives and have no symptoms or signs of their disease. Only traces of leukemia — found by our most sensitive tests — remain,” says Jan Burger, M.D., Ph.D., associate professor of Leukemia and Whittington’s oncologist.
In people with CLL, the white blood cells — specifically B cells — that protect against disease and infection grow out of control. As they multiply, they crowd out healthy cells in the blood, bone marrow, lymph nodes, spleen and liver.
Through a clinical trial Whittington joined two years ago, she’s given ibrutinib, a drug that blocks a protein that aids B cells’ growth. The trial is part of the CLL Moon Shot, which taps the expertise of Burger and colleagues who played leading roles in the early clinical trials of the drug.
“The Moon Shot Program is closely linked to the clinical trial she’s in, where we pursue a large number of laboratory studies to understand resistance to ibrutinib and develop new combination treatments with the goal to eradicate the leukemia,” Burger says.
Goal: Double the cure rate
Combination chemotherapy in which multiple drugs are given simultaneously, including a standard-of-care regimen developed at MD Anderson, has achieved a 35% cure rate for CLL, but comes with severe side effects that can force patients off treatment. CLL Moon Shot leaders think they can double the cure rate to 70% using ibrutinib and other targeted therapies.
Whittington’s CLL was caught by a routine blood test at her annual well-woman checkup in 2013. CLL usually progresses slowly and many patients are monitored for years before treatment becomes necessary.
Whittington sought a second opinion at MD Anderson, where Burger found that her disease had a genetic mutation known as a 17p deletion, which causes CLL to progress faster and resist chemotherapy.
At the time, she stayed with her original oncologist for monitoring and Burger urged her to call when her disease progressed.
Drug thwarts rapid progression
Seven months after diagnosis, Whittington’s white blood cell counts rose to a level that prompted her oncologist to plan for chemo.
“I called Dr. Burger, came to MD Anderson and went on an ibrutinib clinical trial,” she says.
Her white count went up the first few weeks, which is common with ibrutinib because the drug pulls CLL cells into the bloodstream from the lymph nodes, spleen and bone marrow to die.
Her symptoms — night sweats, swollen lymph nodes and spleen, lack of energy — vanished in a week. “I’ve never had any side effects from the drug.”
After six weeks, her white blood cell counts began to plummet and her CLL went into remission. That was in October 2014.
Now Whittington takes three ibrutinib pills a day, comes in every three months for blood tests and has an annual CT scan, bone marrow aspiration and biopsy. She’s never missed more than a day of work.
“I’m excited. I thank God every day because I couldn’t have a better care team,” she says.
CLL — the most common adult leukemia — is a malignancy of immune system B cells (white blood cells that normally produce antibodies against infection). The American Cancer Society estimates almost 19,000 new cases will be diagnosed in 2016 in the U.S., and about 4,600 people will die of CLL.