Frank Meehan spent two decades spearheading the United Food & Commercial Workers’ (UFCW) effort to raise money to defeat blood cancers. As president of the Long Island, NY Local, he was one of the first leaders to act upon the union’s national relationship with The Leukemia & Lymphoma Society (LLS).
Then last spring, in a twist of fate, he ended up losing his life to one of the aggressive leukemias he’d been hoping to see cured.
“It’s so ironic. He worked so hard for this cause,” said his wife Pam. “He kicked off UFCW’s involvement for years. For him to pass from acute myeloid leukemia (AML) just blew us all away.”
Meehan, who was 75, looked and felt fine when he went for his annual physical in December. He had a low level of vitamin B12 that he couldn’t seem to kick but that was it. When a doctor did a bone marrow biopsy in March just to be safe, he was diagnosed with AML. The initial treatment knocked out his white blood cells and when he developed a complication, it couldn’t be treated and he got pneumonia. He died on Easter Sunday, only three weeks after being diagnosed.
At first his family was angry. He did so much to fight leukemia. Why would this happen to him?
“But then you ask why it would happen to a small child,” said Pam Meehan. “There’s no answer. It’s just a devastating loss.”
When he first started his journey in 2010, he didn’t have any connection with leukemia or lymphoma. He signed up for his first Team In Trainingevent when a good friend and fellow dive instructor, Steve, was diagnosed with throat cancer and he decided to ride in his honor. In the early 1990s, they had developed a strong bond while stationed at Navy Dive School in Pearl Harbor working on ships and submarines. Along with a mutual friend Ron, they had many fond memories of their years together and Sena could go on for hours with all the sea stories.
Sena had no idea that Ron had been diagnosed with leukemia in 2009, and four days after signing up for that first event, he heard that Ron had passed away. Determined to use his passing to make a difference, he took to social media and raised $2,800 in four days.
Motivated to beat the disease that took his friend, Sena has been riding, running and swimming in his memory ever since. He’s completed America's Most Beautiful Bike Ride six times (also a mentor and captain), done the Vegas Bike team twice (also a coach), and finished the Pacific Grove and Wildflower triathlons. He wears a picture of Ron on his back for every event.
Robert Hromas, M.D., a blood cancer expert at the University of Florida's College of Medicine, is looking to discover new drugs that will improve the response of elderly AML patients to chemotherapy. His latest research, funded through a Translational Research Program grant from The Leukemia & Lymphoma Society, focuses on inhibiting the DNA repair response.
How would you explain what kind of research you do?
The marrow inside your bones makes white blood cells, which fight infections. Most of these cells must be made new every day, because they only live for less than 24 hours. Once they are made, the bone marrow stops making more. Now imagine if the bone marrow never turned off making these white blood cells, and worse, they lived forever. Then your body would fill up with white blood cells, and this could kill you. This situation is called acute myeloid leukemia (AML). I study ways to kill these immortal leukemia cells in order to prevent them from killing you. Even more importantly, I have come up with some ways to prevent the marrow from making leukemia cells in the first place.
What is novel and innovative about your approach?
There are two novel aspects to our work. First, the most innovative part of what we do is study how to prevent the DNA mutations (called translocations) that cause leukemia.We have found that an FDA-approved ovarian cancer drug called olaparib can prevent translocations when given after a translocation-inducing toxin such as high dose radiation or high dose chemotherapy. The second novel aspect of our work is that we have described a DNA repair protein called Metnase that mediates resistance of leukemia cells to treatment. We have generated a new class of drugs that block Metnase from doing this. These drugs restore the sensitivity of leukemia cells to chemotherapy. Interestingly, these drugs are bi-functional, simultaneously damaging the leukemia cells’ DNA, and then inhibiting Metnase from repairing that DNA.