Our son Harrison was diagnosed with acute lymphoblastic leukemia (ALL) in December 2011. When 4 weeks of chemotherapy did not eliminate the
leukemia from Harrison’s bone marrow, his doctors
looked at the genome of the leukemia cells. They
found an alteration recently detected in leukemia
cells from other children whose ALL did not respond
to chemotherapy. Harrison was the first child with
ALL to have a drug targeted to the effects of the
genomic alteration, the tyrosine-kinase inhibitor
imatinib (Gleevec), added to his chemotherapy. It
put him into complete remission. Although he has
recently had a relapse of the leukemia in his central
nervous system, Harrison’s doctors have turned to
second-generation tyrosine-kinase inhibitors, and
we are hoping they will help the way imatinib did.
Harrison’s diagnosis with ALL came just a few days
after his 10th birthday. He had always been a very
energetic child, constantly outside playing sports. But
for about 2 months before the diagnosis, he hadn’t
been feeling his usual self. Over that time, he gradually
felt worse. Harrison became more and more lethargic,
started having night sweats, and became very pale.
Thinking he had a virus, we took him to the
pediatrician. The pediatrician sent us straight to
the emergency room (ER) at Wake Med, telling
us Harrison either had a virus or leukemia, and
further tests were needed immediately to distinguish
between the two.
A blood test in the ER confirmed that Harrison
had leukemia, and he was transferred right away to
North Carolina Children’s Hospital. Just 2 days later,
he started the intensive induction chemotherapy that
is standard treatment for pediatric ALL.
The goal of induction chemotherapy is to achieve
complete remission, and so the drugs that they use
are very strong. It was a really difficult time for the
whole family, and the chemotherapy took its toll on
Harrison’s body. About 2 weeks into the treatment,
he had a stroke and multiple seizures. He was in the
pediatric intensive care unit for 10 days, and we
didn’t know if he would live.
After 4 weeks of chemotherapy, we found out
there were almost as many leukemia cells in
Harrison’s bone marrow as there had been when
he was diagnosed. He was in the small percentage of
patients who do not go into remission after induction
chemotherapy. We were devastated.
Harrison’s doctors began looking for answers as to
why he was not in remission. One thing they did was
look at the genome of the leukemia cells. They found
the cells contained a recently reported chromosomal
translocation found in cases of pediatric ALL that did
not respond to induction chemotherapy.
Harrison’s doctors contacted the researchers who
had first reported the chromosomal translocation,
and together they decided to add imatinib to the
chemotherapy regimen because imatinib targets the
effects of the chromosomal translocation.
About a week after starting imatinib, Harrison was
in remission. The day we found out—January 24,
2012— was amazing. We were very tense waiting for
the test results, but the doctor came in and said, “We
have a touchdown.” All the nurses, oncologists, and
patients in the clinic erupted in cheers and clapping.
Harrison continued through the standard
chemotherapy protocol for pediatric ALL, which
ended in April 2015. Throughout that time and until
the relapse in his central nervous system was discovered
at the end of June  he took imatinib once a day.
The doctors think the relapse occurred because
imatinib does not penetrate into the central nervous
system very well. So they s witched him to dasatinib
(Sprycel), a second-generation tyrosine-kinase
inhibitor that penetrates the central nervous system
better than imatinib. This drug knocked down the
number of leukemia cells but did not eliminate all
of them. As a result, Harrison has just finished a
course of high-dose chemotherapy and another
drug that targets the effects of the chromosomal
translocation, nilotinib ( Tasigna).
We are hoping that this plan will put Harrison into
complete remission again and allow him to move
on to the consolidation phase of treatment for his
type of leukemia.
We are telling Harrison’s story because we are truly
grateful for the research that led to imatinib and other
drugs like it that have kept our son alive and have the
potential to put him back into complete remission.
His doctors told us if he had been diagnosed just 6
months earlier, he would not have survived because
the research knowledge that led them to their
treatment decisions would not have been there. With
greater public and private support for research, we
believe that more children will survive their cancers.
2% TO 5% OF
KINION \\ AGE 14 \\ WAKE FOREST, NORTH CAROLINA