Annual Meeting Proceedings Part 1 - American Society of Clinical ...

2012 ASCO Annual Meeting Proceedings Special Awards
1s
ABSTRACTS
The American Society of Clinical Oncology
48th Annual Meeting
June 1–5, 2012
McCormick Place
Chicago, Illinois
SPECIAL AWARD LECTURE ABSTRACTS
David A. Karnofsky Memorial Award and Lecture
Saturday, June 2, 9:30 AM
Progress in chronic lymphocytic leukemia (CLL): A tribute to Dr. David A. Karnofsky.
Kanti R. Rai, MB,BS; North Shore-Long Island Jewish Medical Center, New Hyde Park, NY
My own journey in cancer research started in 1958 when I was a 26-year-old resident in pediatrics and was called
upon one day to see and admit a 3-year-old named Laurie. Laurie, it turned out, had acute lymphoblastic
leukemia (ALL).The attending hematologist helped me in making the diagnosis that night. I took care of Laurie
not only that night but throughout her disease course. As, unfortunately, was the case with all children with acute
leukemia in 1958, after whatever treatment we were able to give, Laurie died a few months later. The
hematologist, Dr. Arthur Sawitsky, had watched how very involved I had become in Laurie’s care and how deeply
her death affected me, and counseled me to pursue leukemia research and become a hematologist. After I
completed my hematology fellowship, Dr. Sawitsky helped me join the research team of a world-class
hematologist, Dr. Eugene P. Cronkite, at the Brookhaven National Laboratory. It was while working with Dr.
Cronkite and seeing patients with all hematologic malignancies that I was intrigued by the wide spectrum of life
expectancies of patients carrying the same diagnosis of chronic lymphocytic leukemia (CLL). David Karnofsky
himself had already written about CLL in the 1950s. He, as well as several other hematologists of that era, had
mentioned that CLL, in contrast with ALL, was not a very exciting disease, not much was happening with patients
with CLL. Both Cronkite and Sawitsky encouraged me to study this disease. We then developed a relatively simple
staging system, which was rapidly integrated in practice by clinicians, and it became possible to classify all CLL
patients, on a prospective basis, into three distinct prognosis groups. It became possible to initiate therapeutic
trials and ask research questions. Within two decades after clinical staging was developed, my colleague,
Nicholas Chiorazzi, who is the leader of our CLL basic research team, demonstrated that one of the fundamental
differences between the good prognosis and bad prognosis groups was that the former had somatic
hypermutations in the IgVH genes while the latter did not. CLL has become a disease that, today, fascinates
molecular biologists, immunologists, as well as clinicians. Promising new therapies targeting the B-cell receptor
signaling pathways have become a reality. I feel certain that this progress, indeed, is in the tradition that Dr.
Karnofsky started.
Science of Oncology Award and Lecture
Sunday, June 3, 1:00 PM
Normalizing tumor microenvironment to treat cancer: Bench to bedside to biomarkers.
Rakesh K. Jain, PhD; Harvard Medical School and Massachusetts General Hospital, Boston, MA
For the past three decades our laboratory has focused on one challenge: How do we improve the delivery and
efficacy of therapeutics in cancer patients? Working on the hypothesis that the abnormal tumor microenvironment
fuels tumor progression and treatment resistance, we developed an array of sophisticated imaging
technologies as well as mathematical and animal models to unravel the complex biology of the tumor
microenvironment. Using these tools, we showed that the blood and lymphatic vessels as well as the extracellular
matrix associated with tumors are abnormal. We further showed that these abnormalities generate a hostile tumor
microenvironment (e.g., hypoxia, high interstitial fluid pressure). Our work also revealed how these abnormalities
fuel malignant properties of a tumor as well as prevent treatments from reaching and attacking tumor cells. We
next hypothesized that creative manipulation of the microenvironment should improve treatment outcomes.
Toward this end, we discovered that “normalizing” the tumor vessels and matrix would allow cancer therapies to
penetrate the mass and to function more effectively. Originally designed to destroy tumor vessels, we showed,
first in mice and then in rectal and glioblastoma cancer patients, that antiangiogenic drugs could, paradoxically,