Hadassah Medical University
My romance with the ICRF goes back to 1985, when I was still a postdoctoral fellow in MIT. At that time, I was planning my return to Israel and taking a job at the Lautenberg Center for Immunology at the Medical School of the Hebrew University. During my post-doctoral training in the lab of Nobel Prize laureate Prof. David Baltimore, I worked on a dreadful malignancy known as Chronic Myelogenous Leukemia (CML). This disease already had an
‘Israeli affiliation’, as Eli Canaani, an ICRF fellow, was able to clone the BCR-ABL oncogene, which is the culprit of CML. My work complemented Canaani’s, as I independently cloned the mouse ABL gene and characterized the p210 onco-protein that initiates CML. That same year, I received my first ICRF grant, which in fact, was also the first ever research grant given to me as a Principal Investigator.
ICRF was both a source of powerful moral encouragement and financial support for my ongoing work on the CML oncoproteins, this time as an independent scientist in Jerusalem.
But scientific undertaking goes its own way. This project was completed in Boston before I got back to Jerusalem a year later. I therefore thought to use my ICRF funding for developing a novel therapy for CML.
CML Patients at that time had an average life span of 5 years and were in desperate need of new therapeutic approaches. To this end, I teamed with Alex Levitzki, who had an avant-garde idea to treat cancer with small molecule tyrosine kinase inhibitors. At that point, I had my second rendezvous with ICRF, which provided me with a Research Career Development Award (RCDA). Together with my student, Motti Anafi, we identified some excellent BCR-ABL inhibitors that converted aggressive leukemic cells to innocent red blood cell precursors. These pioneering studies became a platform for the development of the ‘CML magic bullet drug’ Gleevec®, by Novatis, as acknowledged in the first publication of Gleevec.
Twenty years later, I got back to work on CML. Despite the remarkable, unmatched success of Gleevec, CML remains an incurable disease and patients are still dying following CML blast crisis. Now I have matured to win an ICRF Professorship award, which enables me to seek drugs that will surpass Gleevec by their ability to destroy the CML stem cells, thereby providing complete cure of the disease.
Attaining this goal may turn out to be a happy-end of a 30 years love story between the ICRF and me.