Introduction

Radioactive isotopes of phosphorus (Greek: "lightbringing") were among the first artificially produced radioisotopes in the pioneering experiments by Frederic Joliot and Irene Curie in 1934, and by Enrico Fermi and his group in the same year. In 1935, George Hevesy, after having seen the results of Fermi, was the first to produce microcurie quantities of phosphorus-32 (P-32) in Copenhagen by using a strong Ra/Be source given to Niels Bohr, and applying P-32 in a biological experiment to study the bio-distribution in rats (1). Soon, millicurie quantities were being produced by Ernest O. Lawrence in the cyclotron at Berkeley, California, and Lawrence started periodically sending Hevesy a few millicuries of P-32 (2). Later, in 1937, Hevesy was possibly the first to give a dose of a man-made radioactive substance to a human being in a study of the excretion of P-32 in a hospital patient (3). Later work by Hevesy focused on the possible use of P-32 as a red blood cell (RBC) label, which did not turn out to be satisfactory, owing to insufficient stable RBC binding.

In the meantime, Ernest O. Lawrence's brother, John H. Lawrence, a physician, developed an interest in the application of radiation for the treatment of cancer, after having seen his mother being cured of pelvic cancer by the application of a new therapy—external high voltage radiation. By this time, it was common knowledge that overexposure to radiation would lead to a reduction in the formed elements of the blood, thought of as "killing" of the formed elements, and is still not perceived as a suppression of the production by the bone marrow. To hypothesize that radiation might be useful in diseases characterized by too many blood cells, like leukemias and polycythemia, was but a short step. After several experiments in leukemic mice, in 1938, John H. Lawrence applied P-32 in the treatment of chronic myeloid leukemia in a 29-year-old student, and by 1940, he published a report on a total of five patients (4). A coworker of John H. Lawrence was to expand on the use of P-32 in polycythemia vera (PV) (5), and explain that it did not kill the excess RBC, but that it reduced the production of RBC by the bone marrow with a delayed effect of about six weeks to three months, thus necessitating the use of phlebotomy for immediate relief.

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