By Christine Duncan, MD
2009-12-05
The Ham-Wasserman Lecture, named in honor of renowned hematologists Drs. Thomas Hale Ham and Louis R. Wasserman, is given annually by an individual from outside the United States who has contributed significantly to an area of hematology. This year’s honorary lecturer is Professor Melvin Greaves from the Institute of Cancer Research in Sutton, England.
This year the world celebrates the 200th anniversary of Charles Darwin’s birth and the 150th anniversary of the publication of his groundbreaking book, On the Origin of Species. Thus, it is timely and fitting that Prof. Greaves has been selected to give the 51st Ham-Wasserman Lecture. His research focuses on understanding the origins of childhood acute lymphoblastic leukemia (ALL) and is built on — or more appropriately evolved from — Darwin’s principles of natural selection. He has explained his work to the scientific community in a multitude of papers. Scientists and nonscientists alike have been enthralled with his book, Cancer: The Evolutionary Legacy, which provides an evolutionary biologist’s perspective on cancer.
In a series of elegant studies Prof. Greaves has demonstrated how many cases of childhood ALL can be traced to in utero genetic events. The support for this hypothesis comes from monozygotic twin studies, examination of newborn blood spots, and analysis of umbilical cord blood. Prof. Greaves and colleagues reported the concordance rate for ALL in a series of monozygotic twins. They found that in infant ALL the concordance rate is almost 100 percent and 10 percent to 15 percent in B-cell precursor ALL. It was established that the vascular sharing afforded by the placenta resulted in blood chimerism. This work has been supported by a series of chromosomal investigations using stored neonatal blood spots (Guthrie cards) and umbilical cord blood. PCR testing of Guthrie cards and cord blood identified associated chromosomal abnormalities from children who were healthy at birth and developed ALL later in childhood. Additionally, leukemic chromosomal abnormalities were identified in the neonatal blood spots of children who did not develop leukemia. These studies and other work that Prof. Greaves will present led to a two-step model for the development of some childhood ALL with the first chromosomal change taking place in utero and secondary postnatal genetic changes occurring later in childhood. Prof. Greaves will provide rationale for why some children with neonatal leukemic chromosomal abnormalities develop leukemia while the vast majority of children remain healthy.
In On the Origin of Species, Charles Darwin wrote, “Nothing before had ever made me thoroughly realise, though I had read various scientific books, that science consists in grouping facts so that general laws or conclusions may be drawn from them.” The Darwin-esque explanation of the origins of childhood leukemia by Prof. Greaves calls to mind the same sentiment and promises to educate and inspire. Charles Darwin would be proud.
Dr. Duncan indicated no relevant conflicts of interest.
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