George W. Beadle
George E. Burch
Dan H. Campbell
William B. Castle
Robert B. Corey
Charles D. Coryell
Lee A. DuBridge
Vernon M. Ingram
Harvey A. Itano
Alfred E. Mirsky
Robert M. Nalbandian
James V. Neel
A. A. Noyes
Ava Helen Pauling
Walter A. Schroeder
S. Jonathan Singer
Stanley M. Swingle
Ibert C. Wells
Paul L. Wolf
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Harvey A. Itano1920-2010
Harvey Itano Papers, 1946-2000
Location: Mandeville Special Collections Library, Geisel Library, University of California,
Address: UCSD Libraries 0175S, 9500 Gilman Drive, La Jolla, California 92093-0175
Size: 3.8 linear feet
Finding Aid: http://libraries.ucsd.edu/speccoll/testing/html/mss0226a.html
Phone: 858-534-2533 Fax: 858-534-5950
Email: email@example.com Web: http://www.ucsd.edu/portal/site/Libraries
- Letter from Linus Pauling to William Castle. November 6, 1946.
- Letter from Linus Pauling to George Burch. May 25, 1949.
- Memorandum from Linus Pauling to Harvey Itano. January 20, 1950.
- Letter from Linus Pauling to George Burch. October 5, 1951.
- Memorandum from Linus Pauling to Harvey Itano. October 12, 1951.
- Memorandum from Linus Pauling to George Beadle. July 18, 1955.
- Letter from William Castle to Linus Pauling. September 28, 1955.
- Letter from S. J. Singer to Linus Pauling. July 8, 1957.
- Letter from S. J. Singer to Linus Pauling. March 12, 1958.
- Letter from Emile Zuckerkandl to Linus Pauling. June 18, 1964.
- Letter from Linus Pauling to C. Lockard Conley. November 17, 1969.
- Letter from Linus Pauling to William G. Esmond. October 23, 1972.
- Letter from Linus Pauling to C. Lockard Conley. August 1, 1978.
- Greeting Card from Harvey Itano to Linus Pauling. December 22, 1985.
Pictures and Illustrations
Published Papers and Official Documents
Manuscript Notes and Typescripts
"The rapidity and simplicity of this test suggests that it would be useful as a clinical
laboratory procedure for diagnosing sickle cell anemia and sickle cell trait."
Linus Pauling. "A Rapid Diagnostic Test for Sickle Cell Anemia," Blood, 4(1): 66-68, 67. January 1949.
"It appears, therefore, that while some of the details of this picture of the sickling
process are as yet conjectural, the proposed mechanism is consistent with experimental
observations at hand and offers a chemical and physical basis for many of them. Furthermore,
if it is correct, it supplies a direct link between the existence of “defective” hemoglobin
molecules and the pathological consequences of sickle cell disease."
Linus Pauling. "Sickle Cell Anemia, a Molecular Disease." Science 110: 543-548. April 1949.
"The idea of Dr. Linus Pauling that an abnormal hemoglobin molecule might be responsible
for the sickling process initiated the study of the hemoglobin molecule in hereditary
Harvey Itano. "Clinical States Associated with Alterations of the Hemoglobin Molecule." Archives of Internal Medicine, 96: 287-97, 295. 1955.
"The discovery by Dr. Itano of the abnormal human hemoglobins has thrown much light
on the problem of the nature of the hereditary hemolytic anemias, and has changed
these diseases from the status of poorly understood and poorly characterized diseases
into that of well understood and well characterized diseases"
Linus Pauling. Nomination of Harvey Itano for the Theobald Smith Award. July 1955.
"The demonstration that sickle cell hemoglobin differs in electrophoretic mobility
from normal hemoglobin led to the entitled inference: 'Sickle cell anemia, a molecular
disease.' This astonishingly simple concept is of fundamental importance to medicine
for the ultimate understanding of the origins of sickness, and to biology for the
insight into what genes do. In the author's words, 'This investigation...reveals a
clear case of a change produced in a protein molecule by an allelic change in a single
gene involved in synthesis.'"
Samuel H. Boyer IV. Introduction to "Sickle Cell Anemia, a Molecular Disease." Papers on Human Genetics, 115-25. 1963.
"In 1949, application of methods of physical chemistry directly to the study of a
protein produced by a mutated gene led Pauling, Itano, Singer and Wells to identify
the specific change in the protein brought about by the gene. The discovery of the
first of the abnormal human hemoglobins which they described as causing a 'molecular
disease' -- sickle cell anemia -- was followed the identification of a large number
of other proteins, each of which owed its difference from normal structure to a mutated
gene. Ingram then showed that the change due to the mutation, in the case of each
of two abnormal hemoglobins, was confined to a single amino acid residue at one point
in one of the polypeptide chains composing the globin. There could be no doubt that
genes controlled protein structure by specifying the sequence of amino acid residues
in the polypeptide chains. The assumed basic functional correspondence was then altered
from 'one gene-one enzyme' to 'one gene-one polypeptide.'"
L. C. Dunn. "Old and New in Genetics." Bulletin of the New York Academy of Medicine, 40(5): 325-333, 329. May 1964.
"I remember asking a new graduate student, Harvey Itano, what his research problem
was. He said he was going to test your hunch that there was a difference in hemoglobin
molecules between normal people and those with sickle cell anemia. I thought that
was a crazy idea; a complicated human disease could not have any such simple cause.
And so I learned to respect bold simple ideas -- especially those conceived by Linus
Norman Davidson. Letter to Linus Pauling. January 26, 1976.