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Biographical Memoirs: Volume 62
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Biographical Memoirs: Volume 62 JACOB FURTH September 20, 1896-July 23, 1979 BY SIDNEY WEINHOUSE AND JOHN J. FURTH THE TWENTIETH CENTURY has witnessed the phenomenal growth of medical science, and cancer research in particular has advanced from a field of descriptive anatomy to a flourishing, sophisticated biological discipline, pregnant with insights directed toward understanding and control of one of humankind's misfortunes. One of the leaders who helped to transform cancer research to a true scientific endeavor was Jacob Furth. In a career of fifty-seven years he contributed to diverse fields of cancer biology and experimental pathology. He was responsible for major advances in immunology, leukemia and radiation, and viral carcinogenesis. His pioneering work on hormonal effects in tumor development added new dimensions to our understanding of how tumors proliferate. Jacob Furth was born in the city of Miscolcz, then part of the Austro-Hungarian Empire, in 1896. His father, Jonas, had seven children, four of whom died as infants. Jacob was the next to the youngest. His mother, Jetti Sussman, died when he was three. His father remarried Roza Farkas, and they had four more children. Roza was a simple woman and a devoted mother to both her children and her stepchildren. Jacob was particularly close to one brother, Lajos, with whom he played soccer and chess. Lajos came to the
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Biographical Memoirs: Volume 62 United States in 1941, and they remained close until his death in 1969. Jetti's children were all talented. One sister, Margit, wrote first-rate novels and poetry (in Hungarian). Jacob pondered whether to go into medicine or law. He chose medicine over law because, as he put it, "Lawyers can be hired to prove not only the right, but also that the wrong was right."1 This was at the outbreak of World War I; after his first year, having been captured in the first major battle in which his unit was engaged, Jacob spent three years in Russian military prisons. He returned to Hungary as part of a prisoner exchange and completed his medical training in 1921. His experiences as a prisoner during the turmoil of the Bolshevik Revolution, which extended into Hungary on his return, have been recounted by Murray Angevine.2 It was in Prague that Jacob met Olga Berthauer, a medical student at the Czech University, while he was attending the German University. She was to come to the United States a year after Jacob. The immigration authorities were reluctant to let her stay (as a single woman). However, they were married the next day, and, upon presentation of the marriage certificate, the immigration authorities relented. She was to be collaborator, colleague, homemaker, and confidant for over fifty years. Although maintaining a career, first as a pediatrician and later in school health, Olga's devotion to Jacob was complete. Without hesitation she gave up good jobs when he moved. She was good at her vocation, always able to get a good job in the new city (except Boston, for Massachusetts would not license a graduate of a foreign medical school). Her last job was with the School Health Department of New York City, a position she held until the mandatory retirement age of eighty. She died April 21, 1988.
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Biographical Memoirs: Volume 62 EARLY YEARS IN RESEARCH, 1918-32 Jacob had an inquiring mind and a love of learning that attracted him to research, even while a medical student. Under the guidance of Edmund Weil, one of several great scientists who, he acknowledged, had an important influence on his career, Jacob began research in microbiology and immunology, directed to whether bacterial species could be characterized antigenically. This work required keeping open plates for one or two weeks in search of mutants, and these were subject to fungal contamination. In his autobiographical essay,1 Jacob wryly confessed his chagrin at his presumption that the "damned fungi were preventing growth of the bacteria by depriving them of essential nutrients. The possibility that the fungi secreted a bactericidal substance did not cross my mind." He also regretted that he did not write up or follow up on work he started at that time on bacteriophage, just discovered by D'Herelle, recalling the statement by his dean and department chairman Oscar Bail that "this may be the greatest discovery of our period." However, a lasting contribution of the period was Jacob's introduction of the agar plate, which has now become standard practice in microbiology. A turning point in Jacob's career was the sudden death of his mentor, Edmund Weil, and his senior associate, F. Breinl, from typhus, and his own illness and recovery from the same disease. Facing the dilemma of whether to choose a career in clinical research or stay in the laboratory, and weighing his future in postwar Europe, Jacob accepted an offer from Eugene L. Opie of the Henry Phipps Institute of the University of Pennsylvania in Philadelphia. He remained there for two productive years, 1924-26, working on acid-fast organisms and their antigens. Jacob acknowledged with gratitude (naming one of his
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Biographical Memoirs: Volume 62 twin sons Eugene) the profound influence of Opie and an outstanding group of young scientists on his career. During his two years at the Phipps Institute he established immunologic relationships among acid-fast organisms, the antigenicity of microbial lipids, and at the suggestion of Opie he confirmed the observation of Zinnser that new antigens could be created by heat. This last work caught the interest of Karl Landsteiner, the discoverer of the blood groups, who invited Jacob to the Rockefeller Institute as his assistant. His two years there, from 1926 to 1928, were a profound learning experience. From Landsteiner and daily contact with other great scholars at the institute, Jacob learned both the philosophy and strategies of research. It was at the institute that he was introduced to the cancer problem by the brilliant work of Peyton Rous, James Murphy, and especially Alexis Carrel, through whom he was introduced to tissue culture, a tool he used continuously in his future work. With Landsteiner he attempted to transform saprophytic vibrios to cholera vibrios and to transform Drosophila strains. They chose the wrong organism. It was Avery who several years later successfully transformed pneumococcal strains, thereby revealing the hereditary role of DNA! Under Landsteiner's instruction Jacob demonstrated differences in the blood groups among the anthropoid apes, and Landsteiner asked him to stay on to take on Philip Levine's work on minor blood subgroups. Restless to do independent work, however, Jacob accepted an offer in 1928 from Opie to return to the Phipps Institute in Philadelphia. A return to this institution was not without some regret. In his autobiographical essay1 he points out ruefully, ''Now that Philip Levine has attained greatness by the discovery of the Rh factor . . . I see what I have missed."
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Biographical Memoirs: Volume 62 Opie had accepted a generous grant from E. Mallinkrodt, Jr., for experimental work on leukemia and placed Jacob in charge. It was here that Jacob began a long, wide-ranging, and uniquely productive study on leukemia, for which he received widespread recognition. He frequently expressed his gratitude to Mr. Mallinkrodt, who required no reports and even kept his support anonymous until 1957, when he relented on Opie's urging. Jacob took two independent approaches simultaneously. One was to obtain leukemic mouse strains. He succeeded by inbreeding mice in which leukemia occurred spontaneously or was induced by radiation. One strain, the AKR mouse, carries a leukemia virus and has become one of the most common and widely used animals in many diverse experimental studies. The second approach was to attempt to isolate viruses from the various types of leukosis then available. Five leukosis viruses were isolated and studied, one of which was the fowl neurolymphomatosis virus, the agent of Marek's disease, an economic scourge of the poultry industry until its conquest by a vaccine in 1970. Other notable findings of this period were the transmission of avian leukosis by blood-sucking insects, the occurrence of high concentrations of leukemia virus in the serum of leukemic chickens, and the viral nature of the common venereal sarcoma of dogs, transmitted through copulation. It was in Philadelphia that Jacob's twin sons were born. He somehow found time to be a good father. Both sons emulated him and became physicians. One is now in North Carolina, the chairman of the Department of Medicine at East Carolina Medical School, and the other, a coauthor of this memoir, is a professor of pathology at the University of Pennsylvania in Philadelphia.
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Biographical Memoirs: Volume 62 CORNELL, 1932-47 When Opie assumed chairmanship of the Department of Pathology at Cornell Medical College in New York in 1932, Jacob joined him as assistant professor of pathology. Acquainted with New York through his prior two years at the Rockefeller Institute, Jacob found the atmosphere exhilarating. Angevine, his colleague and sometime collaborator at Cornell, has succinctly described this period: The days spent at Cornell were among the happiest of J.F.'s career. The conditions and environment were ideal for investigation with fine, well-equipped laboratories, space for animals, a loyal and efficient technical staff, and adequate financial support.2 Angevine goes on, Initially, when full time was available for the studies on leukemia, [Jacob] was like a human dynamo, working so continuously and relentlessly that although he frequently appeared fatigued, his pace seldom slackened. He seemed to thrive in the midst of the restless activity and ferment of New York City, which served as a catalyst for his boundless energy. His enthusiastic approach to every problem attracted bright young men to his laboratory, most of whom worked hard and completed an arbeit. He was also strongly convinced of the value of student participation in research; perhaps this stemmed from his own experience as a student. Jacob's fifteen years at Cornell were very productive. With Cole and Boon in the early forties he demonstrated important genetic factors in the heritability of leukemia in mice, and in cross-breeding experiments they showed that in some instances the influences of the low leukemia strain predominated, whereas in others the high leukemia strain predominated. He (and others) also showed that heritability was not due to a maternal "milk factor," as it was with high and low mammary tumor strains.
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Biographical Memoirs: Volume 62 A role of the thymus in leukemia was shown by work with McEndy and Boon. In the high leukemia AK strain, removal of the thymus, a primary site in this strain, lowered the incidence from 78 to 11 percent. Removal of the spleen had no effect, and the effect of thymectomy was not inherited, since the offspring of thymectomized mice had the same high incidence as the high leukemia grandparent. Thymectomy also lowered the incidence of methylcholanthrene-induced leukemia but had no effect on the growth of grafted leukemic cells, which grow equally in high and low leukemic mice. During his period at Cornell Jacob received support not only from the Mallinkrodt Fund but also from the Lady Tata Memorial Trust, the International Cancer Research Foundation, the Jane Coffin Childs Fund, and the Anna Fuller Fund. Although research remained his foremost interest, Jacob enthusiastically entered into the other elements of the academic triad, teaching and service. Also in his mind was the tenuous nature of full-time research, particularly at that time. He was in a pathology department and felt he had to become a "compleat" pathologist. He took a minisabbatical to Vienna to learn anatomical pathology from Masters. One of Jacob's major responsibilities was teaching experimental pathology, then a requirement for medical students, who had the choice of spending two semesters on an investigative study proposed by either the staff or the student. He derived much satisfaction in having indoctrinated future physicians in the methods and spirit of research and in some instances having encouraged students toward research careers. Additional wartime responsibilities as acting chairman of the department when Opie retired and other staff members left for wartime service drew
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Biographical Memoirs: Volume 62 him further away from research. He regretted this hiatus in his leukemia studies, causing loss in momentum to other investigators. Much of his most important work on viral causation of leukemia, such as genetic inheritance of the virus causing leukemia in AK mice, went unreported. Another important contribution inadequately reported during the pressure of wartime responsibilities were the effects of thymectomy in preventing viral expression and the use of thymus extracts to activate viral expression. This work, however, marked the beginning of a major career effort, to be described later, on the role of host factors in cancer development. As recognition came and he advanced to full professorship, Jacob became increasingly in demand as a consultant and as a member of committees dealing with the evaluation of research projects and policies for such agencies as the Armed Forces Institute of Pathology, the Atomic Energy Commission, the National Institutes of Health, and the American Cancer Society. As a sometime member with him on such panels, the senior author of this biography saw firsthand how well Jacob performed in these roles. He was a superb adviser on these bodies—forthright in his opinions, backed always by adequate documentation; they were invariably the well-thought, considered, and eminently fair views of an erudite scientist well versed in biomedical science. These same qualities made for extremely effective service on editorial boards for a number of journals such as Blood, Cancer Research, Journal of the National Cancer Institute, and others, to which he gave much time and effort. Jacob modestly attributed his productivity at Cornell to ... a good student body, associates and assistants. We reported on the individuality of various types of leukemia in mice; their transmission by a single cell; a method for preservation of living cells by slow freezing (with
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Biographical Memoirs: Volume 62 C. Breedis); the genetics of spontaneous leukemia (with R. Cole); the role of the thymus in leukemogenesis; the individuality of the monocytes, histiocytes and microglia cells (with H. Dunning) and their relation to reticulum cell sarcoma; differentiation of leukemia and leukemoid reactions (with W. A. Barnes); and the possibilities of experimental therapy of leukemias (with L. Reiner and C. Flory). We also expanded the list of different viruses causing leukemias and sarcomas, and indicated the essential identity of mouse and human leukemias and the neoplastic character of both. . . . The two years Elvin Kabat spent with us at Cornell were highly productive. In addition to work on high-speed sedimentation of leukemia viruses, the histochemical identification of alkaline phosphatases, and the localization of alkaline phosphatase (with C. Breedis) in the proximal convoluted tubules of the kidney led us to identify the site of nephrotoxic agents such as the mercurial compounds, then used in the therapy of syphilis.1 A SHORT STAY IN DALLAS, 1947-49 Disappointed at being passed over for chairmanship of the Pathology Department at Cornell after Opie's retirement, Jacob left to join the Veterans Administration Hospital in Dallas, Texas, in 1947. The Dallas position also carried an academic appointment at Southwestern Medical College, but several unforeseen setbacks made this position much less desirable than he had anticipated. Though accepted wholeheartedly by the faculty, the dean (a retired general of the Army Medical Corps) refused to appoint Jacob to a full professorship, a rank he held at Cornell; nor would the dean allow him to accept any of the research grants from the foundations that supported him in New York. (It would be hard to imagine any of today's deans conducting such an act of self-immolation.) Although a heavy service load severely handicapped Jacob's research, notable observations were still made. With T. Bali he observed some remarkable changes in radiation-induced ovarian tumors, and he isolated a highly functional mast cell tumor.
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Biographical Memoirs: Volume 62 When the Veterans Administration abolished its regional organization, a better opportunity arose in 1949 to chair a department in one of its university-based hospitals. At the same time, however, Jacob received a cordial invitation from Alexander Hollaender to join the Biology Division of Oak Ridge National Laboratory. He accepted on the advice of Shields Warren, a statesman of U.S. science who at the time was head of the Atomic Energy Commission Biology Division, and thus ended a seventeen-year period of broad-based pathology to return once again to the laboratory. RADIATION BIOLOGY AT OAK RIDGE, 1950-54 Jacob had already contributed to radiation carcinogenesis with x-ray induction of leukemia in mice back in 1929, the induction of ovarian tumors as late radiation effects, and some attempts at γ-ray therapy of experimental leukemia. Enthusiastically plunging into the newly developing area of radiation biology, Jacob greatly expanded his perceptions by taking a course in radiation physics. Aided and guided by members of the Biology Division, he entered a renewed surge of research accomplishment in a highly charged atmosphere, of the same type that had nourished and sustained him at Cornell. A unique experiment in which he took part at Oak Ridge was a massive study of radiation effects on mice, resulting from an experimental explosion of an atomic bomb (Operation Greenhouse). As Shields Warren wrote, Jacob was the recipient of large numbers of mice, survivors from a Pacific nuclear test, placed with various degrees of shielding along radii from the point of explosion. He had the foresight to follow these animals to the time of their natural death. As a result of these studies, much new information was developed about the late effects of radiation, about biological dosimetry, and about the similarity of certain radiation effects to those of aging. The meticulous care with which these animals were kept free of
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Biographical Memoirs: Volume 62 Its concentration in blood cells and plasma and relation to the incubation period. J. Exp. Med. 55:465-78. With H. K. Miller. Studies on the nature of the agent transmitting leucosis of fowls. II. Filtration of leucemic plasma . J. Exp. Med. 55:479-93. Studies on the nature of the agent transmitting leucosis of fowls. III. Resistance to desiccation, to glycerin, to freezing and thawing, survival at ice box and incubator temperatures. J. Exp. Med. 55:495-504. 1933 With R. R. Rathbone and H. R. Seibold. Relation of x-rays to lymphomatosis. Proc. Soc. Exp. Biol. Med. 30:754-56. With H. L. Ratcliffe. Studies on the pathogenesis of erythroleucosis. Am. J. Pathol. 9:165-84. 1934 With D. H. Kabakjian. Studies on the effect of continuous exposure of mice to gamma rays of radium. Am. J. Roentgenol. Radium Ther. 32:227-34. Lymphomatosis, myelomatosis, and endothelioma of chickens caused by filterable agent. II. Morphological characteristics of the endotheliomata caused by this agent. J. Exp. Med. 59:501-17. With E. L. Stubbs. Experimental studies on venereal sarcoma of the dog. Am. J. Pathol. 10:275-86. 1935 With H. W. Ferris and P. Reznikoff. Relation of leukemia of animals to leukemia of man. J. Am. Med. Assoc. 105:1824-30. With H. S. Dunning. Studies on the relation between microglia, histiocytes and monocytes . Am. J. Pathol. 11:895-914. 1936 The relation of leukosis to sarcoma of chickens. II. Mixed osteochondrosarcoma and lymphomatosis (Strain 12). III. Sarcomato of strains 11 and 15 and their relation to leukosis. J. Exp. Med. 63:127-35. With O. B. Furth. Neoplastic diseases produced in mice by general irradiation with x-rays. I. Incidence and types of neoplasms. Am. J. Cancer 28:54-65.
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Biographical Memoirs: Volume 62 With J. S. Butterworth. Neoplastic diseases occurring among mice subjected to general irradiation with x-rays. II. Ovarian tumor and associated lesions. Am. J. Cancer 28:66-95. 1937 With M. C. Kahn. The transmission of leukemia of mice with a single cell. Am. J. Cancer 31:276-82. 1938 With A. Tuggle and C. Breedis. Quantitative studies on the effect of x-rays on neoplastic cells. Proc. Soc. Exp. Biol. Med. 38:490-92. With M. C. Kahn. Transmission of mouse sarcoma with small numbers of counted cells. Proc. Soc. Exp. Biol. Med. 38:485-586. With C. Breedis. The feasibility of preserving neoplastic cells in the frozen state. Science 38:531-32. With O. B. Furth. Monocytic leukemia and other neoplastic diseases occurring in mice following intrasplenic injection of 1:2-benzpyrene. Am. J. Cancer 34:169-83. 1939 A neoplasm of monocytes of mice and its relation to similar neoplasms of man. J. Exp. Med. 69:13-30. 1940 With E. A. Kabat. Chemical and immunological studies on the agent producing leukosis and sarcoma of fowls. J. Exp. Med. 71:5570. With W. A. Barnes. A transmissible malignant neoplasm of mice originating in reticular or endothelial cells. Am. J. Pathol. 16:457-65. With E. A. Kabat. Association of the heterogenetic antigen with a material in normal and tumor tissues sedimentable at high speed. Science 91:483-85. 1941 With E. A. Kabat. A histochemical study of the distribution of alkaline phosphatase in various normal and neoplastic tissues. Am. J. Pathol. 17:303-18. With E. A. Kabat. Immunological specificity of material sedimentable at high speed present in normal and tumor tissues. J. Exp. Med. 74:247-56.
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Biographical Memoirs: Volume 62 With E. A. Kabat. Association of the Wassermann antigen with heavy materials present in tissues. Science 94:46-47. With E. A. Kabat. Neutralization of the agent causing leukosis and sarcoma of fowls by rabbit antisera. J. Exp. Med. 74:257-61. With R. K. Cole. Experimental studies on the genetics of spontaneous leukemia in mice. Cancer Res. 1:957-65. 1942 With R. K. Cole and M. C. Boon. The effect of maternal influence upon spontaneous leukemia of mice. Cancer Res. 2:280-83. With D. P. McEndy and M. C. Boon. Induction of leukemia in mice by methylcholanthrene and x-rays. J. Natl. Cancer Inst. 3:227-47. 1943 With W. A. Barnes and O. B. Furth. Studies on the indirect effect of Roentgen rays in single and parabiotic mice. Am. J. Roentgenol. Radium Ther. 49:662-81. With M. C. Boon. Enhancement of leukemogenic action of methylcholanthrene by preirradiation with X-rays. Science 98:138-39. 1944 With M. C. Boon and N. Kaliss. On the genetic character of neoplastic cells as determined in transplantation experiments. With notes on the somatic mutation theory. Cancer Res. 4:1-10. Neoplastic growth. Annu. Rev. Physiol. 6:25-68. With D. P. McEndy and M. C. Boon. On the role of thymus, spleen, and gonads in the development of leukemia in a high-leukemia stock of mice. Cancer Res. 4:377-83. 1946 Recent experimental studies on leukemia. Physiol. Rev. 26:47-76. Prolongation of life with prevention of leukemia by thymectomy in mice. J. Gerontol. 1:46-54. With H. Sobel. Hypervolemia secondary to grafted granulosa-cell tumor. J. Natl. Cancer Inst. 7:103-13. 1947 With H. Sobel. Transplantable luteoma in mice and associated secondary changes. Cancer Res. 7:246-62.
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Biographical Memoirs: Volume 62 With M. C. Boon. Induction of ovarian tumors in mice by x-rays. Cancer Res. 7:241-45. 1949 With T. Ball. A transplantable splenic tumor rich in mast cells. Observations on mast cells in varied neoplasms. Am. J. Pathol. 25:605-25. With T. Ball. Morphological and biological characteristics of x-ray-induced transplantable ovarian tumors. Cancer Res. 9:449-72. 1951 With R. R. Bigelow, M. C. Woods, and R. H. Storey. Endothelial damage by x-rays disclosed by lymph fistula studies. Proc. Soc. Exp. Biol. Med. 76:734-36. Recent studies on the etiology and nature of leukemia. Blood 6:964-75. With W. T. Burnett, Jr. Hormone-secreting transplantable neoplasms of the pituitary induced by I131. Proc. Soc. Exp. Biol. Med. 78:222-24. 1952 With J. B. Kahn, Jr. The pathogenesis of postirradiation anemia. Blood 7:404-16. With E. L. Gadsden and W. T. Burnett, Jr. Autonomous transplantable pituitary tumors arising in growths dependent on absence of the thyroid gland. Proc. Soc. Exp. Biol. Med. 80:4-7. 1953 With M. C. Woods, F. N. Gamble, and R. R. Bigelow. Control of the postirradiation hemorrhagic state by platelet transfusions. Blood 8:545-53. With W. T. Burnett, Jr., and E. L. Gadsden. Quantitative relationship between thyroid function and growth of pituitary tumors secreting TSH. Cancer Res. 13:298-307. Conditioned and autonomous neoplasms: A review. Cancer Res. 13: 477-92. With A. C. Upton. Vertebrate radiobiology: Histopathology and carcinogenesis. Annu. Rev. Nucl. Sci. 3:303-38. With E. L. Gadsden. Effect of thyroid hormone on growth of thyrotrophin-secreting pituitary tumors. Proc. Soc. Exp. Biol. Med. 83:511-14.
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Biographical Memoirs: Volume 62 With A. C. Upton. Induction of pituitary tumors by means of ionizing irradiation. Proc. Soc. Exp. Biol. Med. 84:255-57. With E. L. Gadsden and A. C. Upton. ACTH secreting transplantable pituitary tumors. Proc. Soc. Exp. Biol. Med. 84:253-54. 1954 With A. C. Upton. The effects of cortisone on the development of spontaneous leukemia in mice and on its induction by irradiation. Blood 9:686-95. With A. C. Upton, K. W. Christenberry, W. H. Benedict, and J. Moshman. Some late effects in mice of ionizing radiation from an experimental nuclear detonation. Radiology 63:562-70. With A. C. Upton and K. W. Christenberry. Late effects of thermal neutron irradiation in mice. Cancer Res. 14:682-90. Thyroid-pituitary tumorigenesis. J. Natl. Cancer Inst. 15:687-91. 1955 With J. N. Dent and E. L. Gadsden. On the relations between thyroid depression and pituitary tumor induction in mice. Cancer Res. 15:70-75. With J. N. Dent, W. T. Burnett, Jr., and E. L. Gadsden. The mechanism of induction and the characteristics of pituitary tumors induced by thyroidectomy. J. Clin. Endocrinol. Metab. 15:81-97. With A. C. Upton. Spontaneous and radiation-induced pituitary adenomas of mice. J. Natl. Cancer Inst. 15:1005-21. 1956 With J. N. Dent and E. L. Gadsden. Further studies on induction and growth of thyrotropic pituitary tumors in mice. Cancer Res. 16:171-74. With J. Mayer and C. Zomzely. Body composition and energetics in obesity induced in mice by adrenotropic tumors. Science 123:184. With E. L. Gadsden, K. H. Clifton, and E. Anderson. Autonomous mammotropic pituitary tumors in mice: Their somatotropic features and responsiveness to estrogens. Cancer Res. 16:600-607. With K. H. Clifton, E. L. Gadsden, and R. F. Buffett. Dependent and autonomous mammotropic pituitary tumors in rats: Their somatotropic features. Cancer Res. 16:608-16. With A. C. Upton, G. S. Melville, Jr., M. Slater, and F. P. Conte.
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Biographical Memoirs: Volume 62 Leukemia induction in mice by fast neutron irradiation. Proc. Soc. Exp. Biol. Med. 92:436-38. With R. W. Bates, K. H. Clifton, and E. Anderson. Prolactin and thyrotropin content of functional transplantable pituitary tumors. Proc. Soc. Exp. Biol. Med. 93:525-27. 1957 With R. Bahn, E. Anderson, and E. Gadsden. Morphologic and functional changes associated with transplantable ACTH-producing pituitary tumors of mice. Am. J. Pathol. 33:1075-97. With K. H. Clifton. Experimental pituitary tumors and the role of pituitary hormones in tumorigenesis of the breast and thyroid. Cancer 10:842-53. Discussion of problems related to hormonal factors in initiating and maintaining tumor growth. Cancer Res. 17:454-63. With K. H. Clifton. Hormonal influences on growth and somatotropic actions of autonomous mammotropes. Proc. Soc. Exp. Biol. Med. 94:809-14. With R. Bahn, H. Wilson, L. Kedda, and E. Anderson. Metabolic changes associated with transplantable ACTH-producing pituitary tumors of the mouse. Can. J. Biochem. Biophys. 35:1057-65. With P. Hagen and E. I. Hirsch. Transplantable mastocytoma in the mouse containing histamine, heparin, 5-hydroxytryptamine. Proc. Soc. Exp. Biol. Med. 95:824-28. 1959 With D. Metcalf and R. F. Buffett. Pathogenesis of mouse leukemia caused by Friend virus. Cancer Res. 19:52-58. With N. Haran-Ghera, H.J. Curtis, and R. F. Buffett. Studies on the pathogenesis of neoplasms by ionizing radiation. I. Pituitary tumors. Cancer Res. 19:550-56. With J. D. Levinthal and R. F. Buffett. Prevention of viral lymphoid leukemia of mice by thymectomy. Proc. Soc. Exp. Biol. Med. 100:61924. With N. Haran-Ghera, R. F. Buffett, and K. Yokoro. Studies on the pathogenesis of neoplasms by ionizing radiation. II. Neoplasms of endocrine organs. Cancer Res. 19:1181-87.
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Biographical Memoirs: Volume 62 1960 With N. Haran-Ghera and P. Pullar. Induction of thyrotropin dependent thyroid tumors by thyrotropes. Endocrinology 66:694-701. With E. Bloch and A. I. Cohen. Steroid production in vitro by normal and adrenal tumor-bearing male mice. J. Natl. Cancer Inst. 24:97-107. With U. Kim and K. H. Clifton. A highly inbred line of Wistar rats yielding spontaneous mammosomatotropic pituitary and other tumors. J. Natl. Cancer Inst. 24:1031-55. With K. H. Clifton. Ducto-alveolar growth in mammary glands of adrenogonadectomized male rats bearing mammotropic pituitary tumors. Endocrinology 66:893-97. With G. A. Edwards and R. F. Buffett. The micromorphology of a salivary-gland tumor of a mouse infected with polyoma virus. J. Natl. Cancer Inst. 25:25-51. With K. Yokoro and N. Haran-Ghera. Further observations on pituitary tumorigenesis by X-rays in mice and rats. Radiat. Res. 12(51). With A. C. Upton, A. W. Kimball, K. W. Christenberry, and W. H. Benedict. Some delayed effects of atom-bomb radiations in mice. Cancer Res. 20(Part 2):1-62. With U. Kim. Relation of mammary tumors to mammotropes. I. Induction of mammary tumors in rats. Proc. Soc. Exp. Biol. Med. 103:640-42. With U. Kim. Relation of mammary tumors to mammotropes. II. Hormone responsiveness of 3-methylcholanthrene induced mammary carcinomas. Proc. Soc. Exp. Biol. Med. 103:642-45. With U. Kim and K. H. Clifton. Relation of mammary tumors to mammotropes. III. Hormone responsiveness of transplanted mammary tumors. Proc. Soc. Exp. Biol. Med. 103:646-50. With U. Kim. Relation of mammotropes to mammary tumors. IV. Development of highly hormone dependent mammary tumors. Proc. Soc. Exp. Biol. Med. 105:490-92. 1961 With K. Yokoro and N. Haran-Ghera. Induction of mammotropic pituitary tumors by X-rays in rats and mice. The role of mammotropes in development of mammary tumors. Cancer Res. 21:178-86.
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Biographical Memoirs: Volume 62 With K. Yokoro. Enhancement of induction of breast tumors with x-rays by mammotropin in rats . Radiat. Res. Abstract No. 188. With K. H. Clifton. Changes in hormone sensitivity of pituitary mammotropes during progression from normal to autonomous. Cancer Res. 21:913-30. With K. Yokoro. Relation of mammotropes to mammary tumors. V. Role of mammotropes in radiation carcinogenesis. Proc. Soc. Exp. Biol. Med. 107:921-24. 1962 With H. Takemoto, K. Yokoro, and A. I. Cohen. Adrenotropic activity of mammosomatotropic tumors in rats and mice. I. Biological aspects. Cancer Res. 22:917-24. With K. Yokoro. Determining role of ''mammotropins" in induction of mammary tumors in mice by virus. J. Natl. Cancer Inst. 29:887-909. 1963 Influence of host factors on the growth of neoplastic cells. Cancer Res. 23:21-34. With U. Kim and K. Yannopoulos. Observations on hormonal control of mammary cancer. I. Estrogen and mammotropes. J. Natl. Cancer Inst. 31:233-59. 1964 With A. Kunii. Inhibition of lymphoma induction in virus-infected rats by thymectomy. An affinity of the lymphoma virus of myeloid cells. Cancer Res. 24:493-97. With K. Yokoro, A. Kunii, and P. W. Durbin. Tumor induction with Astatine-211 in rats: Characterization of pituitary tumors. Cancer Res. 24:683-88. 1965 With D. Sinha and R. Pascal. Transplantable thyroid carcinoma induced by thyrotropin. Arch. Pathol. 79:192-98. With A. Kunii and A. Cali. Effect of neonatal thymectomy on induction of leukemia by virus in rats. Proc. Soc. Exp. Biol. Med. 118:815-18. With A. Kunii and H. Takemoto. Leukemogenic filterable agent
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Biographical Memoirs: Volume 62 from estrogen-induced thymic lymphoma in RF mice. Proc. Soc. Exp. Biol. Med. 119:1211-15. 1966 With A. Kunii and L. Berwick. Studies on restoration of sensitivity of thymectomized rats to viral leukemia. Cancer Res. 26:48-59. Discussion/etiology of lymphomas and leukemias. Twentieth Annual Symposium on Fundamental Cancer Research-A Broad Critique, M. D. Anderson Hospital and Tumor Institute, Houston, pp. 196-200, 388-93. (Sessions chaired by Dr. Jacob Furth.) 1967 With P. Moy. Use of antibodies of sera of hypophysectomized animals in pituitary hormone analysis and the application of Landsteiner's inhibition test in agar gel immunoassays. Endocrinology 80:435-46. 1968 With W. Takizawa and P. Moy. Relation of mammotropes to mammary tumors. VI. Immunoassays of rat prolactin and growth hormone. Proc. Soc. Exp. Biol. Med. 127:70-74. With S. Ueda, W. Takizawa, P. Moy, and F. Marolla. Characterization of four transplantable mammotropic pituitary tumor variants in the rat. Cancer Res. 28:1963-75. Pituitary cybernetics and neoplasia. In The Harvey Lectures, Ser. 63. New York: Academic Press. 1970 With S. Takizawa and J.J. Furth. DNA synthesis in autonomous and hormone-responsive mammary tumors. Cancer Res. 30:206-10. 1971 With A. Ito, J. M. Martin, R. E. Grindeland, and S. Takizawa. Mammotropic and somatotropic hormones in sera of normal rats and in rats bearing primary and grafted pituitary tumors. Int. J. Cancer 7:416-29. 1973 With J. M. Martin, P. Moy, and G. Ueda. Growth hormonal activity of thyrotropic pituitary tumors. Proc. Soc. Exp. Biol. Med. 142:511-15.
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Biographical Memoirs: Volume 62 With P. Moy, D. S. Schalch, and G. Ueda. Gonadotropin activities of thyrotropic tumors: Demonstration by immunohistochemical staining. Proc. Soc. Exp. Biol. Med. 142:1180-1184. With P. Moy, J. M. Hershman, and G. Ueda. Thyrotropic tumor syndrome. A multiglandular disease induced by sustained deficiency of thyroid hormones. Arch. Pathol. 96:217-26. With G. Uedo and P. Moy. Multihormonal activities of normal and neoplastic pituitary cells as indicated by immunohistochemical staining. Int. J. Cancer 12:100-14. 1975 Hormones as etiological agents in neoplasia. In Cancer, vol. 1, ed. F. F. Becker, pp. 75-120. New York: Plenum Press. 1976 The making and missing of discoveries: An autobiographical essay. Cancer Res. 36:871-80. With A. Ito and D. K. Kaul. Recent observations of 2 types of transplantable ACTH secreting pituitary tumors in mice and rats. Am. J. Pathol. 82(2):59. With U. Kim. The role of prolactin in carcinogenesis. In Vitamins and Hormones. Advances in Research and Applications, vol. 34, pp. 107-13. New York: Academic Press. 1978 The creation of the AKR strain whose DNA contains the genome of a leukemia virus. In Origins of Inbred Mice, ed. H. C. Morse, pp. 69-97. New York: Academic Press. 1979 With D. K. Kaul. Attempts to induce gonadotropic tumors immunohistochemical observations on the pituitaries of long-term gonadectomized rats. Fed. Proc. 38:102. 1980 With K. H. Clifton. Mammotropin effects in tumor induction and growth. In Hormonal Proteins and Peptides, vol. 8, pp. 75-104. New York: Academic Press.
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Biographical Memoirs: Volume 62 1981 With D. M. Linke. Gonad gonadotrope interactions, plasma gonadotropin levels and tumor induction in long-term castrated rats. Acta Endocrinol, pp. 181-85. 1982 Hormones as etiological agents in neoplasia. In Cancer: A Comprehensive Treatise, vol. 1, Etiology: Chemical and Physical Carcinogenesis, 2nd ed., ed. F. F. Becker, pp. 89-134. New York: Plenum Press.
Representative terms from entire chapter: