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Transplanted Tumors1

Nathan Kaliss

Comprehensive treatments of the research uses of transplanted tumors and reviews of the literature will be found in Hauschka ( 1952), Kaliss ( 1961, 1965), Klein ( 1959), Snell ( 1958), and Woglom ( 1929). Bibliographic compendia appear from time to time ( Handler, 1954 et seq.; 1963 et seq.), and occasional review articles in various areas of experimental cancer research appear in serials (Advances in Cancer Research, 1953 et seq.; Homburger, 1960 et seq.) and in the numerous journals dealing with cancer research and tissue grafting. The genetic relationships governing the fate of transplants apply with equal force to grafts of normal and cancer tissues and are detailed in Chapter 24.

Cancer research, from the beginnings of defined experimental approaches in the 19th century, was naturally concerned primarily with the initiating factors in cancerogenesis. With Pasteur's demonstration of the infectious etiology of disease, the search for similar causative agents for cancer was taken up with particular vigor at the turn of the century. Numerous attempts were made to transmit cancers within and between species by inoculating live tumors or tumor extracts. Some positive results were recorded, particularly in rodents, but the conditions for success were undefinable and the results unpredictable. What did become clear was that live cancer cells were required in the inoculum and that the resultant cancer was truly a graft and not a new growth generated by an infectious "cancer agent." Historical reviews of this exciting and vital period in cancer research will be found in Oberling ( 1952), Triolo ( 1964), and Woglom ( 1913, 1929).

Probably the first breakthrough to an understanding of the causes for the vagaries attending cancer grafting came with Jensen's demonstration that a mouse cancer could be consistently grafted to other mice but that the strain of mice used as host was a deciding factor in success ( Triolo, 1964). Final clarification came first with Tyzzer's demonstration in the mouse that there was a genetic basis for the acceptance or rejection of cancer grafts, and Little's experimental verification of his hypothesis that Mendelian inheritance underlay graft-host compatibility ( Little, 1921). Little advocated the use of inbred mice to provide genetically uniform research animals (Heston, 1949, 1959; Little, 1921, 1947), and inbred mice have since been the chief contributors to the development of experimental cancer research. Most of the important strains still in widespread use derive from those first developed by C.C. Little and L.C. Strong ( Green, 1964; Heston, 1949, 1959; Staats, 1964). They have furnished a wide variety of cancers, indispensable to investigations in cancer biology and to an understanding of transplantation genetics and immunology.

It was suspected very early that the rejection of tumor grafts was accompanied by an immunological reaction ( Triolo, 1964; Woglom, 1913, 1929) and this gave impetus to the hope for realizing an immunotherapy for cancer. In attempts to equate the reactions to grafts with responses to infectious disease, extensive searches were made for specific antibodies in animals with regressing grafts, but without success, More rewarding were studies on the histopathology of the graft site, particularly those of Murphy ( 1926) and his colleagues, who demonstrated involvement of the lymphoid tissues and the lymphocyte in particular in the rejection of grafts. They noted the cellular responses as operative in grafts of both normal tissues and cancers and in infections such as tuberculosis. Though Murphy did not recognize the lymphocytic reaction as immunologically specific and allied to the evocation of antibodies, he foreshadowed the concept that these responses are dual manifestations of immune activity.

The first indication that immunologically specific mechanisms are involved in graft rejection was given by Gorer's ( 1942) demonstration that hemagglutinating antibodies appeared concomitantly with the rejection of tumor homografts in mice. Specificity of the lymphoid response to tumor grafts was demonstrated by Mitchison ( 1955), and Medawar ( 1957) and his colleagues extended this finding to normal tissue grafts. It is now generally recognized that the immunological defenses mobilized against infectious agents are identical with those evoked by tissue isoantigens (equals "alloantigens," Chapter 24), whether resident in normal tissues or cancers ( Gorer, 1961; Chapter 31). This understanding puts in proper perspective the experimental conditions that must be satisfied in a search for cancer-specific antigens and points up the strictures attending the use of transplanted tumors for this purpose ( Hauschka, 1952; Kaliss, 1961, 1965; Klein, 1959; Snell, 1958). Woglom ( 1929) has given an incisive critique of the flood of earlier unsuccessful attempts with tumor transplants and much of his analysis of the reasons for failure still holds true in the light of our present understanding. The paper will repay reading by anyone contemplating immunological researches with transplanted tumors.


Beyond the initial motivations in developing tumor grafting outlined above, transplanted tumors have made major contributions to cancer biology which would otherwise have been unrealizable, or achievable with great difficulty ( Furth, 1959). Accounts of some of the research areas that have been enriched follow.


The term "progression" is broadly inclusive of the changes in characteristics exhibited by tumors during their "lifetime" (Foulds, 1954, 1958; Furth, 1959; Furth et al., 1960; Klein and Klein 1957). Examples are the alteration in endocrine tumors from dependence upon hormones for their survival to their eventual autonomy, the development of metastases, variations in growth rate and invasiveness, and the morphological evolution of chemically induced cancers ( Chapter 27). The changes, seemingly sporadic and unpredictable, are often unobserved in autochthonous ("spontaneous") tumors, since there may be insufficient time for them to develop during the curtailed life of the afflicted animal. They do, however, occur, and the transplanted tumor, whose existence is prolonged beyond that of the original donor, is the essential tool for their detection and study. The information gained is of immediate clinical interest, since the choice of therapeutic measures may depend upon the peculiarities of a given cancer as exemplified in its life-history.

Cancerogenic viruses

The search for infectious cancerogenic agents operative in mammals has received its largest impetus with success achieved within the last three decades ( American Cancer Society, 1960; Dalton and Hagenau, 1962; Gross, 1961; Chapters 27, 30). The chief research instrument has been the variety of inbred strains of mice with well-characterized life-histories detailing the autochthonous tumors peculiar to each strain (Heston, 1949, 1959, 1963; Staats, 1964). Crucial proof that tumors are induced de novo by agents present in ultrafiltrates of tumor homogenates has been provided by the strain (genetic) specificity of such tumors when transplanted. Thus, filtrates prepared from leukemias arising in strain AKR mice produced leukemias when injected into newborn C3H mice. On transplantation, the latter leukemias were accepted by C3H mice but were rejected by AKR mice ( Gross, 1961). This finding and the fact that the C3H strain normally has a very low incidence of leukemia was positive proof that some agent in the filtrate, and not live AKR leukemia cells, was responsible for the initiation of leukemias in the C3H mice injected at birth. We have here an instructive example of how such an understanding of the genetics of transplantation, provided in the first place by studies in inbred mice, in turn supplied the essential tool for demonstrating an infectious origin for a mammalian cancer.

Chromosome morphology in relation to cancer

The suggestion was made early in the history of cancer research that the induction of chromosomal abnormalities ( Chapter 7) — whether in the form of deviations from the normal diploid complement or of aberrant chromosome types — initiated the cancerous transformation ( Bayreuther, 1960; Bielder et al., 1961; Ford et al., 1958; Hauschka, 1961; Hellström et al., 1963; Koller, 1963; Stevens and Bunker, 1964; Wakonig, 1960). There is still disagreement as to whether the departure from mitotic normality observed in many cancers is a consequence of cancerogenesis or is a necessary precondition. Studies of primary and transplanted tumors have shown that the former in many instances are diploid ( Bayreuther, 1960; Hellström et al., 1963; Stevens and Bunker, 1964; Wakonig, 1960) and heteroploidy appears on repeated transplantation. One school of thought holds that heteroploidy is imposed on the cancer cell by its abnormal biology, with selective advantages thereby conferred assuring the continued growth of the cancer ( Koller, 1963). In this respect, transplanted tumors may be considered as examples of the "progression" one might find if a given tumor were examined cytologically from its genesis and at intervals throughout its period of growth. A model study in this manner has been made with testicular teratomas in mice ( Stevens and Bunker, 1964). These tumors permit histological detection at an unusually early stage of their inception. Diploidy was characteristic of the primary tumors, whereas aneuploidy and aberrant chromosomes appeared on transplantation.


Transplanted tumors — rather than "spontaneous" cancers — are most widely used for assaying the therapeutic effectiveness of a large and bewildering array of compounds. The ready availability of grafts in large numbers and under presumably standard biological conditions has made transplanted tumors test objects of choice. An introduction to methodology and statements of the logic of various approaches to a rationale of chemotherapy will be found in a symposium of the American Cancer Society ( 1963). In this country, testing standards and procedures have been set up under the guidance of the National Institutes of Health's Cancer Chemotherapy National Service Center (Cancer Chemotherapy National Service Center, 1962). Periodic reports on the relative effectiveness of compounds are to be found in supplements to Cancer Research ( Leiter, 1958 et seq.).

An interesting ancillary development has been the discovery that some radiomimetic drugs will suppress the immune response to grafts or normal or cancer tissues ( Glynn et al., 1963; Hitchings and Elion, 1963; Humphreys et al., 1961, 1963; Uphoff, 1961). An extensive research field has developed in an attempt to use such drugs clinically to ensure survival of homografts of normal tissues and organs. This finding stresses the necessity for caution in interpreting the data of chemotherapeutic assays, since there may be a balance between the effects of a given drug on the cancer graft and on the immune response of the host. It emphasizes the fact that the host-graft relationship for a given assay combination must be clearly defined ( Teller et al., 1964), for it cannot be taken for granted that the host may be simply acting as a passive provider of the conditions necessary for the graft's growth.


Fundamental to the development of prophylaxis and therapy is an understanding of the biological properties peculiar to cancers, and biochemical characterization is essential for this understanding. Biochemical investigations concern the nature of both cancerous tissues ( American Cancer Society, 1956; Bergel, 1961; Busch and Starbuck, 1964; Greenstein, 1954; Kit, 1960; LePage and Henderson, 1960; Potter, 1962) and the cancer-bearing animal ( Furth, 1959; Greenstein, 1954). Transplanted tumors, as a putative source of large quantities of tissue of uniform character, seem to offer unique material for study. The choice of tumor, however, must be governed by the validity of its being specifically comparable with the normal tissue from which the tumor presumably arose, and this is not always unequivocally achievable, particularly with long-transplanted tumors. Potter ( 1962) has stated the problem and outlined the criteria to be met in choosing a model tumor. Statements of the main theories of the biochemistry of cancerogenesis will be found in a symposium of the American Cancer Society ( 1956) and in Bergel ( 1961), Busch and Starbuck ( 1964), and Potter ( 1962).


Types of tumors

The spectrum of transplanted tumors carried in mice reflects the range of autochthonous and experimentally produced tumors found in the laboratory ( Chapter 27). Dunham and Stewart ( 1953) listed and briefly described 159 tumors, most of which were maintained by United States investigators. Stewart et al. ( 1959) have given detailed descriptions of the history, histology, and growth characteristics of 30 tumors selected as prototypes of the variety to be found in the mouse. Many more tumors have since been reported from a number of countries and new ones continually appear in the literature. It would be much beyond the scope of this chapter to attempt to list them.

Tumors originally of similar histological type may exhibit considerable changes on continued transplantation ( Chapter 27; Stewart et al., 1959). Some tumors, for example, may lose their identity and become undifferentiated. It is, therefore, advisable to fix pieces (perhaps at every fifth transfer) for microscopic evaluation. Growth rates may vary considerably for tumors of the same histological type ( Stewart et al., 1959), and some tumors characteristically metastasize to the lymph nodes or organs distant from the site of tumor inoculation, while others do not ( Stewart et al., 1959) the growth patterns of tumors may vary with the histological type, or may vary for tumors of the same type ( Chapter 27; Stewart et al., 1959). Thus, certain lymphatic leukemias regularly disseminate when inoculated subcutaneously, while others produce only localized growths. Some endocrine tumors have special hormonal requirements for their continued growth on transplantation. Of particular note are the so-called dependent pituitary tumors which arise and will grow only in mice radiothyroidectomized by I131 ( Furth et al., 1960). The tumors may become "autonomous" on continued transplantation and will then grow in normal hosts. These and other transplanted endocrine tumors have been of particular value in studying the interrelationships underlying the hormonal genesis of cancers (Chapters 20, 27).

The designation (coding) of transplanted tumor lines constitutes an esoteric and bewildering language of its own. This reflects the fact that there is no generally accepted convention for coding transplanted tumors, and each investigator devises his own system. Tumors reported for the first time should be precisely identified by a statement of their origin, their histological characterization, and their peculiarities on initial and continued transplantation.

Ascites tumors

Some tumors will grow as a dispersal of cells, free of a supporting stroma or vasculature, when innoculated intraperitoneally ( Klein and Klein, 1960). A large volume of peritoneal fluid develops as the tumor cells multiply. This form of growth offers a particularly convenient research tool, since it permits rather precise cellular quantitation of an inoculum. (With solid tumors, quantitation is more difficult and inaccurate at best, though methods have been devised to disperse the growths into discrete cells [ Boyse, 1960; Snell, 1953].) Ascites growths provide a relatively "pure culture" of tumor cells, though the fluid will contain some lymphoid cells and it may eventually become suffused with red blood cells. An account of the different research uses of ascites tumors will be found in Miner ( 1956).

Nongenetic factors affecting growth of tumor transplants

Even when there is genetic identity between tumor graft and host — and the graft is therefore expected to grow uniformly and without hindrance — extrinsic factors may alter the rate of growth and sometimes completely prevent it. Infectious contaminants — viral or bacterial — which transplanted tumors often acquire are a common source of trouble. The ambient temperature may alter the growth rate of subcutaneous grafts. Discussion of a variety of nongenetic conditions affecting tumor grafting will be found in Kaliss ( 1961), Klein ( 1959), and Snell ( 1958).

It is not an unusual experience that the primary transplant of a tumor originating in an inbred mouse will not grow in 100 per cent of hosts of the same inbred strain. With continued transfers the grafts will grow in all hosts and often at a much increased rate, so that transfers have to be made at shorter intervals to avoid losing the tumor line. The bases for these changes are not understood, and they have been variously attributed to "increased virulence" or to "antigenic simplification." "Virulence" is a descriptive general term for the unrestrained growth that distinguishes cancer as a disease and which is still the chief puzzle of cancer biology. "Antigenic simplification" implies that an autochthonous cancer may be immunogenic to its host and, by extension, to inbred mice when grafted to all individuals of the same strain, a possibility which is increasingly being demonstrated as a reality ( Kaliss, 1965; Old and Boyse, 1965; Prehn, 1965).

Transplantation sites

A variety of sites has been used including the eye, brain, ovarian capsule, and splenic capsule, but the most usual are the subcutaneous (actually subpannicular in the mouse, in which the panniculus carnosus muscle layer is intimately associated with the overlying dermis), intraperitoneal, and intramuscular. Subcutaneous inoculations are usually placed in the dorsum or the flanks. For routine maintenance of most solid tumors, the inoculum is placed subcutaneously; the intraperitoneal site is used for ascites growths. As much as is feasible, the sterile procedures attending surgery should be observed during transplantation (Cancer Chemotherapy, National Service Center, December, 1962). This is not so much to protect the host as to prevent infection of the graft.


Tumors can be kept viable in the frozen state for prolonged periods ( Hauschka et al., 1959; Kilsileva, 1961; Klein et al., 1957; Morgan et al., 1956; Schmidt and Tessenow, 1960; Sugiura, 1961). Successful storage for as long as 2 years has been reported ( Hauschka et al., 1959). The earlier methods used mechanical freezers or dry-ice chests maintaining a temperature of about -78°C. Preservation is better at even lower temperatures, and containers of simple design are now available for storage in liquid nitrogen (-147°C). Mechanical freezers are also made that can maintain temperatures much below that of dry ice. The usual method for preparing solid tumors for freezing is to immerse small pieces in various media (glycerol-glucose, for example) in sealed sterile ampoules. Ascitic tumors are likewise mixed in various proportions with a conditioning medium such as glycerol-glucose and sealed in sterile ampoules. The consensus is that the tumor-medium mixture should be slowly cooled to the final storage temperature and rapidly thawed (at 37°C) on removal. The tumors should be immediately inoculated after thawing. Not all tumors can be successfully stored.

Some authors ( Hauschka et al., 1959; Kilsileva, 1961; Klein et al., 1957) found no change in chromosome number or morphology, H-2 antigenic specificity, strain specificity, or response to chemotherapeutic drugs after storage, whereas, to the contrary, others have reported changes in transplantation specificity ( Morgan et al., 1956). A slight increase in "latent period" sometimes occurs with the first transplant, but subsequent transplants directly from an animal donor will revert to the growth characteristic of a given tumor prior to freezing.


Transplanted tumors were used from the beginning of experimental cancer research in parallel attempts to show that cancers were transmitted by infectious agents and that immunization against these agents could be achieved. These objectives were not realized, but it was demonstrated that transplanted cancers derived from live cells in the graft inoculum and that genetic identity between graft and host is necessary for successful transplantation. It was also shown that graft rejection has an immunological basis whose operation is identical for grafts of cancers and normal tissues. With clarification of the conditions attending successful cancer transplantation, it has become possible to show that some cancers are generated by filterable agents, and that cancer-specific antigens are realities. These findings have been made possible mainly by the establishment of a number of highly inbred strains of mice.

Transplanted cancers have contributed to several aspects of cancer biology: "progression," host-cancer interactions, cancer viruses, chromosome morphology, biochemistry. They are the chief test objects for possible therapeutic agents. Methods for maintaining transplanted tumors are described.

1The writing of this chapter was supported in part by Public Health Service Research Grant CA 01594 from the National Cancer Institute, and in part by grant E-25 from the American Cancer Society.


Advances in Cancer Research. 1953 et seq.. Academic Press, New York.

American Cancer Society. 1956. Symposium on a critical appraisal of the biochemical characteristics of morphologically separable cancers. Cancer Res. 16: 639-724.

American Cancer Society. 1960. Symposium on the possible role of viruses in cancer. Cancer Res. 20: 669-830.

American Cancer Society. 1963. Symposium on problems basic to cancer chemotherapy. Cancer Res. 23: 1181-1497.

Bayreuther, K. 1960. Chromosomes in primary neoplastic growth. Nature 186: 6-9.
See also PubMed.

Bergel, F. 1961. Chemistry of Enzymes in Cancer. Charles C Thomas, Springfield, Ill. 122 p.

Bielder, J.F., L.J. Old, and D.A. Clarke. 1961. Chromosomal lesion associated with carcinogen-induced tumours in mice. Nature 192: 286-288.

Boyse, E.A. 1960. A method for the preparation of viable cell suspensions from solid tumors. Transpl. Bull. 7(25): 100-104.
See also PubMed.

Busch, H., and W.C. Starbuck. 1964. Biochemistry of cancer. Ann. Rev. Biochem. 33: 519-570.
See also PubMed.

Cancer Chemotherapy National Service Center. April, 1962. A Manual on Quantitative Drug Evaluation in Experimental Tumor Systems. Cancer Chemotherapy Reports No. 17. Public Health Service, Washington, D.C. 178 p.

Cancer Chemotherapy National Service Center. December, 1962. Protocols for Screening. Cancer Chemoherapy Reports No. 25. Public Healh Service, Washington, D.C., 184 p.

Dalton, A.J., and F. Hagenau [ed.] 1962. Tumors induced by viruses: ultrastructural studies. Academic Press, New York, 229 p.

Dunham, L.J., and H. L. Stewart. 1953. A survey of transplantable and transmissible animal tumors. J. Nat. Cancer Inst. 13: 1299-1377.
See also PubMed.

Ford, C.E., J.L. Hamerton, and R.H. Mole. 1958. Chromosomal changes in primary and transplanted reticular neoplasms of the mouse. J. Cell. Comp. Physiol. 52 (Suppl. 1): 235-269.
See also PubMed.

Foulds, L. 1954. The experimental study of tumor progression: a review. Cancer Res. 14: 327-339.
See also PubMed.

Foulds, L. 1958. The natural history of cancer. J. Chrom. Dis. 8: 2-37.
See also PubMed.

Furth, J. 1959. A meeting of ways in cancer research. Thoughts on the evolution and nature of neoplasms. Cancer Res. 19: 241-258.
See also PubMed.

Furth, J., U. Kim, and K.H. Clifton. 1960. On evolution of the neoplastic state: progression from dependence to autonomy. National Cancer Institute Monograph 2: 149-178.
See also PubMed.

Glynn, J.P., S.R. Humphreys, G. Trivers, A.R. Bianco, and A. Goldin. 1963. Studies on immunity to leukemia L1210 in mice. Cancer Res. 23: 1008-1015.
See also PubMed.

Gorer, P.A. 1942. The role of antibodies in immunity to transplanted leukemia in mice. J. Pathol. Bacteriol. 54: 51-65.

Gorer, P.A. 1961. The antigenic structure of tumors. Adv. Immunol. 1: 345-393.

Green, E.L. [ed.] 1964. Handbook on Genetically Standardized Jax Mice. The Jackson Laboratory, Bar Harbor, Maine. 82 p.

Greenstein, J.P. 1954. Biochemistry of Cancer, 2nd ed. Academic Press, New York. 653 p.

Gross, L. 1961. Oncogenic Viruses. Pergamon Press, New York. 393 p.

Handler, A.H. Bibliography of Tumor Transplantation. Transplant. Bull. 1953-1962; Transplantation, 1963 et seq. (Issued from time to time.)

Hauschka, T.S. 1952. Immunologic aspects of cancer: a review. Cancer Res. 12: 615-633.
See also PubMed.

Hauschka, T.S. 1961. The chromosomes in ontogeny and oncogeny. Cancer Res. 21: 957-974.
See also PubMed.

Hauschka, T.S., J.T. Mitchell, and D.J. Niederpruem. 1959. A reliable frozen tissue bank: viability and stability of 82 neoplastic and normal cell types after prolonged storage at -78°C. Cancer Res. 19: 643-653.
See also PubMed.

Hellström, K.E., I. Hellström, and H.O. Sjögren. 1963. Further studies on karyotypes of a variety of primary and transplnated mouse polyoma tumors. J. Nat. Cancer Inst. 31: 1239-1253.

Heston, W.E. 1949. Development of inbred strains in the mouse and their use in cancer research. p. 9-31. In Genetics Cancer, Growth and Social Behavior. Roscoe B. Jackson Memorial Laboratory 20th Commemoration, Bar Harbor, Maine.
See also MGI.

Heston, W.E. 1959. The impact of genetics upon cancer research. Roswell Park Mem. Inst. Bull. 4: 105-122.

Heston, W.E. 1963. Genetics of neoplasia. p. 247-264. In W.J. Burdette [ed.] Methodology in Mammalian Genetics. Holden-Day, San Francisco.
See also MGI.

Hitchings, G.H., and G.B. Elion. 1963. Chemical suppression of the immune response. Pharmacol. Rev. 15: 365-405.
See also PubMed.

Homburger, F. [ed.] 1960 et seq. Progress in Experimental Tumor Research. Lippincott, Philadelphia, and Hafner, New York.

Humphreys, S.R., M.A. Chirigos, K.L. Milstead, N. Mantel, and A. Goldin. 1961. Studies on the supression of the homograft response with folic acid antagonists. J. Nat. Cancer Inst. 27: 259-276.
See also PubMed.

Humphreys, S.R., J.P. Glynn, and A. Goldin. 1963. Suppression of the homograft response by pretreatment with antitumor agents. Transplantation. 1: 65-69.
See also PubMed.

Kaliss, N. 1961. The transplanted tumor as a research tool in cancer immunology. Cancer Res. 21: 1203-1208.
See also PubMed.

Kaliss, N. 1965. Immunological enhancement and inhibition of tumor growth: relationship to various immunological mechanisms. Fed. Proc. 24: 1024-1029.
See also PubMed.

Kilsileva, N.S. 1961. The effect of prolonged storage in frozen state of transplantable tumors on the growth, metastatic spreading and strain specificity. Probl. Oncol. 7(2): 22-27 [translated from Russian; Vop. Onkol. 7: 179-187].

Kit, S. 1960. Nucleic acid synthesis in the neoplastic cell and impact of nuclear changes in the biochemistry of tumor tissue: a review. Cancer Res. 20: 1121-1148.
See also PubMed.

Klein, G. 1959. The usefulness and limitations of tumor transplantation in cancer research: a review. Cancer Res. 19: 343-358.
See also PubMed.

Klein, G., and E. Klein. 1957. The evolution of independence from specific growth stimulation and inhibition in mammalian tumour-cell populations. Symp. Soc. Exp. Biol. 11: 305-328.
See also PubMed.

Klein, G. and E. Klein. 1960. Conversion of solid neoplasms into ascites tumors. Ann. N.Y. Acad. Sci. 63: 640-661.

Klein, G., L. Révész, and E. Klein. 1957. Experiences with a frozen tumor bank. Transplant. Bull. 4: 31-33.
See also PubMed.

Koller, P.C. 1963. The role of chromosome anomalies in cancer. Ciba Symp. 11: 54-63.

Leiter, J. [ed.] 1958 et seq. Cancer chemotherapy screening data. Cancer Res. (Supplements). (Issued from time to time.)

LePage, G.A., and J.F. Henderson. 1960. Biochemistry of tumors. Progr. Exp. Tumor Res. 1: 441-476.
See also PubMed.

Little, C.C. 1921. The relations of genetics to the problems of cancer research. Harvey Lectures, Series 17: 65-68.

Little, C.C. 1947. The genetics of cancer in mice. Biol. Rev. 22: 315-343.

Medawar, P.B. 1957. The immunology of transplantation. Harvey Lectures, Series 52: 144-176.
See also PubMed.

Miner, R.W. [ed.] 1956. Ascites tumors as tools in quantitative oncology. Ann. N.Y. Acad. Sci. 63: 637-1030.

Mitchison, N.A. 1955. Studies on the immunological response to foreign tumor transplants in the mouse. I. The role of lymph node cells in conferring immunity by adoptive transfer. J. Exp. Med. 102: 157-177.
See also PubMed.

Morgan, J.F., L.F. Guerin, and H.J. Morgan. 1956. The effect of low temperature and storage on the viability and mouse strain specificity of ascitic tumor cells. Cancer Res. 16: 907-911.
See also PubMed.

Murphy, J.B. 1926. The Lymphocyte in Resistance to Tissue Grafting, Malignant Disease, and Tuberculous Infection. Monogr. Rockefeller Inst. Med. Res. No. 21. 168 p.

Oberling, C. 1952. The Riddle of Cancer (translated by W.H. Woglom). Yale, New Haven. 238 p.

Old, L.J., and E.A. Boyse. 1965. Antigens of tumors and leukemias induced by viruses. Fred. Proc. 24: 1009-1017.
See also PubMed.

Potter, V.R. 1962. Enzyme studies on the deletion hypothesis of carcinogenesis. p. 367-399. In The Molecular Basis of Neoplasia. 15th Ann. Sympos. Fundamental Cancer Res. University of Texas Press, Austin.

Prehn, R.T. 1965. Cancer antigens in tumors induced by chemicals. Fed. Proc. 24: 1018-1022.
See also PubMed.

Schmidt, F., and W. Tessenow. 1960. Methodische Versuche zur Einrichtung einer Tumorbank. Z. Krebforsch. 63: 284-293.
See also PubMed.

Snell, G.D. 1953. A cytosieve permitting sterile preparation of suspensions of tumor cells for transplantation. J. Nat. Cancer Inst. 13: 1511-1515.
See also PubMed.

Snell, G.D. 1958. Transplantable tumors, p. 293-345. In F. Homburger [ed.] The Pathophysiology of Cancer, 2nd ed. Hoeber-Harper, New York.

Staats, J. 1964. Standardized nomenclature for inbred strains of mice, Third listing. Cancer Res. 24: 147-168.
See also PubMed.

Stevens, L.C., and M.C. Bunker. 1964. Karyotype and sex of primary testicular teratomas in mice. J. Nat. Cancer Inst. 33: 65-78.
See also PubMed.

Stewart, H.L., K.C. Snell, L.J. Dunham, and S.M. Schlyen. 1959. Transplantable and Transmissible Tumors of Animals. Atlas of Tumor Pathology, Sect. XII, Fasc. 40. Armed Forces Institute of Pathology, Washington, D.C. 378 p.

Sugiura, K. 1961. Frozen storage of 34 various solid and ascites tumors. Cancer Res. 21: 496-501.

Teller, M.N., R. Wolff, and S.F. Wagshul. 1964. Host-tumor-drug relationships in experimental chemotherapy systems with allogenic and xenogenic host-tumor combinations. Cancer Res. 24: 114-119.
See also PubMed.

Triolo, V.A. 1964. Nineteenth century foundations of cancer research. Cancer Res. 24: 4-27.
See also PubMed.

Uphoff, D.E. 1961. Drug-induced immunological "tolerance" for homotransplantation. Transplant. Bull. 28: 12-16.
See also PubMed.

Wakonig, R. 1960. Aneuploidy in neoplasia — cause or result. Can. J. Genet. Cytol. 2: 344-356.
See also PubMed.

Woglom, W.H. 1913. The Study of Experimental Cancer. A Review. Columbia University Press, New York. 288 p.

Woglom, W.H. 1929. Immunity to tranplantable tumors. Cancer Rev. 4: 129-214.

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