28
LEROY C. S T E V E N S
indicating that some of the cells are female. This has led to the formulation of several conflicting theories concerning the initiation of teratocarcinogenesis.
Under certain conditions, human and mouse teratomas form structures
that are morphologically similar to normal human and mouse embryos.
The mouse embryoid bodies not only look like normal mouse embryos
but have similar embryonic potency. It is concluded that they are
homologous to embryos.
Teratomas can be induced in adult fowl and mice by injecting zinc
or copper salts into the testis followed by the administration of hormones.
They may be induced in strain 129 and A/He mice by grafting genital
ridges of 12.5-day fetuses into the testes of adults. Most of the male
genital ridges develop into testes with multiple teratomatous foci. There
is a sharply defined critical period during which primordial germ cells
are susceptible to teratocarcinogenesis. At 13.5 days of gestation the
germ cells of strain 129 fetuses are resistant to this process. The site
of the graft is also critical. The spleen and other parts of the body do
not exert the strong teratocarcinogenetic influence found in the testis.
Teratomas can be initiated in plants, and the pattern of growth and
differentiation can be experimentally directed. Single teratomatous cells
can give rise to normal fertile adult plants.
Acknowledgments
Part of the work presented here was supported by grant CA 02662 from the
U.S. Public Health Service, and a grant from The John A. Hartford Foundation.
The author is grateful to the editors of the Journal of the National
Cancer
Institute for permission to use Figs. 1, 6, 7, and 8, and to the editors of Developmental Biology (Academic Press) for permission to use Fig. 5.
References
Abell, M. R., and Holtz, F. (1963). Cancer 16, 965.
Abell, M. R., and Holtz, F. (1964). Cancer 17, 881.
Abell, M. R., Johnson, V. J., and Holtz, F. (1965). Am. J. Obstet. Gynecol. 92,
1059.
Ashley, D. J. B., and Theiss, E. A. (1958). Science 128, 1434.
Azzopardi, J. G., Mostofi, F. K., and Theiss, E. A. (1961). Am. J. Pathol. 38, 207.
Bagg, H. J. (1936). Am. J. Cancer 26, 69.
Borum, K. (1961). Exptl. Cell Res. 24, 495.
Braun, A. (1965). Sei. Am. 213, 75.
Bresler, V. M. (1959). Probl. Oncol. (USSR) (Engl. Transi.) 5, 24.
Bresler, V. M. (1964). "Cyto logical Mechanisms of Carcinogenesis in the Testis."
Izv. Akad. Nauk SSSR, Moscow (Russian).
Budde, M. (1926). Beitr. Pathol. Anat. Allegm. Pathol. 75, 357.
Bunker, M. C. (1966). Can. J. Genet. Cytology 8, 312.
Cabanne, F. (1957). Arch. Anat. Pathol. Semaine Hop. 5, 165.
Campbell, J. G. (1962). Brit. J. Cancer 16, 258.
LEROY C. S T E V E N S
indicating that some of the cells are female. This has led to the formulation of several conflicting theories concerning the initiation of teratocarcinogenesis.
Under certain conditions, human and mouse teratomas form structures
that are morphologically similar to normal human and mouse embryos.
The mouse embryoid bodies not only look like normal mouse embryos
but have similar embryonic potency. It is concluded that they are
homologous to embryos.
Teratomas can be induced in adult fowl and mice by injecting zinc
or copper salts into the testis followed by the administration of hormones.
They may be induced in strain 129 and A/He mice by grafting genital
ridges of 12.5-day fetuses into the testes of adults. Most of the male
genital ridges develop into testes with multiple teratomatous foci. There
is a sharply defined critical period during which primordial germ cells
are susceptible to teratocarcinogenesis. At 13.5 days of gestation the
germ cells of strain 129 fetuses are resistant to this process. The site
of the graft is also critical. The spleen and other parts of the body do
not exert the strong teratocarcinogenetic influence found in the testis.
Teratomas can be initiated in plants, and the pattern of growth and
differentiation can be experimentally directed. Single teratomatous cells
can give rise to normal fertile adult plants.
Acknowledgments
Part of the work presented here was supported by grant CA 02662 from the
U.S. Public Health Service, and a grant from The John A. Hartford Foundation.
The author is grateful to the editors of the Journal of the National
Cancer
Institute for permission to use Figs. 1, 6, 7, and 8, and to the editors of Developmental Biology (Academic Press) for permission to use Fig. 5.
References
Abell, M. R., and Holtz, F. (1963). Cancer 16, 965.
Abell, M. R., and Holtz, F. (1964). Cancer 17, 881.
Abell, M. R., Johnson, V. J., and Holtz, F. (1965). Am. J. Obstet. Gynecol. 92,
1059.
Ashley, D. J. B., and Theiss, E. A. (1958). Science 128, 1434.
Azzopardi, J. G., Mostofi, F. K., and Theiss, E. A. (1961). Am. J. Pathol. 38, 207.
Bagg, H. J. (1936). Am. J. Cancer 26, 69.
Borum, K. (1961). Exptl. Cell Res. 24, 495.
Braun, A. (1965). Sei. Am. 213, 75.
Bresler, V. M. (1959). Probl. Oncol. (USSR) (Engl. Transi.) 5, 24.
Bresler, V. M. (1964). "Cyto logical Mechanisms of Carcinogenesis in the Testis."
Izv. Akad. Nauk SSSR, Moscow (Russian).
Budde, M. (1926). Beitr. Pathol. Anat. Allegm. Pathol. 75, 357.
Bunker, M. C. (1966). Can. J. Genet. Cytology 8, 312.
Cabanne, F. (1957). Arch. Anat. Pathol. Semaine Hop. 5, 165.
Campbell, J. G. (1962). Brit. J. Cancer 16, 258.