2
LEROY C. STEVENS
tumor formation, and parthenogenesis, in that it results in the activation
of development of germ cells. Either sex may show a predilection for
teratomas, and this varies from one species to another. They can be
experimentally induced in adult cocks and in fetal and adult mice. In
mice, their growth and differentiation has been shown to be under
genetic control. A single major gene is responsible for susceptibility to
experimental teratocarcinogenesis in mice, but the spontaneous tumors
depend upon the actions of this gene and several modifying genes. The
patterns of growth and differentiation of experimentally induced testicular teratomas are also under environmental control. The composition
of mouse teratomas that have been serially transplanted for many generations may change. They may progress toward a more malignant
or a more benign state. The differentiation of descendants of the stem
cell into morphologically and functionally normal cells is an example of
a transformation from malignant, progressively growing cells to nonproliferating benign cells. These puzzling aspects of the growth and
differentiation of teratomas have provoked many investigations of their
nature. The biology of teratomas has been reviewed extensively in the
past (Friedman and Moore, 1946; Dixon and Moore, 1952; Willis, 1958,
1962a; Pierce, 1961; Stevens, 1962; Bresler, 1964), but recent developments of animal materials and methods have made it possible to probe
more deeply into factors underlying the process of teratocarcinogenesis.
Throughout this article the disease under discussion will be referred
to as teratoma. Commonly used synonyms include embryonal carcinoma,
embryoma, teratocarcinoma, dysembryoma, dermoid cyst, and teratoid
tumor. In general, neoplasms of germ cell origin including teratomas are
homologous in the male and female (Teilum, 1965).
II. Classification
Perhaps the most widely accepted classification of testicular tumors is
that proposed by Dixon and Moore (1953). There are germinal and nongerminal tumors. The human germinal tumors, which comprise 96% of
testicular tumors, are composed of one or any combination of four
morphologic patterns and may be classified as: seminoma, embryonal
carcinoma, teratoma, and choriocarcinoma. Seminomas are relatively
low in malignancy and are made up of characteristically large, uniform
cells that resemble spermatogonia. They are distinct and separable from
the other types of germinal tumors in that they arise from germ cells
that are not pluripotent. The other three groups of germinal tumors arise
from pluripotent germ cells, and the earliest form is embryonal carcinoma. Embryonal carcinomas are composed of highly malignant, multipotential, anaplastic cells that may be entirely undifferentiated or may
show slight differentiation toward somatic or trophoblastic cells. Tera-
LEROY C. STEVENS
tumor formation, and parthenogenesis, in that it results in the activation
of development of germ cells. Either sex may show a predilection for
teratomas, and this varies from one species to another. They can be
experimentally induced in adult cocks and in fetal and adult mice. In
mice, their growth and differentiation has been shown to be under
genetic control. A single major gene is responsible for susceptibility to
experimental teratocarcinogenesis in mice, but the spontaneous tumors
depend upon the actions of this gene and several modifying genes. The
patterns of growth and differentiation of experimentally induced testicular teratomas are also under environmental control. The composition
of mouse teratomas that have been serially transplanted for many generations may change. They may progress toward a more malignant
or a more benign state. The differentiation of descendants of the stem
cell into morphologically and functionally normal cells is an example of
a transformation from malignant, progressively growing cells to nonproliferating benign cells. These puzzling aspects of the growth and
differentiation of teratomas have provoked many investigations of their
nature. The biology of teratomas has been reviewed extensively in the
past (Friedman and Moore, 1946; Dixon and Moore, 1952; Willis, 1958,
1962a; Pierce, 1961; Stevens, 1962; Bresler, 1964), but recent developments of animal materials and methods have made it possible to probe
more deeply into factors underlying the process of teratocarcinogenesis.
Throughout this article the disease under discussion will be referred
to as teratoma. Commonly used synonyms include embryonal carcinoma,
embryoma, teratocarcinoma, dysembryoma, dermoid cyst, and teratoid
tumor. In general, neoplasms of germ cell origin including teratomas are
homologous in the male and female (Teilum, 1965).
II. Classification
Perhaps the most widely accepted classification of testicular tumors is
that proposed by Dixon and Moore (1953). There are germinal and nongerminal tumors. The human germinal tumors, which comprise 96% of
testicular tumors, are composed of one or any combination of four
morphologic patterns and may be classified as: seminoma, embryonal
carcinoma, teratoma, and choriocarcinoma. Seminomas are relatively
low in malignancy and are made up of characteristically large, uniform
cells that resemble spermatogonia. They are distinct and separable from
the other types of germinal tumors in that they arise from germ cells
that are not pluripotent. The other three groups of germinal tumors arise
from pluripotent germ cells, and the earliest form is embryonal carcinoma. Embryonal carcinomas are composed of highly malignant, multipotential, anaplastic cells that may be entirely undifferentiated or may
show slight differentiation toward somatic or trophoblastic cells. Tera-