T H E BIOLOGY OF T E R A T O M A S
15
other hand, Abell and Holtz (1964) concluded that the majority of
germ cell neoplasms that are detected in adolescence do not represent
alterations in behavior in neoplasms present before puberty, but arise
de novo several years after puberty, not coincident with puberty.
Abell et al. (1965) studied a series of germinal tumors of the ovary
and found that the youngest patients were those with embryonal carcinoma, followed by those with mixed germ cell neoplasms, then partially
differentiated teratomas, and differentiated teratomas. Although the
differences were not statistically significant, Abell et al. (1965) believed
that they supported the concept that all of these lesions are related and
represent a spectrum of teratomatous neoplasms arising from embryonal
carcinoma. Melicow (1955) offered a similar interpretation based on
studies of human testicular teratomas.
The simplest explanation of the origin and development of teratomas
in strain 129 mice, and the one that fits the observed facts, begins with
the process of ephebogenesis (teratocarcinogenesis) : the spontaneous development of a male germ cell believed to result in chorionic carcinoma
or teratoma of the testis. The neoplastic process is initiated at 12.5 days
of gestation in a primordial germ cell. Older germ cells are resistant to
this neoplastic change (Stevens, 1964). The germ cell proliferates and
acquires the characteristics of early undifferentiated embryonal cells.
The neoplastic germ cells may give rise to other cells that may become
progenitors of nearby foci. These foci, composed of undifferentiated cells
like those in early normal mouse embryos grow, invade, and rupture the
tubules in which they originated, and neoplastic cells and normal germ
cells spill out into the interstitial area (Figs. 6-8). About the time of
birth, some embryonal cells form vesicles lined by primitive epithelium
(Fig. 8). This epithelium becomes similar in appearance and in histogenetic capacity to ectoderm or endoderm, and mesenchymal cells between
the ectodermal and endodermal vesicles represent mesoderm (Fig. 9).
These primary germ layers give rise to all the varied histological components of a teratoma, which may include formations similar in morphology and histogenetic potency to parts of early mouse embryos. This
developmental system resembles normal mouse development in some
respects, but it does not, nor should it be expected to, mimic normal
development completely.
X. Genetic and Environmental Influences on Teratocarcinogenesis
A. Multiple Gene Influences
Several genetic and environmental factors which influence teratocarcinogenesis have been identified. There is an apparent race difference
in incidence of germinal tumors in American males (Dixon and Moore,
15
other hand, Abell and Holtz (1964) concluded that the majority of
germ cell neoplasms that are detected in adolescence do not represent
alterations in behavior in neoplasms present before puberty, but arise
de novo several years after puberty, not coincident with puberty.
Abell et al. (1965) studied a series of germinal tumors of the ovary
and found that the youngest patients were those with embryonal carcinoma, followed by those with mixed germ cell neoplasms, then partially
differentiated teratomas, and differentiated teratomas. Although the
differences were not statistically significant, Abell et al. (1965) believed
that they supported the concept that all of these lesions are related and
represent a spectrum of teratomatous neoplasms arising from embryonal
carcinoma. Melicow (1955) offered a similar interpretation based on
studies of human testicular teratomas.
The simplest explanation of the origin and development of teratomas
in strain 129 mice, and the one that fits the observed facts, begins with
the process of ephebogenesis (teratocarcinogenesis) : the spontaneous development of a male germ cell believed to result in chorionic carcinoma
or teratoma of the testis. The neoplastic process is initiated at 12.5 days
of gestation in a primordial germ cell. Older germ cells are resistant to
this neoplastic change (Stevens, 1964). The germ cell proliferates and
acquires the characteristics of early undifferentiated embryonal cells.
The neoplastic germ cells may give rise to other cells that may become
progenitors of nearby foci. These foci, composed of undifferentiated cells
like those in early normal mouse embryos grow, invade, and rupture the
tubules in which they originated, and neoplastic cells and normal germ
cells spill out into the interstitial area (Figs. 6-8). About the time of
birth, some embryonal cells form vesicles lined by primitive epithelium
(Fig. 8). This epithelium becomes similar in appearance and in histogenetic capacity to ectoderm or endoderm, and mesenchymal cells between
the ectodermal and endodermal vesicles represent mesoderm (Fig. 9).
These primary germ layers give rise to all the varied histological components of a teratoma, which may include formations similar in morphology and histogenetic potency to parts of early mouse embryos. This
developmental system resembles normal mouse development in some
respects, but it does not, nor should it be expected to, mimic normal
development completely.
X. Genetic and Environmental Influences on Teratocarcinogenesis
A. Multiple Gene Influences
Several genetic and environmental factors which influence teratocarcinogenesis have been identified. There is an apparent race difference
in incidence of germinal tumors in American males (Dixon and Moore,