THE BIOLOGY OF TERATOMAS
13
coelomic epithelium, somitic material, and yolk sac; all were in the
proper spacial relationships to each other (Fig. 5).
Another theory of the origin of teratomas, which will be discussed
in detail under Section IX, postulates that they arise as a consequence
of three unlikely events: (1) premature reductional division of germ
cells, (2) fusion of two haploid cells in the gonad, and (3) neoplastic
transformation of the product of this fusion. This theory is gaining in
popularity but the author does not think it applies to teratocarcinogenesis
in the mouse.
The most widely accepted theory is that teratomas are derived from
diploid germ cells (Azzopardi et al., 1961; Cabanne, 1957; Carleton
et al., 1953; Dixon and Moore, 1953; Neubecker and Breen, 1962; Pierce
and Beals, 1964; Stevens and Bunker, 1964; Stevens, 1964). There is
evidence to support this theory. Teratomas are much more common in
the gonads than in any other site. Carleton et al. (1953) concluded that
teratocarcinogenesis in the fowl testis begins in the seminiferous tubule.
All of the early teratomas observed in strain 129 mice are within the
seminiferous tubules (Fig. 6), demonstrating that teratocarcinogenesis is
initiated in either the primordial germ cells or in the supporting cells,
which will become the Sertoli cells (Stevens, 1962). The neoplastic
process does not endow affected cells with new embryonic potencies.
Neoplastic cells of mammary gland origin, for example, do not give rise
to neural or muscular cells. There is no evidence to support the concept
that supporting cells of the testis can be transformed to totipotent cells,
and it is known that primordial germ cells are totipotent. The observation that testicular teratomas may have a male and/or female nuclear
sex has been used to support the theory that germ cells give rise to
teratomas.
Pierce and Beals (1964) studied the fine structure of primordial germ
cells and embryonal carcinoma using as a rationale that many of the
ultrastructural features characteristic of normal cells may be retained
by their neoplastic counterparts. Embryonal carcinoma cells from a
transplanted teratoma of strain 129 origin bore a striking resemblance
to primordial germ cells and to embryonal carcinoma cells of man. The
same similarity was observed in electron micrographs of early induced
teratomas (Pierce, Stevens, and Nakane, unpublished).
Bresler's finding (1959, 1964) that teratomas can be induced in the
testes of mature mice is important. If it is assumed that these tumors
an outer layer of endoderm and an inner layer of ectoderm and undifferentiated
embryonal cells. X 300.
FIG. 5. Embryoid body showing some morphogenesis in the anterior chamber of
the eye. Note neuroepithelium (NE), mesenchyme in somitic region (ME), yolk sac
(YS), epithelium resembling coelomic epithelium (GE), and amnion (AM), χ 300.
13
coelomic epithelium, somitic material, and yolk sac; all were in the
proper spacial relationships to each other (Fig. 5).
Another theory of the origin of teratomas, which will be discussed
in detail under Section IX, postulates that they arise as a consequence
of three unlikely events: (1) premature reductional division of germ
cells, (2) fusion of two haploid cells in the gonad, and (3) neoplastic
transformation of the product of this fusion. This theory is gaining in
popularity but the author does not think it applies to teratocarcinogenesis
in the mouse.
The most widely accepted theory is that teratomas are derived from
diploid germ cells (Azzopardi et al., 1961; Cabanne, 1957; Carleton
et al., 1953; Dixon and Moore, 1953; Neubecker and Breen, 1962; Pierce
and Beals, 1964; Stevens and Bunker, 1964; Stevens, 1964). There is
evidence to support this theory. Teratomas are much more common in
the gonads than in any other site. Carleton et al. (1953) concluded that
teratocarcinogenesis in the fowl testis begins in the seminiferous tubule.
All of the early teratomas observed in strain 129 mice are within the
seminiferous tubules (Fig. 6), demonstrating that teratocarcinogenesis is
initiated in either the primordial germ cells or in the supporting cells,
which will become the Sertoli cells (Stevens, 1962). The neoplastic
process does not endow affected cells with new embryonic potencies.
Neoplastic cells of mammary gland origin, for example, do not give rise
to neural or muscular cells. There is no evidence to support the concept
that supporting cells of the testis can be transformed to totipotent cells,
and it is known that primordial germ cells are totipotent. The observation that testicular teratomas may have a male and/or female nuclear
sex has been used to support the theory that germ cells give rise to
teratomas.
Pierce and Beals (1964) studied the fine structure of primordial germ
cells and embryonal carcinoma using as a rationale that many of the
ultrastructural features characteristic of normal cells may be retained
by their neoplastic counterparts. Embryonal carcinoma cells from a
transplanted teratoma of strain 129 origin bore a striking resemblance
to primordial germ cells and to embryonal carcinoma cells of man. The
same similarity was observed in electron micrographs of early induced
teratomas (Pierce, Stevens, and Nakane, unpublished).
Bresler's finding (1959, 1964) that teratomas can be induced in the
testes of mature mice is important. If it is assumed that these tumors
an outer layer of endoderm and an inner layer of ectoderm and undifferentiated
embryonal cells. X 300.
FIG. 5. Embryoid body showing some morphogenesis in the anterior chamber of
the eye. Note neuroepithelium (NE), mesenchyme in somitic region (ME), yolk sac
(YS), epithelium resembling coelomic epithelium (GE), and amnion (AM), χ 300.