THE BIOLOGY OF TERATOMAS
5
and comprise the most common form of malignancy encountered in male
patients from 20 to 35 years of age (Dixon and Moore, 1953).
Malignant mediastinal teratomas are much more common in males
than females (Willis, 1962a), and Campbell (1962) stated that, "It is
perhaps not without significance that pineal teratomas are practically
confined to the human male."
Like the situation in human beings, teratomas have been observed
more frequently in female than in male mice (except for strain 129).
Ovarian teratomas have been reported in several colonies, and they
usually grow progressively when transplanted. Testicular teratomas are
almost unknown in mice except for strain 129, and most of these tumors
differentiate into adult type tissues, and proliferation ceases at 20-30
days of age. There is no evidence to help explain why the sex of the
bearer influences the incidence and malignancy of teratomas.
All inbred strain 129 mice are genetically identical except for forced
heterozygosis at the C locus and the sex chromosomes. An explanation
for the sex difference in tumor incidence in this strain may be postulated
considering the following facts. (1) Teratocarcinogenesis in the testis is
initiated at 12.5 days of gestation and not later (Stevens, 1964). (2) It
is probable that ovarian teratomas also arise prenatally. (3) Germ cells
in female mice stop oogonial division along with sex differentiation, and
most of the germ cells enter into meiosis on the fourteenth day of
gestation (Borum, 1961). This happens simultaneously for all oocytes
during the course of 1 or 2 days. The female germ cells remain in meiotic
prophase, and do not undergo mitotic division henceforth. Thus, the
male germ cells continue to proliferate throughout the life span of the
mouse, while female cells cease to divide during fetal life. It is possible
that the prenatal cessation of mitosis in female strain 129 germ cells
prevents the development of ovarian teratomas. According to Willis
(1951), human ovarian teratomas probably arise prenatally. Possibly,
the reason they do not arise later is associated with the prenatal cessation of mitosis in germ cells.
C. Laterality
It is difficult to comprehend why laterality should play a role in
teratocarcinogenesis of the testis. But Willis (1960) found that human
testicular teratomas occur more frequently on the right than the left side.
Stevens and Mackensen (1961) observed 597 teratomas in strain 129
mice of which 71% were in the left testis, 27% in the right, and 2% were
bilateral. Guthrie (1964) summarized the results from induced teratomas
in fowl testes and found that 18% of the right-sided and 47% of the leftsided growths were dwarf tumors. Apparently, the pattern of growth of
induced teratomas in fowl is also influenced by laterality.
5
and comprise the most common form of malignancy encountered in male
patients from 20 to 35 years of age (Dixon and Moore, 1953).
Malignant mediastinal teratomas are much more common in males
than females (Willis, 1962a), and Campbell (1962) stated that, "It is
perhaps not without significance that pineal teratomas are practically
confined to the human male."
Like the situation in human beings, teratomas have been observed
more frequently in female than in male mice (except for strain 129).
Ovarian teratomas have been reported in several colonies, and they
usually grow progressively when transplanted. Testicular teratomas are
almost unknown in mice except for strain 129, and most of these tumors
differentiate into adult type tissues, and proliferation ceases at 20-30
days of age. There is no evidence to help explain why the sex of the
bearer influences the incidence and malignancy of teratomas.
All inbred strain 129 mice are genetically identical except for forced
heterozygosis at the C locus and the sex chromosomes. An explanation
for the sex difference in tumor incidence in this strain may be postulated
considering the following facts. (1) Teratocarcinogenesis in the testis is
initiated at 12.5 days of gestation and not later (Stevens, 1964). (2) It
is probable that ovarian teratomas also arise prenatally. (3) Germ cells
in female mice stop oogonial division along with sex differentiation, and
most of the germ cells enter into meiosis on the fourteenth day of
gestation (Borum, 1961). This happens simultaneously for all oocytes
during the course of 1 or 2 days. The female germ cells remain in meiotic
prophase, and do not undergo mitotic division henceforth. Thus, the
male germ cells continue to proliferate throughout the life span of the
mouse, while female cells cease to divide during fetal life. It is possible
that the prenatal cessation of mitosis in female strain 129 germ cells
prevents the development of ovarian teratomas. According to Willis
(1951), human ovarian teratomas probably arise prenatally. Possibly,
the reason they do not arise later is associated with the prenatal cessation of mitosis in germ cells.
C. Laterality
It is difficult to comprehend why laterality should play a role in
teratocarcinogenesis of the testis. But Willis (1960) found that human
testicular teratomas occur more frequently on the right than the left side.
Stevens and Mackensen (1961) observed 597 teratomas in strain 129
mice of which 71% were in the left testis, 27% in the right, and 2% were
bilateral. Guthrie (1964) summarized the results from induced teratomas
in fowl testes and found that 18% of the right-sided and 47% of the leftsided growths were dwarf tumors. Apparently, the pattern of growth of
induced teratomas in fowl is also influenced by laterality.