THE BIOLOGY OF TERATOMAS
21
ality as well as the maternal environment, influence the incidence of
testicular teratomas. The genetic and environmental influences involved
in teratocarcinogenesis appear to be similar to those which determine the
penetrance of non-neoplastic inherited characters that are controlled by
genetically complex multifactorial and modifying mechanisms.
Gross chromosomal changes are not involved in teratocarcinogenesis
in strain 129 mice.
XI. Sex of Teratomas
Many investigators have confirmed the finding of Hunter and Lennox
(1954), that cells of human testicular teratomas may contain sex
chromatin indicating that the cells were female, or they may be without
sex chromatin like normal male cells. There is no experimental approach
to elucidate these observations in human beings, and it is difficult to
explain them.
Hunter and Lennox (1954) advanced a theory involving self-fertilization of two haploid cells which could produce XX, XY, or YY combinations in males. Tavares (1955) and Rivière (1956) suggested the
parthenogenetic division of haploid cells followed by chromosome reduplications, which in males would form 50% XX and 50% YY cells.
Ashley and Theiss (1958) and Theiss et al. (1960) interpreted their
findings as indicating a premature reductional division of primordial
germ cells, fusion, and a neoplastic change in the product of this
autofertilization.
Meyers (1959b) studied teratomas of females, and sex chromatin was
present uniformly throughout the tumors in well differentiated tissues.
The majority of the teratomas from females were benign and nuclear
sexing of the tissues was relatively easy and reliable. Nearly a quarter
of the testicular teratomas were "mosaics," and contained both male
and female regions. Meyers pointed out that it is highly improbable that
all the teratomas with diverse nuclear morphology represent fused
multiple growth, and that there is, as yet, no adequate explanation of
the presence of chromatin masses in teratomas of males. Neither of the
previously proposed theories alone can explain the occurrence of mosaics.
Meyers proposed that local factors inherent in the nature and growth
of teratomas may be responsible for the mosaic pattern. Nuclei with
unbalanced numbers of chromosomes could result from mitotic errors
such as nondisjunction, displacement and clumping of chromosomes,
endomitosis, polyploidy, and spindle abnormalities.
Taylor (1963) found sex chromatin discrepancies in 8 of 50 teratomas
(3 of these were from males and 5 from females), and in 4 of 49 other
embryonic tumors (one from a female and three from males). She sug-
21
ality as well as the maternal environment, influence the incidence of
testicular teratomas. The genetic and environmental influences involved
in teratocarcinogenesis appear to be similar to those which determine the
penetrance of non-neoplastic inherited characters that are controlled by
genetically complex multifactorial and modifying mechanisms.
Gross chromosomal changes are not involved in teratocarcinogenesis
in strain 129 mice.
XI. Sex of Teratomas
Many investigators have confirmed the finding of Hunter and Lennox
(1954), that cells of human testicular teratomas may contain sex
chromatin indicating that the cells were female, or they may be without
sex chromatin like normal male cells. There is no experimental approach
to elucidate these observations in human beings, and it is difficult to
explain them.
Hunter and Lennox (1954) advanced a theory involving self-fertilization of two haploid cells which could produce XX, XY, or YY combinations in males. Tavares (1955) and Rivière (1956) suggested the
parthenogenetic division of haploid cells followed by chromosome reduplications, which in males would form 50% XX and 50% YY cells.
Ashley and Theiss (1958) and Theiss et al. (1960) interpreted their
findings as indicating a premature reductional division of primordial
germ cells, fusion, and a neoplastic change in the product of this
autofertilization.
Meyers (1959b) studied teratomas of females, and sex chromatin was
present uniformly throughout the tumors in well differentiated tissues.
The majority of the teratomas from females were benign and nuclear
sexing of the tissues was relatively easy and reliable. Nearly a quarter
of the testicular teratomas were "mosaics," and contained both male
and female regions. Meyers pointed out that it is highly improbable that
all the teratomas with diverse nuclear morphology represent fused
multiple growth, and that there is, as yet, no adequate explanation of
the presence of chromatin masses in teratomas of males. Neither of the
previously proposed theories alone can explain the occurrence of mosaics.
Meyers proposed that local factors inherent in the nature and growth
of teratomas may be responsible for the mosaic pattern. Nuclei with
unbalanced numbers of chromosomes could result from mitotic errors
such as nondisjunction, displacement and clumping of chromosomes,
endomitosis, polyploidy, and spindle abnormalities.
Taylor (1963) found sex chromatin discrepancies in 8 of 50 teratomas
(3 of these were from males and 5 from females), and in 4 of 49 other
embryonic tumors (one from a female and three from males). She sug-