22
L E R O Y C. S T E V E N S
gested that sex chromatin discrepancies in these tumors may be the
expression of abnormal sex chromosome complements such as XO or
XXY produced by one or more errors of mitosis such as nondisj unction
or anaphase lagging at or soon after the inception of the tumor. Bunker
(1966) showed that a transplanted teratoma of the mouse had lost the
Y chromosome. This loss occurred long after the initiation of teratocarcinogenesis, and so was not associated with that process.
Dayan (1963) summarized previously published findings of sex of
teratoma cells and determined the sex in 37 additional testicular teratomas. All investigators found testicular teratomas with male or female
nuclear sex, and three found mosaics. Dayan (1963) pointed out
that all this work has relied on the concept that the number of chromatin
bodies is one less than the number of X chromosomes in the nucleus and
that in a diploid cell the absence of sex chromatin implies the XY
constitution, and the presence of sex chromatin indicates the XX constitution. According to Dayan (1963) it is not safe to assume the karyotype
from the nuclear sex, and the hypothesis of autofertilization of haploid
gametes is incorrect. Dayan (1963) felt it more likely that polyploidy,
nondisj unction, or other errors of mitosis in tumor cells would explain
the presence of sex chromatin in some cells of testicular teratomas.
Miles (1959) examined 11 female and 10 male human tumors cultured
in vitro for the presence of sex chromatin. All but two of the female
tissues showed sex chromatin in high percentages of cells. None of the
male tissues contained sex chromatin.
The identification of sex chromatin in more malignant tumors became
progressively more difficult with increasing anaplasia (Meyers, 1959a).
In tumors from both males and females, the incidence of typical
chromatin masses at the nuclear membrane varied considerably, and
frequently one or more masses simulating sex chromatin were free within
the nucleoplasm or adjacent to the nuclear membrane. Nuclear constituents other than sex chromatin can form discrete chromatin masses of
similar size and shape, and hence the designation of such particles in
malignant tumors as "sex chromatin" becomes very questionable and
unreliable. The identification of sex chromatin in more malignant tumors
was frequently impossible.
As Meyers (1959b) pointed out, there have been no studies of human
teratomas to determine their chromosome numbers or to detect abnormalities in mitosis. It remains for further investigations to determine
the nature of these anomalies and whether they are related to the origin
of teratomas.
Stich and Hsu (1960) have shown that the sex of mouse cells can be
determined by observing the morphology of the heteromorphic X and Y
L E R O Y C. S T E V E N S
gested that sex chromatin discrepancies in these tumors may be the
expression of abnormal sex chromosome complements such as XO or
XXY produced by one or more errors of mitosis such as nondisj unction
or anaphase lagging at or soon after the inception of the tumor. Bunker
(1966) showed that a transplanted teratoma of the mouse had lost the
Y chromosome. This loss occurred long after the initiation of teratocarcinogenesis, and so was not associated with that process.
Dayan (1963) summarized previously published findings of sex of
teratoma cells and determined the sex in 37 additional testicular teratomas. All investigators found testicular teratomas with male or female
nuclear sex, and three found mosaics. Dayan (1963) pointed out
that all this work has relied on the concept that the number of chromatin
bodies is one less than the number of X chromosomes in the nucleus and
that in a diploid cell the absence of sex chromatin implies the XY
constitution, and the presence of sex chromatin indicates the XX constitution. According to Dayan (1963) it is not safe to assume the karyotype
from the nuclear sex, and the hypothesis of autofertilization of haploid
gametes is incorrect. Dayan (1963) felt it more likely that polyploidy,
nondisj unction, or other errors of mitosis in tumor cells would explain
the presence of sex chromatin in some cells of testicular teratomas.
Miles (1959) examined 11 female and 10 male human tumors cultured
in vitro for the presence of sex chromatin. All but two of the female
tissues showed sex chromatin in high percentages of cells. None of the
male tissues contained sex chromatin.
The identification of sex chromatin in more malignant tumors became
progressively more difficult with increasing anaplasia (Meyers, 1959a).
In tumors from both males and females, the incidence of typical
chromatin masses at the nuclear membrane varied considerably, and
frequently one or more masses simulating sex chromatin were free within
the nucleoplasm or adjacent to the nuclear membrane. Nuclear constituents other than sex chromatin can form discrete chromatin masses of
similar size and shape, and hence the designation of such particles in
malignant tumors as "sex chromatin" becomes very questionable and
unreliable. The identification of sex chromatin in more malignant tumors
was frequently impossible.
As Meyers (1959b) pointed out, there have been no studies of human
teratomas to determine their chromosome numbers or to detect abnormalities in mitosis. It remains for further investigations to determine
the nature of these anomalies and whether they are related to the origin
of teratomas.
Stich and Hsu (1960) have shown that the sex of mouse cells can be
determined by observing the morphology of the heteromorphic X and Y