18
LEROY C. STEVENS
have evidence of genetic influences, none have been shown to result
from a single gene. Instead they are inherited as threshold characters.
However, single genes can have a very strong effect on the incidence of
certain tumors.
B. Single Gene Influences
Single specific genes which influence susceptibility to teratocarcinogenesis in strain 129 mice have been identified.
To determine the effect of single genes on teratocarcinogenesis we
introduced several mutant genes onto the strain 129 background by
repeated backcrosses of animals carrying the mutation to strain 129
mice. The gene Steel (Sl
J
) was selected because it exerts striking effects
upon the development of primordial germ cells and has effects on pigment
which makes its presence detectable. The tumor incidence in males in
which the gene Sl
J
and its wild type allele were segregating was determined, and animals carrying the Sl
J
gene had more than twice as many
teratomas as their + / + littermates (Stevens and Mackensen, 1961).
Of the last 500 Sl
+
males observed in our laboratory, 14% of them had
spontaneous teratomas. Six percent of 500 of their + / + littermates had
tumors.
An allele of SI, Sl
d , has similar effects on the development of red
blood, pigment, and germ cells. Another locus, W, also affects these three
systems. Sl
d
and several alleles of W were introduced onto the strain
129 genetic background to test their influence on teratocarcinogenesis.
Four percent of the mutant-carrying mice developed testicular teratomas,
as did 4% of their wild-type littermates (Table I ) . Of the genes tested,
only Sl
J
doubles the incidence of teratomas in strain 129 mice. This may
mean that the tumor enhancing influence of Sl
J
is independent of the
slightly deleterious effect of Sl
J
on the development of germ cells, and
that it is another pleiotropic effect of this gene. Alternatively, the
deleterious effect of Sl
J
may operate differently from that of the other
genes tested.
The gene Yellow (A
v ) increases the incidence of pulmonary tumors,
mammary tumors in females, hepatomas in male mice (Heston and
Vlahakis, 1961), and induced skin tumors (Vlahakis and Heston, 1963).
The gene Yellow was introduced onto the strain 129 genetic background
by repeated backcrosses of A^-carrying animals to strain 129 mice. The
incidence of teratomas in A
y
animals was 4/420 and in their normal
littermates, 35/437. Yellow-bearing mice have only about one-tenth as
many teratomas as wild type.
The experimental induction of testicular teratomas in strain 129 mice
will be discussed in a later section, but it is appropriate to cite some
evidence on genetic control of susceptibility here. There is preliminary
LEROY C. STEVENS
have evidence of genetic influences, none have been shown to result
from a single gene. Instead they are inherited as threshold characters.
However, single genes can have a very strong effect on the incidence of
certain tumors.
B. Single Gene Influences
Single specific genes which influence susceptibility to teratocarcinogenesis in strain 129 mice have been identified.
To determine the effect of single genes on teratocarcinogenesis we
introduced several mutant genes onto the strain 129 background by
repeated backcrosses of animals carrying the mutation to strain 129
mice. The gene Steel (Sl
J
) was selected because it exerts striking effects
upon the development of primordial germ cells and has effects on pigment
which makes its presence detectable. The tumor incidence in males in
which the gene Sl
J
and its wild type allele were segregating was determined, and animals carrying the Sl
J
gene had more than twice as many
teratomas as their + / + littermates (Stevens and Mackensen, 1961).
Of the last 500 Sl
+
males observed in our laboratory, 14% of them had
spontaneous teratomas. Six percent of 500 of their + / + littermates had
tumors.
An allele of SI, Sl
d , has similar effects on the development of red
blood, pigment, and germ cells. Another locus, W, also affects these three
systems. Sl
d
and several alleles of W were introduced onto the strain
129 genetic background to test their influence on teratocarcinogenesis.
Four percent of the mutant-carrying mice developed testicular teratomas,
as did 4% of their wild-type littermates (Table I ) . Of the genes tested,
only Sl
J
doubles the incidence of teratomas in strain 129 mice. This may
mean that the tumor enhancing influence of Sl
J
is independent of the
slightly deleterious effect of Sl
J
on the development of germ cells, and
that it is another pleiotropic effect of this gene. Alternatively, the
deleterious effect of Sl
J
may operate differently from that of the other
genes tested.
The gene Yellow (A
v ) increases the incidence of pulmonary tumors,
mammary tumors in females, hepatomas in male mice (Heston and
Vlahakis, 1961), and induced skin tumors (Vlahakis and Heston, 1963).
The gene Yellow was introduced onto the strain 129 genetic background
by repeated backcrosses of A^-carrying animals to strain 129 mice. The
incidence of teratomas in A
y
animals was 4/420 and in their normal
littermates, 35/437. Yellow-bearing mice have only about one-tenth as
many teratomas as wild type.
The experimental induction of testicular teratomas in strain 129 mice
will be discussed in a later section, but it is appropriate to cite some
evidence on genetic control of susceptibility here. There is preliminary