| Non-Scientific Abstract T Cells are one of the most important types of
cells in the immune systems of humans.When these cells grow out of control, however, they can lead to
many different types of cancers. One molecule that is important in the growth of these cells is called
Ras, a molecule that normally regulates cell growth.When Ras gets mutated it can cause cells to become
cancerous. This study shows how Ras may cause cancer in T Cells.There are three main ways in which Ras
could cause cancer: by increasing the survival time of the cells,by increasing the rate of replication
of the cells, or by protecting the cells from death.Any of these three mechanisms would cause an
excess of T cells, which could lead to cancer. The results show that the mutated Ras causes T Cells to
survive longer and multiply more, leading to a cancerous state but that Ras does not protect the cell
against death.
Abstract The Ras proto-oncogene is a gene that is normally found in cells and,when activated by cell receptors, tells cells to grow and multiply. The V12
mutation of Ras induces an oncogenic state, causing the cell to grow uncontrollably. This study characterizes this mutation in T Cells. Primary
murine T Cells were infected with a retroviral vector containing either V12 Ras or V12 Ras with a second mutation in the effector region of the
Ras protein. These cells were then assayed to characterize the survival, proliferation, apoptosis prevention, and molecular signaling conferred
by the inserted gene. Results show that only the single V12 mutant increases the survival of T Cells. Only V12 and one of the effector mutants,
C40, increased proliferation of the T Cells. No mutants provided protection against drug-induced cell death. These results provide conclusive
evidence that V12 Ras is oncogenic in T Cells through excessive growth and that residue 40 in the effector region is not a crucial component of
the signaling pathway.The Ras proto-oncogene is a gene that is normally found in cells and,when activated by cell receptors, tells cells to grow and multiply. The V12
mutation of Ras induces an oncogenic state, causing the cell to grow uncontrollably. This study characterizes this mutation in T Cells. Primary
murine T Cells were infected with a retroviral vector containing either V12 Ras or V12 Ras with a second mutation in the effector region of the
Ras protein. These cells were then assayed to characterize the survival, proliferation, apoptosis prevention, and molecular signaling conferred
by the inserted gene. Results show that only the single V12 mutant increases the survival of T Cells. Only V12 and one of the effector mutants,
C40, increased proliferation of the T Cells. No mutants provided protection against drug-induced cell death. These results provide conclusive
evidence that V12 Ras is oncogenic in T Cells through excessive growth and that residue 40 in the effector region is not a crucial component of
the signaling pathway. |
