When tumor
suppressor genes work properly, they «slow down cell division,» repair broken DNA, and trigger programmed cell death.
Not exact matches
Working with colleagues at St. Vincent's Hospital in Sydney, Martin identified two individuals who had the characteristics of hereditary nonpolyposis colorectal cancer, which is usually caused by a mutation that inactivates one of a person's two copies of the tumor
suppressor gene MLH1, but who showed no signs of mutation.
On the other hand, our earlier
work also showed that this enzyme acts to silence tumor -
suppressor genes.
In a previous study, his team
worked with other collaborators to identify the potential role of extra copies of the tumor
suppressor gene (p53) that increase the elephant's ability to eliminate pre-cancerous cells with DNA damage.
After
working on the genetics of yeasts during a Ph.D. in pharmacy at the University of Valencia, Gil moved to the United States for a postdoc on human
suppressor genes.
BRCA1 and 2,
genes whose proteins are supposed to
work as tumor
suppressors and also repair DNA damage, were the first known risk factor
genes for familial breast cancer as well as ovarian and other cancers.
The drug, lapatinib, activates the
suppressor called FOXO, in HER2 + breast cancer cells, but then FOXO becomes a turncoat molecule,
working with an epigenetic regulator that controls
gene expression.
During his 11 years of extensive
work experience in the fields of cell and cancer biology (including
work on the famous tumor
suppressor gene BRCA1), and biochemistry he has successfully published in peer - reviewed journals such as Molecular and Cell Biology and Cancer Research.
In their study paper, the authors note that a «hallmark of advanced prostate cancer» is that two tumor
suppressor genes — PTEN and p53 — do not
work properly because they are mutated.
Her graduate
work culminated in multiple publications in the field of cancer epigenetics and in a thesis entitled «Aberrant epigenetic silencing of tumor
suppressor genes in human cancer: the roles of DNA hypermethylation and the histone code.»
«We expected Ezh2 to be an oncogene in this aggressive tumor, but our
gene - editing
work revealed it to be a tumor
suppressor,» said corresponding author Martine Roussel, Ph.D., a member of the Department of Tumor Cell Biology at St. Jude Children's Research Hospital.
When mutated, or not
working properly, cells with abnormal tumor
suppressor genes are more likely to grow out of control and lead to the development of cancer.
These
suppressor genes are inactivated in tumors, and since cancer drugs
work by reducing the activity of enzymes, they won't
work on such
suppressors because a drug can't inhibit a
gene that is already inactivated.»