The researchers therefore decided to take a closer look at the protein - encoding
genes in the mouse tumors.
If they succeed, they will then «knock out» either the p14ARF gene or the p53
gene in mouse tumors to see how the drug fares.
Not exact matches
Northwestern Medicine scientists have identified a small RNA molecule called miR - 182 that can suppress cancer - causing
genes in mice with glioblastoma mulitforme (GBM), a deadly and incurable type of brain
tumor.
Now,
in a provocative study that raises unsettling questions about the widespread use of vitamin supplements, Swedish researchers have showed that relatively low doses of antioxidants spur the growth of early lung
tumors in cancer - prone
mice, perhaps by hindering a well - known
tumor suppressor
gene.
However, cancer cells may instead be coaxed to turn back into normal tissue simply by reactivating a single
gene, according to a study that found that restoring normal levels of a human colorectal cancer
gene in mice stopped
tumor growth and re-established normal intestinal function within only 4 days.
Mice engineered to express Lin28
in their kidneys developed Wilms
tumor, which regressed when Lin28 was withdrawn, indicating that strategies aimed at blocking or deactivating the
gene hold therapeutic promise for children with Wilms.
In this mouse model, mutations in Kras and p53 genes resulted in the formation of individual tumor cell populations that were labeled with different color
In this
mouse model, mutations
in Kras and p53 genes resulted in the formation of individual tumor cell populations that were labeled with different color
in Kras and p53
genes resulted
in the formation of individual tumor cell populations that were labeled with different color
in the formation of individual
tumor cell populations that were labeled with different colors.
A virus that has shown promise as a vector for human
gene therapy causes liver
tumors in neonatal
mice.
BCL - 2 is present
in high amounts
in many
tumors and helps cancer cells to survive, but when the BCL - 2
gene is blocked by MM41
in mice, the cancer cells succumb to apoptosis and die.»
By deleting the
gene that expresses p300, the researchers safely reduced Treg function and limited
tumor growth
in mice.
Researchers at The Rockefeller University have shown that a new technique using RNA interference is able to find
genes that cause epidermal
tumor growth
in months rather than the decades it may take using traditional methods employing specially bred, genetically altered
mice.
«When we compared the
gene signature activity of glioblastoma cells from around 60 patients we found that a large number of patients could be divided into subgroups that showed a correlation between
gene activity,
tumor cell characteristics and cell of origin similar to the one we had seen
in the
mouse study.
Yilmaz, who studies colon cancer and how it is influenced by
genes, diet, and aging, decided to adapt this approach to generate colon
tumors in mice.
Using the
gene - editing system known as CRISPR, MIT researchers have shown
in mice that they can generate colon
tumors that very closely resemble human
tumors.
They've used a gun powered by pressurized helium to fire microscopic gold bullets, coated with
genes, into skin cells surrounding
tumors in mice.
«A new
tumor suppressor
gene for breast cancer
in mice.»
Humans have an ortholog of the murine Nrk
gene, and considering that the
gene expression pattern
in breast
tumor in Nrk mutant
mice was similar to that
in human luminal B breast cancer, the findings of this study may lead to further understanding of the mechanisms of human breast cancer suppression and to advances
in its diagnosis and therapy.
In any case, she and Yang have found that a week of
gene shots three to five times daily not only shrinks the
tumors but lengthens the lives of the
mice.
Radiation oncologist Anna Saran at the Italian National Agency for New Technologies, Energy and the Environment
in Rome and colleagues studied
mice with a mutation
in a
gene called Patched that makes them susceptible to brain
tumors early
in life.
The analysis also found that a significant fraction of
tumors contained rearrangements and mutations of a
gene called PREX2, and experiments confirmed that cancer - associated mutations of PREX2 promoted the growth of human melanoma cells
in mice.
Next steps include He's collaboration with Piedmont Atlanta Hospital to retrieve T cells, liver cancer cells and healthy tissue normally removed from patients during surgery, put the
mouse receptor
genes on these T cells and monitor
in a dish both how those cells now fight the
tumor and react to healthy human tissue.
In this latter group, they found thirteen
gene - environment interactions, also called «genetic loci,» which contribute to the
tumor susceptibility when the
mouse is exposed to low - dose radiation.
Bradner and Mitsiades had reported
in Cell
in 2011 that the inhibitor blocks the Myc cancer
gene and thereby slows the growth of multiple myeloma
tumors in mice.
However, their initial finding demonstrated that progenitor derived from iPSCs generated using lentiviral
gene transduction led to the high incidence of highly aggressive
tumors in immunodeficient
mice after transplantation under the kidney capsule.
After implanting the
tumor, they gave the
mice a drug to trigger the
tumor cells to express the aquaporin reporter
gene, which made the
tumor look darker
in MRI images.
The researchers showed that this technique was successful
in monitoring
gene expression
in a brain
tumor in mice.
His lab has extensive experience evaluating and modulating T cell responses to
tumors and viruses, including introducing
genes into T cells to impart specificity and modulate function, designing strategies to overcome tolerance and enhance
in vivo activity, and developing
mouse models that more accurately model human immune responses to candidate vaccines.
Scientists exploit
gene therapy to shrink
tumors in mice with an aggressive form of breast cancer.
This modification is of special interest to p53 - dependent anti-senescence and pro-longevity functions because genetically engineered
mice with p53 serine18 mutated to alanine (p53S18A) show increased ROS levels, metabolic stress,
tumor frequency, premature aging symptoms and defects
in regulation of a subset of p53 target
genes that include sestrins.
Thus, chronically increased p53 activity causes premature aging
in mice, whereas transgenic
mice with extra copies of p53 and ARF
genes under normal regulation show
tumor resistance and extended life span.
One
mouse was sequenced to 15x coverage, and among the handful of somatic nonsynonymous mutations found, one was recurrent, not only
in the APL
mice, but also
in the same
gene in human
tumors.
We are also applying CRISPR / Cas9 - mediated genome engineering to develop novel
mouse models
in order to explore the impact of
gene dosage alterations on
tumor development
in vivo.
These
mice developed multiple independent mammary
tumors of which the majority resembled human ILC
in terms of morphology and
gene expression.
These kind of
mice are an extraordinary resource for modeling human disease; for instance, research has found that
mice that are genetically mutated to carry the BRCA1
gene (a human breast cancer
gene) behave more similarly to human cancer patients than those
mice who have had a
tumor physically transplanted
in.