And in an ironic twist, the work could yield a new way to treat common ailments such as heart disease and
cancer with gene therapies.
Not exact matches
The company will now be able to sell health risk reports on three variants found on the BRCA1 and BRCA2
genes, which are linked
with a higher risk of breast, ovarian, and prostate
cancer.
Cancer has a lot to do
with the
genes in our body and our family history, too.
At last year's Brainstorm Health conference in San Diego, Bergh found himself sitting at dinner
with Othman Laraki, the cofounder and CEO of Color Genomics — a company that extracts the DNA from a customer's submitted saliva sample and then looks for a set number of
gene mutations known to be associated
with increased risk for developing certain hereditary
cancers or heart conditions (depending on the test).
Editas, founded in 2013 in Cambridge, Massachusetts, is a visionary
gene - therapy company
with a pipeline of therapies for
cancer and lung, liver, muscle, eye, and blood diseases.
Novartis drug Kymriah was just approved in the U.S. to edit
cancer - fighting
genes in children
with leukemia.
Gilead, fresh from its CAR - T
cancer drug victory last year, has struck a deal
with gene - editing specialist Sangamo that could be worth up to $ 3 billion (
with $ 150 million in upfront cash).
His research has spanned hematopoiesis,
gene therapy, stem cell biology, genomics and
cancer, consistently focusing on bringing the very latest research advances to patients
with heretofore incurable diseases.
The Kamens claim the main thing that distinguishes their foundation from other brain tumor foundations is their focus on pediatric brain
cancer specifically, as well as their close ties
with pharmaceutical and biotech companies working in the fields of immunotherapy and target
gene therapy.
iPS cells tend to age prematurely and die; they are also created
with cancer - causing
genes, which could make them dangerous to use therapeutically.
Those who feel there is something «unnatural» about introducing human
genes into animals or plants forget that we share a high proportion of our
genes with these species already: it is precisely this collective heritage that allows experiments on frogs to spawn treatments for human
cancer.
Each of us
with breast
cancer (and I include men) has a different set of
genes, personal backgrounds and lifestyles.
The scientists were interested in understanding what factors influenced women to share test results, particularly
with their children, who might also be affected by the
cancer - conferring
genes.
Health matters: A recent study found that women
with good nutrition are more likely to have babies born
with a
cancer - suppressing
gene variant
About 41,000 women and 300 men are diagnosed
with breast
cancer every year, and in five per cent of cases the disease is caused by a hereditary mutation in the BRCA1 and BRCA2 breast
cancer genes.
With new tests to identify women who are at heightened risk of breast
cancer, new drugs aimed at preventing allergies, and the discovery of new
genes that are key to the progression of conditions like Alzheimer's - to give just three examples - we are at the dawn of a whole new era:
KRAS and p53 are
genes often associated
with cancer.
Inherited Neanderthal
genes come in alleles that help fight off nasty viruses such as Epstein - Barr — associated
with several kinds of
cancer, says Stanford University immunologist Laurent Abi - Rached.
The study, led by Dr Len Stephens and Dr Phill Hawkins and published today in the journal Molecular Cell, reveals why loss of the PTEN
gene has such an impact on many people
with prostate
cancer, as well as in some breast
cancers.
One - third of yeast
genes have counterparts in the human genome, many of which are associated
with diseases, such as
cancer.
Altered
gene imprinting at other times has been associated
with developmental disorders and
cancer.
Teixeira and his team also found that a malfunctioning tumor - suppressing
gene that's associated
with certain
cancers, such as colon and pancreatic, and is known as Stk11, additionally influenced the development of BPH.
These findings allowed researchers to create a chimera virus: a mouse virus
with a human viral
gene that can be used to test molecules that inhibit human LANA protein in an animal model of disease, treating not only human herpes virus infection but also its associated
cancers.
So Sandra Ryeom at the Children's Hospital in Boston and colleagues bred mice
with three
genes to find out if an extra copy gave them extra protection against
cancer.
Women
with precancer or
cancer were most likely to have particular versions of the viral
gene E7, which researchers are now interested in targeting.
The results, still in a preliminary stage, show that patients
with a specific variant in the RET
gene - a proto - oncogene or
cancer driver
gene; variant G2071A - could be more sensitive to this drug.
He and his colleagues are now investigating how
gene profiles are altered and whether these techniques could ease symptoms in people
with high blood pressure, inflammatory bowel disease and multiple myeloma, a type of bone marrow
cancer.
Mutations in these
genes have been associated
with one of the deadliest types of ovarian
cancer, called clear cell carcinoma.
Silencing five
genes whose expression negatively correlated
with caspase activity significantly increased
cancer cells» sensitivity to radiation (Genome Research, DOI: 10.1101 / gr.122044.111).
AN EXTRA copy of a
gene on chromosome 21 may explain why people
with Down's syndrome are less likely to get breast and lung
cancer than the rest of the population.
«We found 74
genes with 123 aberrations involved in
cancer growth.
Molecular characterization of the cells that undergo cell fate transition upon oncogenic Pik3ca expression demonstrated a profound oncogene - induced reprogramming of these newly formed cells and identified
gene expression signatures, characteristic of the different cell fate switches, which was predictive of the
cancer cell of origin, tumour type and clinical outcomes in women
with breast
cancers.
They started
with pairs of fat yellow mice known to scientists as agouti mice, so called because they carry a particular
gene — the agouti
gene — that in addition to making the rodents ravenous and yellow renders them prone to
cancer and diabetes.
«The reversible nature of the m6A methylmark adds a new layer to the regulation of
gene expression now termed «epitranscriptomics» and warrants further research to establish links
with human disease such as
cancer,» adds Dr Irmgard Haussmann of Coventry University.
The researchers are working
with the company Oxford BioMedica to develop this idea into a
gene therapy for
cancer.
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.
Novel abnormalities in the FGFR
gene, called FGFR fusions, were identified in a spectrum of
cancers, and preliminary results
with cancer cells harboring FGFR fusions suggested that some patients with these cancers may benefit from treatment with FGFR inhibitor drugs, according to data published in Cancer Discovery, a journal of the American Association for Cancer Res
cancer cells harboring FGFR fusions suggested that some patients
with these
cancers may benefit from treatment
with FGFR inhibitor drugs, according to data published in
Cancer Discovery, a journal of the American Association for Cancer Res
Cancer Discovery, a journal of the American Association for
Cancer Res
Cancer Research.
Women
with high levels of FGF1 were less likely to respond to platinum - based drugs, but blocking the
gene makes their cells lose their resistance (British Journal of
Cancer, DOI: 10.1038 / bjc.2012.410).
Because of a chromosomal abnormality, this
gene sometimes fuses
with another
gene and forms a hybrid, or a
gene fusion, resulting in a
gene product
with an entirely different function, causing
cancers.
Studies have shown that more than 50 % of all human
cancers carry defects in the p53
gene, and almost all other
cancers with a normal p53 function carry other defects which indirectly impair the
cancer - fighting function of p53.
This unexpected result suggests that mutations in NPM1 behave as gatekeepers for this
cancer; once a mutation in this
gene occurs in a cell
with particular previously accumulated pre-leukaemic mutations, the disease progresses rapidly to become leukemia.
Researchers at Moffitt
Cancer Center hope to improve NSCLC patient survival
with the results of a study that found that inherited genetic variations in interleukin
genes are associated
with improved patient survival and response to therapy.
«We don't want people coming into our clinic for intellectual disability and coming out
with a
cancer gene; this is not what they came for,» says Reis.
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.
Reviewing thousands of genome wide associate studies (GWAS) to identify genetic variants in single nucleotide polymorphisms (SNPs), investigators at Dartmouth's Norris Cotton
Cancer Center found that some alleles (one of a pair of
genes located on a specific chromosome) are more frequently risk - associated
with disease than protective.
PARP inhibitors have shown efficacy for a small group of patients
with breast
cancer with inherited mutations in BRCA
genes, but have failed in the more aggressive triple - negative disease.
PARP inhibitors are used primarily to treat tumors linked to defects in BRCA
genes, but may show promise in other
cancers when combined
with other drugs.
This study, published in the journal Microarrays, shows that lack of SOST in the bone microenvironment promotes the expression of many
genes associated
with cell migration and / or invasion, including long non-coding RNA MALAT1 in prostate
cancer, suggesting that SOST has an inhibitory effect on prostate
cancer invasion.
The researchers demonstrated that blocking the PGD enzyme genetically or
with a pharmacologic inhibitor reversed the epigenetic reprogramming and malignant
gene expression changes detected in distant metastases, and also strongly inhibited their tumor - forming capacity,
with no effect on normal cells or peritoneal pancreatic
cancer controls.
«Every woman
with breast
cancer is now tested for that
gene.