Sentences with phrase «genes in cancer cells»

«We saw hundreds of changes in genes in cancer cells that had not been identified before, and for each of these, HHMI research associate Alberto Bardelli had to perform comparisons with the normal tissues of the same patient, to see if the mutation was specific to the cancer,» he said.

Biologist Michael Wigler of Cold Spring Harbor Laboratory, who led the study, started out studying genes in cancer cells but soon realized he was seeing unexpected patterns in the healthy cells he examined for reference.

But the cells also changed shape and other properties in the absence of the protein in ways that reduced the likelihood that they would travel away from the tumor — a sign that myoferlin not only changes genes in cancer cells, but also alters the cells» mechanical properties.

This question has been challenging to address experimentally because attempts to restore function to lost or mutated genes in cancer cells often trigger excess gene activity, causing other problems in normal cells.

Her laboratory seeks to describe and understand the molecular mechanisms governing the activity of the GLI2 gene in cancer cells.

My laboratory seeks to describe and understand the molecular mechanisms governing the activity of the GLI2 gene in cancer cells.

Not exact matches

Cancer - focused CRISPR technology involves taking a set of molecular shears and the guiding molecule Cas9 in order to cut out unwanted genes in immune cells that may help proliferate cancers.

One of the key caveats at the time, however, was that the technique required the use of a virus to introduce several genes into the skin (or other) cell, and these would remain in the cell, and so might contaminate the resulting stem cell or create cancer risks.

Davies and Lineweaver suggest that genes active in embryogenesis and switched off later may be reactivated because of damage, causing the accelerated cell division of these rogue cancer cells.

She demonstrated that early experience leads to lasting changes in the molecular structure of the brain and discovered a gene involved in the spread of brain cancer cells into healthy brain tissue.

However, the impact of the two methylation - regulating enzymes was still seen at 10 to 15 months, when scientists found decreased expression of hundreds of genes — many of which are key tumor suppressor genes such as BMP3, SFRP2 and GATA4 — in the smoke - exposed cells and a five - or - more-fold increase in the signaling of the KRAS oncogene that is known to be mutated in smoking - related lung cancers.

«Cancer cells disguise themselves by switching off genes, new research reveals: A genome - wide map of the genes switched off in aggressive tumors reveals a «signature».»

Chronic cigarette smoke exposure, as noted in many human cancers, tends to block these cell maturation genes from properly turning on, says Baylin.

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.

If this gene plays a role in energy homeostasis and energy balance in the context of obesity, Wang reasoned, perhaps it could play a role in the energy requirements of liver cancer cells.

«In addition, changes in how the genes are expressed (turned on or off) could be used in the future to predict how and when the cancer cells will spread to other parts of the body and how fast they will grow.&raquIn addition, changes in how the genes are expressed (turned on or off) could be used in the future to predict how and when the cancer cells will spread to other parts of the body and how fast they will grow.&raquin how the genes are expressed (turned on or off) could be used in the future to predict how and when the cancer cells will spread to other parts of the body and how fast they will grow.&raquin the future to predict how and when the cancer cells will spread to other parts of the body and how fast they will grow.»

«We think that these genes, which are normally only expressed in the placenta to facilitate invasion, are becoming reactivated in cancer cells and supporting invasion in this context too,» she says.

Mutations in these genes have been associated with one of the deadliest types of ovarian cancer, called clear cell carcinoma.

Lewis is now skimming through these genes to check their function; of those he's looked at so far, several are involved in growth and development, cell differentiation, cell death, and protecting against cancer.

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.

Sutherland says the genes she studies are already silenced in healthy adult tissue, so theoretically researchers should be able to design therapies that re-silence them in cancer cells without side effects.

Carlo Croce, a cancer researcher at Ohio State University in Columbus, and his colleagues created a diagram of interacting miRNAs for normal body cells by connecting them according to which genes they target and the function of those genes, in a way similar to analyses of human social networks.

Together, these signals activate ADAR1, which edits specific RNA in a way that stabilizes a gene that can make cancer stem cells more aggressive.

He identified gene mutations in breast cancer cells that affect their ability to recognize viruses, including some mutations that would be expected to significantly increase the cells» vulnerability to viruses implicated in breast cancer.

Over the past 15 years, the GFP gene has enabled scientists to watch a plethora of previously murky biological processes in action: how nerve cells develop in the brain, how insulin - producing beta cells form in the pancreas of an embryo, how proteins are transported within cells, and how cancer cells metastasize through the body.

«Fibroblast growth factor receptor inhibitors are new therapies being developed in clinical trials for patients whose cancer cells have genetic alterations in this family of genes,» says Roychowdhury, a member of the OSUCCC — James Translational Therapeutics Program.

The findings by a team of Massachusetts General Hospital (MGH) investigators, which will be published in the April 24 issue of Cell and are receiving advance online release, support the importance of epigenetics — processes controlling whether or not genes are expressed — in cancer pathology and identify molecular circuits that may be targeted by new therapeutic approaches.

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 Rescancer 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 ResCancer Discovery, a journal of the American Association for Cancer ResCancer Research.

In these canine cells we induced a morphological change similar to what happens in cancer progression and we have seen displayed significant alterations in the modulation of genes, called epigenetic lesions,» says Manel EstelleIn these canine cells we induced a morphological change similar to what happens in cancer progression and we have seen displayed significant alterations in the modulation of genes, called epigenetic lesions,» says Manel Estellein cancer progression and we have seen displayed significant alterations in the modulation of genes, called epigenetic lesions,» says Manel Estellein the modulation of genes, called epigenetic lesions,» says Manel Esteller.

Their analysis of more than 4,000 individual tumor cells, the largest effort to date in brain tumors, finds three developmental categories of cancer cells — one resembling neural stem cells and two characterized by sets of genes indicting paths towards differentiation.

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.

Bloch's colleagues at the National Institute of Environmental Health Sciences tested the oils in gene expression studies on lab - grown human breast cancer cells and found that they could mimic estrogens, the primary female sex hormones, and inhibit androgens, the primary male sex hormones.

Moreno and his team already have shown that when cell - competition genes are knocked out in mice, cancer growth is inhibited.

Ovarian cancer cells use autophagy all of the time, but also lose several copies of autophagy genes resulting in a compromised capacity.

In the study, they found that miR - 182 suppressed Bcl2L12, a cancer gene that blocks cancer cell death in response to chemo - and radiation therapIn the study, they found that miR - 182 suppressed Bcl2L12, a cancer gene that blocks cancer cell death in response to chemo - and radiation therapin response to chemo - and radiation therapy.

Moreno also found a homologue of a human cancer gene involved in cell competition.

Now, by harnessing advances in genome editing to slice and dice genes in donor T cells, researchers have created a new type of cancer immunotherapy.

«We'd like to extend this further to examine for driver genes in other types of lung cancer, such as squamous cell lung cancer.»

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.

These include the ability to bring new, innovative products to the market; progress in oncology, such as the approval of Genentech's drug Avastin for breast cancer and advances in the use of gene therapy, despite some setbacks; continuing progress in research on stem cells; the emergence of treatments for previously untreated diseases; and solutions for food and fuel shortages, such as biocrops and biofuels.

Whether investigating fat cells, immunotherapy or use of the CRISPR - Cas 9 gene - editing tool, which a federal panel recently approved for a select number of patients suffering from three types of cancers, including multiple myeloma, approaches beyond attacking cancer cells are needed in the fight against many cancers.

The scientists have shown that, in all cancers, a sort of «identity crisis» is observed in cancerous cells: in the organs or tissues in which a tumor develops, genes specific to other tissues or to other stages of the development of the organism express themselves in an aberrant manner.

As cells divide and grow, mutations may crop up in cancer - associated genes.

Vogelstein, Kenneth Kinzler, and other colleagues found a minor change in the APC gene, which normally holds cell growth in check and can cause colon cancers when mutated.

Genes with increased activity are in metabolic pathways that allowed cancer cells to bypass BRAF altogether and continue to grow and divide.

In cancer, these switches inappropriately activate or silence important genes, such as those that regulate cell growth and life cycle, ultimately leading to tumors.

By providing a woman's family history of these cancers, including the ages they were diagnosed, the programs calculate a probability that the patient carries a harmful mutation in BRCA1 or BRCA2 (genes involved in controlling malignant cell growth).

Epigenetic therapies are thought to work in two ways to fix these errors in cancer cells — by correcting the «position» of the gene switches and by making the cell appear as though it's infected by a virus, triggering the immune system.

Previous studies of genetic alterations in lymphoma and lung cancer have found that certain genetic mutations — specifically when part of a gene breaks off and gets fused to another — can inappropriately switch on ALK, driving cancer cells to grow and divide.