Sentences with phrase «mutations in lung»

, Lee - Lin S, Varmus H (2015) Evidence that synthetic lethality underlies the mutual exclusivity of oncogenic KRAS and EGFR mutations in lung adenocarcinoma.

3) Unni A *, †, Lockwood WW *, †, Zejnullahu K, Lee - Lin S, Varmus H (2015) Evidence that synthetic lethality underlies the mutual exclusivity of oncogenic KRAS and EGFR mutations in lung adenocarcinoma.

Although previous studies have identified common somatic mutations in lung cancers, they primarily focused on a small set of genes

By contrast, they concluded that more than two - thirds of the mutations in lung cancer were due to environmental factors, mostly smoking.

Since the initial discovery of EGFR mutations in lung cancer 10 years ago, EGFR targeted therapies such as erlotinib (Tarceva) and afatinib (Gilotrif) have become a fundamental component of lung cancer therapy.

Although we know that chemicals in tobacco smoke cause mutations in lung cells that lead to lung cancers and ultraviolet light causes mutations in skin cells that lead to skin cancers, we have remarkably little understanding of the biological processes that cause the mutations which are responsible for the development of most cancers.

And pinpointing a genetic signature, such as EGFR mutations in lung cancer or HER2 mutations in breast cancer, can guide therapy decisions.

Paweletz and his colleagues are now developing a PCR - based test to detect drug resistance mutations in lung tumors.

«It became clear after reading the paper that crizotinib might also work in patients with the ALK mutation in lung cancer,» Shaw says.

Not exact matches

They'll also jointly market Pfizer's drug Xalkori, which is approved in more than 75 countries for treating non-small cell lung cancer in patients with a certain genetic mutation.

Geoff Oxnard, an assistant professor of medicine at Dana - Farber Cancer Institute and Harvard Medical School in Boston and one of Paweletz's collaborators, remarks that «I had a hospitalized patient last week, she's sick with metastatic lung cancer, and she's exactly the kind of patient who might have an [epithelial growth factor receptor (EGFR)-RSB- mutation, but I simply didn't have enough tissue to ask those questions yet.»

Brueckner's group looked for gene defects in two strains of mice with situs inversus, a mutation in which the heart, lungs, and other organs are inverted, like a mirror image.

Since the Lung Cancer Mutation Consortium trial began in 2009, many patients are now tested for mutated or altered genes before treatment.

Among patients who have this type of lung cancer, nearly one in three will carry a particular genetic mutation on their cancer cells.

To identify the relevant mutations the scientists analyzed the blood samples of 1,858 men from three independent cohorts in Europe and North America: the Swiss arm of the European Randomized Study for Prostate Cancer Screening, the large American Screening trial, Prostate, Lung, Colorectal, and Ovarian (PLCO), Princess Margaret Cancer Centre (University Health Network) and Mount Sinai Hospital (Sinai Health System) in Toronto.

Published in the Proceedings of the National Academy of Sciences, the study found that many species from the two plateaus underwent different mutations to produce the same result: hemoglobins more adept at snaring oxygen from the lungs before sharing it with the other organs that depend on it.

The approach is already routine for some cancer patients, such as women and men with breast cancer tumors that have high levels of a protein called HER2, or lung cancer tumors with mutations in the EGFR gene.

Many people with lung cancer harbour mutations in a gene called EGFR.

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.

Identification of a specific genetic mutation in patients with non-small-cell lung cancer (NSCLC) helps clinicians select the best treatment option.

(The K - Ras gene is mutated in 20 percent of lung cancer cases, and G12C is the most frequent mutation of K - Ras.)

Among patients with advanced non-small cell lung cancer without a mutation of a certain gene (EGFR), conventional chemotherapy, compared with treatment using epidermal growth factor receptor tyrosine kinase inhibitors, was associated with improvement in survival without progression of the cancer, but not with overall survival, according to a study in the April 9 issue of JAMA.

«High concordance between EGFR mutations from circulating - free tumor DNA and tumor tissue in non-small cell lung cancer.»

Epidermal growth factor receptor (EGFR) mutations found in the circulating free tumor DNA (ctDNA) from the plasma of advanced non-small cell lung cancer (NSCLC) patients correlates well with the EGFR mutations from patient - matched tumor tissue DNA.

According to the National Cancer Institute, more than a third of all human cancers, including a high percentage of pancreas, lung and colon cancers are driven by mutations in a family of genes known as Ras.

In the malignant tissue, they found up to 1500 genes with mutations — a level higher than has been found for either lung cancer in smokers or skin cancer in patients with heavy exposure to ultraviolet radiatioIn the malignant tissue, they found up to 1500 genes with mutations — a level higher than has been found for either lung cancer in smokers or skin cancer in patients with heavy exposure to ultraviolet radiatioin smokers or skin cancer in patients with heavy exposure to ultraviolet radiatioin patients with heavy exposure to ultraviolet radiation.

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are the preferred treatment option for patients with advanced non-small cell lung cancer (NSCLC) who have mutations in the EGFR gene.

They found that exposing lung cells with the ΔF508 mutation to VX - 770 long - term — mimicking what happens in patients who take the drug for extended periods — often made the CFTR protein function poorly when compared with short - term exposure.

B - raf gene mutations have known roles in the development of many human cancers including melanoma, lung and thyroid cancer.

Importantly, patients with mutations in a single copy of NKX2.1 often have Brain - Lung - Thyroid Syndrome, which is characterized by respiratory distress after birth and accompanied by decreased surfactant protein expression.

Rejection of lung melanoma metastasis in mice lacking the gene for Cbl - b (down left) or carrying a mutation in this gene (down right), as compared to Cbl - b sufficient mice (upper panels).

The study, called «Molecular Determinants of Drug - Specific Sensitivity for Epidermal Growth Factor Receptor (EGFR) Exon 19 and 20 Mutants in Non-Small Cell Lung Cancer,» and published online in the journal Oncotarget, demonstrates how computer modeling of EGFR mutations found in lung cancer can elucidate their molecular mechanism of action and consequently optimize the selection of therapeutic agents to treat patieLung Cancer,» and published online in the journal Oncotarget, demonstrates how computer modeling of EGFR mutations found in lung cancer can elucidate their molecular mechanism of action and consequently optimize the selection of therapeutic agents to treat patielung cancer can elucidate their molecular mechanism of action and consequently optimize the selection of therapeutic agents to treat patients.

«Rare mutation may extend survival in lung cancer patients with brain metastases.»

In 2015, Tomasetti and Vogelstein published a widely covered Science paper that found that R mutations explain the dramatic variation in cancer incidence among human tissues better than hereditary or environmental factors — helping to illuminate why tissues in the lung or colon give rise to cancer far more frequently than tissues in bone or brain, for examplIn 2015, Tomasetti and Vogelstein published a widely covered Science paper that found that R mutations explain the dramatic variation in cancer incidence among human tissues better than hereditary or environmental factors — helping to illuminate why tissues in the lung or colon give rise to cancer far more frequently than tissues in bone or brain, for examplin cancer incidence among human tissues better than hereditary or environmental factors — helping to illuminate why tissues in the lung or colon give rise to cancer far more frequently than tissues in bone or brain, for examplin the lung or colon give rise to cancer far more frequently than tissues in bone or brain, for examplin bone or brain, for example.

In less than five minutes, Ingber, the institute's 56 - year - old director, has pointed out a mattress that could prevent life - threatening sleep apnea in newborns; simulated lungs, intestines, and hearts made of silicone rubber using microchip manufacturing technology; and a machine that forces mutations in bacteria, directing their evolution so they can produce low - cost biofuels and drugIn less than five minutes, Ingber, the institute's 56 - year - old director, has pointed out a mattress that could prevent life - threatening sleep apnea in newborns; simulated lungs, intestines, and hearts made of silicone rubber using microchip manufacturing technology; and a machine that forces mutations in bacteria, directing their evolution so they can produce low - cost biofuels and drugin newborns; simulated lungs, intestines, and hearts made of silicone rubber using microchip manufacturing technology; and a machine that forces mutations in bacteria, directing their evolution so they can produce low - cost biofuels and drugin bacteria, directing their evolution so they can produce low - cost biofuels and drugs.

A new drug that targets not only common cancer - causing genetic mutations in patients with non-small cell lung cancer (NSCLC), but also a form of the mutation that causes resistance to treatment, has shown promising results in patients in a phase I / II clinical trial.

A small number of these mutations have been found previously in other cancers, and drugs have been developed to target these mutations,» said lead author Raphael Bueno, MD, chief of the Division of Thoracic Surgery at BWH and co-director of the BWH Lung Center.

Researchers at UT Southwestern Medical Center have identified mutations in two genes that cause a fatal lung scarring disease known as familial pulmonary fibrosis.

«The risk of lung cancer development in never - smoking carriers is greater than the risk of heavy smokers with or without the mutation,» says Dr. Gazdar, who is an IASLC member.

In one of the two studies, researchers found that germline EGFR T790M mutation results in a rare and unique lung cancer hereditary syndrome associated with an estimated 31 % risk for the disease in never - smokerIn one of the two studies, researchers found that germline EGFR T790M mutation results in a rare and unique lung cancer hereditary syndrome associated with an estimated 31 % risk for the disease in never - smokerin a rare and unique lung cancer hereditary syndrome associated with an estimated 31 % risk for the disease in never - smokerin never - smokers.

They want to find healthy individuals who have genetic mutations that usually cause serious disease in those who carry them, such as those for the lung disorder cystic fibrosis.

They found that the mutation occurred in approximately 1 % of NSCLCs and in less than one in 7,500 subjects without lung cancer.

Two studies are providing new insight into germline epidermal growth factor receptor (EGFR) T790M mutation in familial non-small cell lung cancer (NSCLC).

Alice Shaw recalls a signal moment in 2004 — just as she was finishing her oncology fellowship at MIT — when scientists discovered that mutations in a gene for epidermal growth factor receptor (EGFR) were the culprits in about 10 to 15 percent of lung cancer patients.

Columbia University Medical Center (CUMC) scientists have identified new genetic mutations that can cause pulmonary arterial hypertension (PAH), a rare fatal disease characterized by high blood pressure in the lungs.

To test VX - 770, the doorman drug, researchers used lung cells from a CF patient with the G551D mutation — the same one sickening the Cheevers girls, who required only a doorman drug to function in healthy mode.

In patients with this mutation, called G551D, the distorted protein obstructs the flow of salt and fluids through the surface of cells, causing mucus in the lungs to thicken like oatmeaIn patients with this mutation, called G551D, the distorted protein obstructs the flow of salt and fluids through the surface of cells, causing mucus in the lungs to thicken like oatmeain the lungs to thicken like oatmeal.

In collaboration with researchers in the Netherlands at University Hospital in Groningen and Rehab Beatrixoord in Haren, Howard found that a mutation in IL13 was associated with extreme contraction of the lungs in response to an inhaled chemical, a symptom of asthmIn collaboration with researchers in the Netherlands at University Hospital in Groningen and Rehab Beatrixoord in Haren, Howard found that a mutation in IL13 was associated with extreme contraction of the lungs in response to an inhaled chemical, a symptom of asthmin the Netherlands at University Hospital in Groningen and Rehab Beatrixoord in Haren, Howard found that a mutation in IL13 was associated with extreme contraction of the lungs in response to an inhaled chemical, a symptom of asthmin Groningen and Rehab Beatrixoord in Haren, Howard found that a mutation in IL13 was associated with extreme contraction of the lungs in response to an inhaled chemical, a symptom of asthmin Haren, Howard found that a mutation in IL13 was associated with extreme contraction of the lungs in response to an inhaled chemical, a symptom of asthmin IL13 was associated with extreme contraction of the lungs in response to an inhaled chemical, a symptom of asthmin response to an inhaled chemical, a symptom of asthma.

In patient samples of lung adenocarcinoma, 3 percent were found to have HER2 amplification and another 3 percent were found to have HER2 mutation.

The researchers, including scientists from pharmaceutical company AstraZeneca, report in an advanced online publication in Nature Medicine on May 4, that their findings indicate «an underappreciated genomic heterogeneity» in mechanisms of resistance to tyrosine kinase inhibitor (TKI) drugs that target the Epidermal Growth Factor Receptor (EGFR) mutation that drive some cases of non-small cell lung cancer (NSCLC).