Sentences with phrase «by mutations in specific genes»

Familial cancer, also known as hereditary cancer is a condition caused by mutations in specific genes that is passed from parent to child.

Luxturna is the first of a crop of treatments that target diseases caused by mutations in specific genes, and thus is referred to by many as the first gene therapy in the U.S.

Luxturna is the first gene therapy approved in the U.S. that targets a disease caused by mutations in a specific gene.

Many idiopathic epileptics have inherited epilepsy: epilepsy caused by a mutation in a specific gene that they inherited from their parents.

Not exact matches

In fact, there are two specific mechanisms for activation of BRAF implicated in PA formation: by fusion of the gene with nearby gene KIAA1549 (K: B fusion) or by point mutations of the BRAF gene itselIn fact, there are two specific mechanisms for activation of BRAF implicated in PA formation: by fusion of the gene with nearby gene KIAA1549 (K: B fusion) or by point mutations of the BRAF gene itselin PA formation: by fusion of the gene with nearby gene KIAA1549 (K: B fusion) or by point mutations of the BRAF gene itself.

By also examining this genetic region in two other families with similar disorders, the researchers were able to pinpoint a mutation in a specific gene, NT5E, which is involved in breaking down calcification in the arteries.

And while scientists have had some success in switching off genes by inserting or deleting random sequences, they have not yet been able to use CRISPR / Cas9 to paste in (or «knock in») specific new sequences to correct mutations in T cells.

She found, for example, that by using a technique called the polymerase chain reaction to amplify genes, she could detect mutations or rearrangements in cancer - specific genes in irradiated tissue that had turned cancerous.

However, researchers have been frustrated by the lack of methods to target mutations to specific genes in the zebrafish.

Chen, also an expert in the processes by which genes are turned on and off, has pioneered cutting - edge organoid systems that recreate prostate tumors and will allow the team to much more easily test the activity of various drugs against tumors with specific mutations.

Programmable nucleases, ZFN, TALEN and RGENs enable gene knockout in cultured cells and organisms by producing site - specific DNA double - strand breaks, whose repair via error - prone non-homologous end joining (NHEJ) or microhomology - mediated end joining (MMEJ) gives rise to frameshift mutations.

A specific codon (34) in U2AF1 harbored missense mutations in multiple AML tumors, suggesting a gain - of - function for the splicing factor encoded by that gene.

These mutant kinases are attractive therapeutic targets, as demonstrated by the efficacy of imatinib in BCR - ABL — positive chronic myelogenous leukemia (CML), 5 as well as in MPD associated with activating alleles involving PDGFRA or PDGFRB.2, 6,7 In addition, activating mutations in the FLT3 receptor tyrosine kinase are the most common genetic event in acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin BCR - ABL — positive chronic myelogenous leukemia (CML), 5 as well as in MPD associated with activating alleles involving PDGFRA or PDGFRB.2, 6,7 In addition, activating mutations in the FLT3 receptor tyrosine kinase are the most common genetic event in acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin MPD associated with activating alleles involving PDGFRA or PDGFRB.2, 6,7 In addition, activating mutations in the FLT3 receptor tyrosine kinase are the most common genetic event in acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowIn addition, activating mutations in the FLT3 receptor tyrosine kinase are the most common genetic event in acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin the FLT3 receptor tyrosine kinase are the most common genetic event in acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknown.

There are two general types of resistance genes found in wheat: Race - specific genes confer a high - level of resistance to specific strains of leaf rust but can be easily overcome by genetic mutation in pathogen populations, while slow rusting (APR) resistance provides partial resistance to a broad spectrum of races, but is typically effective only at the adult stage of plant growth.

The focus of the conference was connecting how epigenetics (cellular and physiological phenotypic trait variations that are caused by external or environmental factors that switch genes on and off and affect how cells read genes instead of being caused by changes in the DNA sequence — in other words nutrition and lifestyle choices) impact whether or not an individual actually develops a specific health issue even though they have a SNP mutation.