Sentences with phrase «aberrant dna»

«Many of the carcinogens present in mainstream smoke are known to exert their effects through a genotoxic mode of action, which is based on their ability to induce DNA damage and mutations, although an epigenetic mode of action, e.g., through aberrant DNA methylation and histone modifications, is also beginning to emerge for a few of these carcinogenic compounds.»
Aberrant DNA Methylation in Human iPSCs Associates with MYC - Binding Motifs in a Clone - Specific Manner Independent of Genetics
Transformed cells such as the Jurkat line may show aberrant DNA methylation patterns at specific loci [57], possibly complicating analyses of cytosine methylation and HIV - 1 latency.
Some researchers have conjectured, however, that the normal WS protein quashes formation of aberrant DNA structures in humans, a process that might go awry when the gene suffers a mutation.
Aberrant DNA methylation, or abnormal methylation, has been associated with an increased rate of malignancy.

Not exact matches

In cancers, both gene mutations and aberrant regulation of genes (promoter inhibition by methylation of DNA) are known to play pivotal roles regulating cancer growth.
The other marker is an aberrant pattern in the chromosomes; the DNA shows a greater number of abnormalities than normal, including DNA that is missing or moved.
Cancer cells that have a relatively large number of mutations in their DNA express aberrant proteins — or neoantigens — that reveal the cancer to the immune system.
DNA hypermethylation in prostate cancer is a consequence of aberrant epithelial differentiation and hyperproliferation.
This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma cell lines by modulating cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B - lymphoma cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B - cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T - cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent gene expression program.
The therapy is an 18 - letter string of DNA that corrects aberrant splicing by binding a unique sequence on SMN2 «s messenger RNA located just downstream of the crucial seventh exon, thereby obstructing components of the RNA splicing machinery (see «Bring to one's antisenses»).
Her graduate work culminated in multiple publications in the field of cancer epigenetics and in a thesis entitled «Aberrant epigenetic silencing of tumor suppressor genes in human cancer: the roles of DNA hypermethylation and the histone code.»
The generation of double - strand DNA breaks as a result of aberrant AID activity is strongly implicated in the genesis of MYC / IG translocations (Robbiani et al., 2008; Dorsett et al., 2007).
She also had to worry that any telomerase activity she saw was an aberrant result caused by one of the DNA polymerases that replicate the middle of the chromosomes.
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