But by hierarchical clustering of observed alterations in endocytosis, the researchers identified two distinct cancer phenotype clusters, one
marked by mutations in the oncogene KRAS in mesenchymal cells and the other by changes in epithelial cells.
Not exact matches
Using gene sequencing tools, scientists from Johns Hopkins Medicine and the University of British Columbia have found a set of genetic
mutations in samples from 24 women with benign endometriosis, a painful disorder
marked by the growth of uterine tissue outside of the womb.
A rare eye disorder
marked by color blindness, light sensitivity, and other vision problems can result from a newly discovered gene
mutation identified
by an international research team, including scientists from Columbia University Medical Center (CUMC).
By performing DNA sequencing of more than 4,000 families affected by neurological problems, the two research teams independently discovered that a disease marked by reduced brain size and sensory and motor defects is caused by a mutation in a gene called CLP1, which is known to regulate tRNA metabolism in cell
By performing DNA sequencing of more than 4,000 families affected
by neurological problems, the two research teams independently discovered that a disease marked by reduced brain size and sensory and motor defects is caused by a mutation in a gene called CLP1, which is known to regulate tRNA metabolism in cell
by neurological problems, the two research teams independently discovered that a disease
marked by reduced brain size and sensory and motor defects is caused by a mutation in a gene called CLP1, which is known to regulate tRNA metabolism in cell
by reduced brain size and sensory and motor defects is caused
by a mutation in a gene called CLP1, which is known to regulate tRNA metabolism in cell
by a
mutation in a gene called CLP1, which is known to regulate tRNA metabolism in cells.
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.