1014 results for "1993+article+mouse+line+professor+BA+psychology"

in 6.36 milliseconds.

• Genetic Landscape of Esophageal Squamous Cell Carcinoma Defined by Exome Sequencing on Chinese Patient Cohort and Cell Lines

  Esophageal Squamous Cell Carcinoma (ESCC) is one of the deadliest cancers worldwide. To define the genetic landscape of ESCC, whole exome sequencing was performed on 113 pairs of tumor and normal DNA samples collected from Chinese individuals with treatment-naive primary ESCC, along with 8 cell lines, including 7 from KYSE series ESCC cell lines and one immortalized esophageal squamous epithelial cell line Het-1A.

  Study EGAS00001000932

• Sequencing of liver cancer cell lines

  Liver cancer is a dreadful disease with limited therapeutic options. How to translate genomic findings into biomarkers and precision treatment is challenging. A large cell line-based platform was established, termed as Liver Cancer Model Repository. Heterogeneities in patients were faithfully recapitulated by 81 liver cancer cell lines at genomic and transcriptomic levels. This platform provides a rich resource and models to study cancer drivers and drug responses in liver cancer.

  Study EGAS00001002237

• GBM-ZEB1: RNA sequencing of parental tumors used for cell line generation

  This dataset contains RNA sequencing raw data from four parental tumors that were used for classification of gene expression subtypes (Verhaak, Cancer Cell 2010) using ssGSEA.

  Dataset EGAD00001001627

• ChIP-seq and Hodgkin lymphoma

  ChIP-seq data (H3K4Me3, H3K27Ac histone modifications) of Hodgkin lymphoma cell line L-428. Samples were processed as previously described (Sud et al., 2018). The files are in bam format, aligned to build 37 of the human genome.

  Dataset EGAD00001004322

• Whole genome sequencing of an individual's genomic DNA and that of its lymphoblastoid cell line.

  The genetic consequences of cellular transformation by Epstein-Barr-Virus were assessed by comparing whole genome sequences of the original genome (before transformation) and the genome after transformation.

  Dataset EGAD00001000693

• 10x Genomics Single Cell Gene Expression for SA1056

  10x Genomics Single Cell Gene Expression for Telomerase immortalized breast epithelium cell line 184-hTERT-22 L9 116.126

  Dataset EGAD00001009112

• 10x Genomics Single Cell Gene Expression for SA1188

  10x Genomics Single Cell Gene Expression for Telomerase immortalized breast epithelium cell line 184-hTert L9 116.66

  Dataset EGAD00001009114

• RNA-seq bulk

  This dataset gather all RNA-sequencing data in MM.1S cell line in control and Dex condition; both in 3 biological replicates

  Dataset EGAD00001011137

• HiChIP bulk

  This dataset gather HiChIP data for H3K27ac mar in MM.1S cell line in control and Dex condition, both in two biological replicates

  Dataset EGAD00001011138

• LCCC1122: Defining the Triple Negative Breast Cancer Kinome Response to GSK1120212

  In this study the investigators looked at adaptive reprogramming impact on the kinome when a MEK inhibitor called GSK1120212 (trametinib) was administered in a "window of opportunity" trial. GSK1120212 is not yet approved by the FDA for use in breast cancer patients. The investigators gave GSK1120212 for a short period of time (one week) to examine MEK and the other kinase expression in cancer cells both before and after the study drug is given. The investigators gave this drug for research purposes only. The length of time it was given is not intended to treat cancer. Recently researchers at UNC developed a process that can comprehensively profile the majority of the individual kinases in the kinome and examine the impact on kinase expression of kinase inhibitors (Duncan et al, Cell 2012, PMID: 22500798). This can tell us which kinases need to be concurrently blocked to augment responsiveness and prevent acquired resistance so that the investigators can design the best combinations of kinase blocking drugs for triple negative breast cancer. This is especially important for individuals with triple negative breast cancer (TNBC) because there are no targeted drugs available that can block molecules that affect tumor growth. The investigators believe that kinase-blocking drugs have the potential to be a more effective treatment for people with TNBC. In this recently published study (Zawistowski et al, Cancer Discovery 2017, PMID: 28108460), TNBC patients treated with trametinib for 7 days resulted in a transcriptional response characterized by significant reprogramming of the tyrosine kinome, and this adaptive bypass response in human tumors was found to be similar to that seen in preclinical models including TNBC cell lines and mouse xenografts. In this study we also examined whether reprogramming differed between TNBC molecular subtypes, finding that basal-like and claudin-low human TNBC cells and mouse tumor subtypes had different adaptive transcriptional responses to MEK-ERK inhibition. Mechanistically we found that genome-wide enhancer remodeling drove the adaptive transcriptional response, suggesting that epigenetic approaches to reprogramming may be more durable than kinase inhibitor polypharmacology.

  Study phs001405