Author: Timothy A. Dinh; Ramja Sritharan; F. Donelson Smith; Adam B. Francisco; Rosanna K. Ma; Rodica P. Bunaciu; Matt Kanke; Charles G. Danko; Andrew P. Massa; John D. Scott; Praveen Sethupathy
Title: Hotspots of aberrant enhancer activity in fibrolamellar carcinoma reveal molecular mechanisms of oncogenesis and intrinsic drug resistance Document date: 2020_1_18
ID: bf4qpsy7_67
Snippet: Transcriptional signal was quantified from enhancers and gene bodies as described above. Gene body and enhancer counts were normalized separately using DESeq2 and the Pearson correlation coefficients between the log2(normalized counts + 1) for genes and enhancers were calculated. To determine the statistical significance of the calculated correlation coefficients, we constructed a null distribution that consisted of correlation coefficients from .....
Document: Transcriptional signal was quantified from enhancers and gene bodies as described above. Gene body and enhancer counts were normalized separately using DESeq2 and the Pearson correlation coefficients between the log2(normalized counts + 1) for genes and enhancers were calculated. To determine the statistical significance of the calculated correlation coefficients, we constructed a null distribution that consisted of correlation coefficients from genes and enhancers on different chromosomes. For gene-enhancer pairs within 100 kb of each other, we calculated the empirical p-value based on the null distribution and adjusted for multiple testing using the Benjamini-Hochberg (FDR) procedure (Benjamini and Hochberg, 1995) .
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