Rachana Jayaraman
A5088555795- Melanoma and MAPK Pathways
- Cancer Research and Treatments
- Mechanisms of cancer metastasis
- Cancer Genomics and Diagnostics
- Glioma Diagnosis and Treatment
- Cancer Cells and Metastasis
- RNA Research and Splicing
- RNA modifications and cancer
- CRISPR and Genetic Engineering
- Trace Elements in Health
- RNA regulation and disease
- Cancer-related Molecular Pathways
Ontario Genomics
2023
University of California, Los Angeles
2021
Focal amplifications (FA) can mediate targeted therapy resistance in cancer. Understanding the structure and dynamics of FAs is critical for designing treatments that overcome plasticity-mediated resistance. We developed a melanoma model dual MAPK inhibitor (MAPKi) bears BRAFV600 through either extrachromosomal DNA (ecDNA)/double minutes (DM) or intrachromosomal homogenously staining regions (HSR). Cells harboring BRAFV600E displayed mode switching between DMs HSRs, from both de novo genetic...
Abstract Accurately modeling and predicting RNA biology has been a long-standing challenge, bearing significant clinical ramifications for variant interpretation the formulation of tailored therapeutics. We describe foundation model biology, “BigRNA”, which was trained on thousands genome-matched datasets to predict tissue-specific expression, splicing, microRNA sites, binding protein specificity from DNA sequence. Unlike approaches that are restricted missense variants, BigRNA can identify...
Abstract Cancer cells display two modes of focal amplifications (FA): extrachromosomal double minutes (DMs/ecDNAs) and intrachromosomal homogenously staining regions (HSRs). Understanding the plasticity these is critical for preventing targeted therapy resistance. We developed a combined BRAF plus MEK inhibitor resistance melanoma model that bears high through both ecDNA HSR modes, investigated FA dynamics in context drug plasticity. Cells harboring FAs displayed mode switching between...
<div>Abstract<p>Focal amplifications (FA) can mediate targeted therapy resistance in cancer. Understanding the structure and dynamics of FAs is critical for designing treatments that overcome plasticity-mediated resistance. We developed a melanoma model dual MAPK inhibitor (MAPKi) bears <i>BRAF</i><sup>V600</sup> through either extrachromosomal DNA (ecDNA)/double minutes (DM) or intrachromosomal homogenously staining regions (HSR). Cells harboring...
Supplementary Figure from Plasticity of Extrachromosomal and Intrachromosomal <i>BRAF</i> Amplifications in Overcoming Targeted Therapy Dosage Challenges
Supplementary Figure from Plasticity of Extrachromosomal and Intrachromosomal <i>BRAF</i> Amplifications in Overcoming Targeted Therapy Dosage Challenges
<div>Abstract<p>Focal amplifications (FA) can mediate targeted therapy resistance in cancer. Understanding the structure and dynamics of FAs is critical for designing treatments that overcome plasticity-mediated resistance. We developed a melanoma model dual MAPK inhibitor (MAPKi) bears <i>BRAF</i><sup>V600</sup> through either extrachromosomal DNA (ecDNA)/double minutes (DM) or intrachromosomal homogenously staining regions (HSR). Cells harboring...
<title>Abstract</title> Accurately modeling and predicting RNA biology has been a long-standing challenge, bearing significant clinical ramifications for variant interpretation the formulation of tailored therapeutics. We describe foundation model biology, “BigRNA”, which was trained on thousands genome-matched datasets to predict tissue-specific expression, splicing, microRNA sites, binding protein specificity from DNA sequence. Unlike approaches that are restricted missense variants,...