Juliann Chmielecki

Mixed responses to targeted therapy driven by chromosomal instability through p53 dysfunction and genome doubling

Longitudinal Analyses of Circulating Tumor DNA for the Detection of EGFR Mutation-Positive Advanced NSCLC Progression During Treatment: Data From FLAURA and AURA3

Candidate mechanisms of acquired resistance to first-line osimertinib in EGFR-mutated advanced non-small cell lung cancer

Analysis of acquired resistance mechanisms to osimertinib in patients with EGFR-mutated advanced non-small cell lung cancer from the AURA3 trial

Early Clearance of Plasma <i>Epidermal Growth Factor Receptor</i> Mutations as a Predictor of Outcome on Osimertinib in Advanced Non–Small Cell Lung Cancer; Exploratory Analysis from AURA3 and FLAURA

Biomarker-Directed Phase II Platform Study in Patients With EGFR Sensitizing Mutation-Positive Advanced/Metastatic Non-Small Cell Lung Cancer Whose Disease Has Progressed on First-Line Osimertinib Therapy (ORCHARD)

Osimertinib in Patients With Epidermal Growth Factor Receptor Mutation–Positive Non–Small-Cell Lung Cancer and Leptomeningeal Metastases: The BLOOM Study

Early clearance of plasma EGFR mutations as a predictor of response to osimertinib and comparator EGFR-TKIs in the FLAURA trial.

Programmed Cell Death Ligand 1 Expression in Untreated EGFR Mutated Advanced NSCLC and Response to Osimertinib Versus Comparator in FLAURA

Adavosertib with chemotherapy (CT) in patients (pts) with platinum-resistant ovarian cancer (PPROC): An open label, four-arm, phase II study.

Mechanisms of acquired resistance to first-line osimertinib: Preliminary data from the phase III FLAURA study

Analysis of resistance mechanisms to osimertinib in patients with EGFR T790M advanced NSCLC from the AURA3 study

Mechanisms of acquired resistance to first-line osimertinib: Preliminary data from the phase III FLAURA study

Analysis of 100,000 human cancer genomes reveals the landscape of tumor mutational burden

FGFR1 and NTRK3 actionable alterations in “Wild-Type” gastrointestinal stromal tumors

Activation Mechanism of Oncogenic Deletion Mutations in BRAF, EGFR, and HER2

Recurrent Loss of NFE2L2 Exon 2 Is a Mechanism for Nrf2 Pathway Activation in Human Cancers

Comprehensive Genomic Profiling Identifies a Subset of Crizotinib-Responsive <i>ALK</i>-Rearranged Non-Small Cell Lung Cancer Not Detected by Fluorescence In Situ Hybridization

Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors

Near universal detection of alterations in <scp><i>CTNNB1</i></scp> and <scp>Wnt</scp> pathway regulators in desmoid‐type fibromatosis by whole‐exome sequencing and genomic analysis

Emergence of RET rearrangement co-existing with activated EGFR mutation in EGFR -mutated NSCLC patients who had progressed on first- or second-generation EGFR TKI

Prospective Comprehensive Genomic Profiling of Advanced Gastric Carcinoma Cases Reveals Frequent Clinically Relevant Genomic Alterations and New Routes for Targeted Therapies

Comprehensive genomic profiling of biliary tract cancers to reveal tumor-specific differences and genomic alterations.

Anchored multiplex PCR for targeted next-generation sequencing

Comprehensive Genomic Analysis of Rhabdomyosarcoma Reveals a Landscape of Alterations Affecting a Common Genetic Axis in Fusion-Positive and Fusion-Negative Tumors

Whole-Exome Sequencing Reveals Frequent Genetic Alterations in <i>BAP1</i> , <i>NF2</i> , <i>CDKN2A</i> , and <i>CUL1</i> in Malignant Pleural Mesothelioma

A Pan-Cancer Analysis of Transcriptome Changes Associated with Somatic Mutations in U2AF1 Reveals Commonly Altered Splicing Events

Identifying <i>ALK</i> rearrangements that are not detected by FISH with targeted next-generation sequencing of lung carcinoma.

Whole-exome sequencing identifies a recurrent NAB2-STAT6 fusion in solitary fibrous tumors

Lung cancers with acquired resistance to EGFR inhibitors occasionally harbor <i>BRAF</i> gene mutations but lack mutations in <i>KRAS, NRAS,</i> or <i>MEK1</i>