Publications by authors named "C J Weeden"
Article Synopsis
- Oncogene amplification on extrachromosomal DNA (ecDNA) is linked to treatment resistance and poorer survival in cancer patients, particularly those with glioblastoma, contributing to genetic diversity in tumors.* ! -
- The study used a new computational model called 'SPECIES' to analyze tumor samples from 94 glioblastoma patients, providing insights into how ecDNA evolves in time and space within tumors.* ! -
- Findings reveal significant patterns in ecDNA copy number variation, indicating strong positive selection on certain oncogenes and suggesting that ecDNA accumulation occurs before major cell growth phases.* !
Mutations in the epidermal growth factor receptor (EGFR) are common in non-small cell lung cancer (NSCLC), particularly in never-smoker patients. However, these mutations are not always carcinogenic, and have recently been reported in histologically normal lung tissue from patients with and without lung cancer. To investigate the outcome of EGFR mutation in healthy lung stem cells, we grow murine alveolar type II organoids monoclonally in a three-dimensional Matrigel.
View Article and Find Full Text PDFEnvironmental carcinogens increase cancer incidence via both mutagenic and non-mutagenic mechanisms. There are over 500 known or suspected carcinogens classified by the International Agency for Research on Cancer. Sequencing of both cancerous and histologically non-cancerous tissue has been instrumental in improving our understanding of how environmental carcinogens cause cancer.
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- The study investigates the role of the APOBEC3B (A3B) enzyme in lung cancer, specifically in non-small-cell lung cancer (NSCLC) driven by the epidermal growth factor receptor (EGFR).
- It was found that A3B expression can limit tumor growth in mouse models but is linked to resistance against EGFR-targeted therapies in tumors.
- The research suggests that A3B could be targeted to improve the effectiveness of cancer treatments, as its upregulation was observed in both preclinical models and patients undergoing EGFR-targeted therapy.
The discovery of frequent 8p11-p12 amplifications in squamous cell lung cancer (SQLC) has fueled hopes that FGFR1, located inside this amplicon, might be a therapeutic target. In a clinical trial, only 11% of patients with 8p11 amplification (detected by FISH) responded to FGFR kinase inhibitor treatment. To understand the mechanism of FGFR1 dependency, we performed deep genomic characterization of 52 SQLCs with 8p11-p12 amplification, including 10 tumors obtained from patients who had been treated with FGFR inhibitors.
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