Publications by authors named "M Dietzen"
Article Synopsis
- - The study introduces the SPRINTER algorithm, which analyzes single-cell DNA sequencing to identify and classify the proliferation rates of different cancer cell clones within tumors, shedding light on the variability of cell growth among these clones.
- - Applying SPRINTER to nearly 15,000 non-small cell lung cancer cells showed significant differences in clone proliferation, which was corroborated by various imaging techniques and indicated that more proliferative clones also had a higher likelihood of metastasis and altered genetic replication patterns.
- - The algorithm's effectiveness was further demonstrated in breast and ovarian cancer datasets, where it uncovered higher proliferation rates and genetic variations in specific, more rapidly growing cell clones.
- Update articles supplement or update information found in full-length articles previously published in . These updates, written by at least one author of the previous article, provide a brief synopsis that emphasizes important new information such as technological advances, revised imaging protocols, new clinical guidelines involving imaging, or updated classification schemes.
View Article and Find Full Text PDFDuring each cell cycle, the process of DNA replication timing is tightly regulated to ensure the accurate duplication of the genome. The extent and significance of alterations in this process during malignant transformation have not been extensively explored. Here, we assess the impact of altered replication timing (ART) on cancer evolution by analysing replication-timing sequencing of cancer and normal cell lines and 952 whole-genome sequenced lung and breast tumours.
View Article and Find Full Text PDFArticle Synopsis
- 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.