Author

E. Lieschke

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cancer Biology· 5

Signature Assays, Organisms & Methods

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Research Focus:drug response / drug discovery· 4 Organism:human· 4 Research Focus:cancer & tumor microenvironment· 3 Assay:DNA methylation· 3 Approach:experimental assay· 3 Approach:genetic perturbation / CRISPR· 3 Research Focus:cell type annotation· 2 Assay:bulk RNA-seq· 1

Frequent Co-Authors

C. L. Scott· 3 shared O. Kondrashova· 3 shared A. DeFazio· 2 shared C. Vandenberg· 2 shared D. Bowtell· 2 shared M. J. Wakefield· 2 shared N. Traficante· 2 shared O. McNally· 2 shared

Activity by Year

2019-2020 · peak 4/yr

Co-Author Collaboration Network

10 top collaborators · 40 mutual co-author links

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3 shared papersCancer Biology

C. L. Scott

Mutual co-authors in cluster

Author profile →

5 papers

Recent·Most cited

Acquired RAD51C promoter methylation loss causes PARP inhibitor resistance in high grade serous ovarian carcinoma

K. Nesic, O. Kondrashova, R. M. Hurley, C. McGehee, C. J. Vandenberg, G.-Y. Ho, E. Lieschke, G. Dall, N. Bound, K. Shield-Artin, M. R. Radke, A. Musafer, Z. Qing Chai, M. R. Eftekhariyan Ghamsari, M. I. Harrell, , C. L. Scott

This study shows that loss of RAD51C promoter methylation leads to PARP inhibitor resistance in high-grade serous ovarian carcinoma, independent of BRCA1 methylation status.

bioRxiv · Dec 10, 2020Cancer Biology

Ovarian carcinosarcoma genomics and pre-clinical models highlight the N-MYC pathway as a key driver and susceptibility to EMT-targeting therapy

G. Y. Ho, E. Kyran, J. Bedo, M. Wakefield, D. Ennis, H. Mirza, S. Cooke, E. Lieschke, C. Vandenberg, O. Kondrashova, R. Upstill-Goddard, U.-M. Bailey, S. Biankin, P. Roxburgh, R. Glasspool, , H. Barker

This study identifies N-MYC pathway activation and susceptibility to EMT-targeting therapy in ovarian carcinosarcoma using genomic and pre-clinical models.

bioRxiv · Nov 24, 2020 · PreprintCancer Biology

CHK2 inhibition provides a strategy to suppress hematological toxicity from PARP inhibitors.

Z. Xu, C. Vandenberg, E. Lieschke, C. L. Scott, I. J. Majewski

This study identifies CHK2 inhibition as a strategy to reduce hematological toxicity from PARP inhibitors by targeting the p53 pathway in blood cells.

bioRxiv · Jul 28, 2020Cancer Biology

Loss of mutant TP53 does not impair the sustained proliferation, survival ormetastasis of diverse cancer cells

Z. Wang, F. Vailllant, C. Chang, C. Riffkin, E. Lieschke, S. Diepstraten, D. Huang, J. E. Visvader, M. J. Herold, G. Kelly, A. Strasser

This study shows that removing mutant TP53 does not affect cancer cell survival, proliferation, or metastasis, suggesting GOF effects are not universally required for malignant growth.

bioRxiv · Mar 30, 2020 · PreprintCancer Biology

Inhibition of RNA Polymerase I Transcription Activates Targeted DNA Damage Response and Enhances the Efficacy of PARP Inhibitors in High-Grade Serous Ovarian Cancer

E. Sanij, K. M. Hannan, S. Yan, X. Xuan, J. E. Ahern, K. T. Chan, J. Son, O. Kondrashova, E. Lieschke, M. J. Wakefield, A. S. Trigos, D. Frank, S. Ellis, C. Cullinane, J. Kang, , R. B. Pearson

This study shows CX-5461, an RNA polymerase I inhibitor, enhances PARP inhibitor efficacy in HR-deficient HGSOC by inducing replication stress and DNA damage, overcoming resistance mechanisms.

bioRxiv · Apr 29, 2019 · PreprintCancer Biology