Elizabeth Lieschke

发表

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

N. Traficante, A. deFazio, D. Bowtell, 2020, bioRxiv.

Review Discussion of some ‘knowns’ and some ‘unknowns’ about the tumour suppressor p 53

A. Strasser, G. Kelly, Elizabeth Lieschke, 2019 .

Phase 1 trial of olaparib and oral cyclophosphamide in BRCA breast cancer, recurrent BRCA ovarian cancer, non-BRCA triple-negative breast cancer, and non-BRCA ovarian cancer

C. Scott, P. Francis, M. Friedlander, 2019, British Journal of Cancer.

CX-5461 activates the DNA damage response and demonstrates therapeutic efficacy in high-grade serous ovarian cancer

E. Berns, K. Khanna, R. Pearson, 2020, Nature Communications.

Acquired RAD51C Promoter Methylation Loss Causes PARP Inhibitor Resistance in High-Grade Serous Ovarian Carcinoma

N. Traficante, A. deFazio, D. Bowtell, 2021, Cancer Research.

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

N. Traficante, A. deFazio, D. Bowtell, 2020, bioRxiv.

Methylation of all BRCA1 copies predicts response to the PARP inhibitor rucaparib in ovarian carcinoma

S. Fox, S. Lade, N. Traficante, 2018, Nature Communications.

Mutant TRP53 exerts a target gene-selective dominant-negative effect to drive tumor development

A. Strasser, G. Smyth, Yunshun Chen, 2018, Genes & development.

Discussion of some ‘knowns’ and some ‘unknowns’ about the tumour suppressor p53

A. Strasser, G. Kelly, Zi-lu Wang, 2018, Journal of molecular cell biology.

Methylation of all BRCA1 copies predicts response to the PARP inhibitor rucaparib in ovarian carcinoma

S. Fox, K. Byth, S. Lade, 2018, Nature Communications.

CX-5461 activates the DNA damage response and demonstrates therapeutic efficacy in high-grade serous ovarian cancer

E. Berns, C. Scott, K. Khanna, 2020, Nature Communications.

Flow cytometric single cell-based assay to simultaneously detect cell death, cell cycling, DNA content and cell senescence

A. Strasser, G. Kelly, Catherine Chang, 2022, Cell Death & Differentiation.

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

C. Scott, C. Vandenberg, I. Majewski, 2020, bioRxiv.

The anti-cancer agent APR-246 can activate several programmed cell death processes to kill malignant cells

O. Sieber, J. Visvader, A. Strasser, 2023, Cell Death & Differentiation.

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

J. Visvader, A. Strasser, F. Vaillant, 2020, bioRxiv.

CHK2 Inhibition Provides a Strategy to Suppress Hematologic Toxicity from PARP Inhibitors

C. Scott, C. Vandenberg, I. Majewski, 2021, Molecular Cancer Research.

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. Berns, C. Scott, K. Khanna, 2019, bioRxiv.

BRCA1 secondary splice-site mutations drive exon-skipping and PARP inhibitor resistance

N. Traficante, A. deFazio, J. Bedő, 2023, medRxiv.

Epithelial-to-Mesenchymal Transition Supports Ovarian Carcinosarcoma Tumorigenesis and Confers Sensitivity to Microtubule Targeting with Eribulin

N. Traficante, A. deFazio, D. Bowtell, 2022, Cancer research.