Andjelija Zivanovic Bujak
A5052828461- Advanced Breast Cancer Therapies
- HER2/EGFR in Cancer Research
- Cancer Treatment and Pharmacology
- PI3K/AKT/mTOR signaling in cancer
- Cancer Genomics and Diagnostics
- BRCA gene mutations in cancer
- Ovarian cancer diagnosis and treatment
- Cancer Cells and Metastasis
- Radiopharmaceutical Chemistry and Applications
- Cancer therapeutics and mechanisms
- Click Chemistry and Applications
- Lung Cancer Treatments and Mutations
- Cancer Immunotherapy and Biomarkers
- Chronic Lymphocytic Leukemia Research
- PARP inhibition in cancer therapy
- Genetic factors in colorectal cancer
Peter MacCallum Cancer Centre
2018-2022
The University of Melbourne
2018-2020
Abstract Venetoclax, a potent and selective BCL2 inhibitor, synergizes with endocrine therapy in preclinical models of ER-positive breast cancer. Using phase Ib 3 + dose-escalation expansion study design, 33 patients ER BCL2-positive metastatic disease (mean prior regimens, 2; range, 0–8) were treated daily tamoxifen (20 mg) venetoclax (200–800 mg). Apart from uncomplicated “on-target” lymphopenia, no dose-limiting toxicities or high-grade adverse events observed the escalation (15...
Abstract There is limited knowledge on the benefit of α-subunit–specific PI3K inhibitor alpelisib in later lines therapy for advanced estrogen receptor–positive (ER+) HER2− and triple-negative breast cancer (TNBC). We conducted a phase II multicohort study monotherapy patients with pathway mutant ER+HER2− TNBC. In intention-to-treat ER+ cohort, overall response rate was 30% clinical 36%. A decline circulating tumor DNA (ctDNA) levels from baseline to week 8 while significantly associated...
Background Metastatic breast cancer (mBC) is a heterogenous disease with increasing availability of targeted therapies as well emerging genomic markers therapeutic resistance, necessitating timely and accurate molecular characterization disease. As minimally invasive test, analysis circulating tumour DNA (ctDNA) positioned for real-time profiling to guide treatment decisions. Here, we report the results prospective testing program established assess feasibility ctDNA clinical management mBC...
1055 Background: Mutations of genes involved in the PI3K signalling pathway occur frequently BC. We performed a phase II study BYL719, selective PI3Kα inhibitor, BC to evaluate its efficacy and identify biomarkers that correlate with tumor response. Methods: Eligible patients had advanced ER+/HER2- documented genetic alteration detected either or plasma. Patients received BYL719 350mg orally daily. The primary end point was RECIST objective response rate (ORR). Secondary endpoints were...
<p>Supplementary Tables S1-5</p>
<p>Supplementary Tables S1-5</p>
<div>Abstract<p>There is limited knowledge on the benefit of α-subunit–specific PI3K inhibitor alpelisib in later lines therapy for advanced estrogen receptor–positive (ER<sup>+</sup>) HER2<sup>−</sup> and triple-negative breast cancer (TNBC). We conducted a phase II multicohort study monotherapy patients with pathway mutant ER<sup>+</sup>HER2<sup>−</sup> TNBC. In intention-to-treat ER<sup>+</sup> cohort, overall...
<div>Abstract<p>There is limited knowledge on the benefit of α-subunit–specific PI3K inhibitor alpelisib in later lines therapy for advanced estrogen receptor–positive (ER<sup>+</sup>) HER2<sup>−</sup> and triple-negative breast cancer (TNBC). We conducted a phase II multicohort study monotherapy patients with pathway mutant ER<sup>+</sup>HER2<sup>−</sup> TNBC. In intention-to-treat ER<sup>+</sup> cohort, overall...
Supplementary Data from Alpelisib Monotherapy for PI3K-Altered, Pretreated Advanced Breast Cancer: A Phase II Study
Supplementary Data from Alpelisib Monotherapy for PI3K-Altered, Pretreated Advanced Breast Cancer: A Phase II Study
Supplementary Figure from Alpelisib Monotherapy for PI3K-Altered, Pretreated Advanced Breast Cancer: A Phase II Study
Supplementary Figure from Alpelisib Monotherapy for PI3K-Altered, Pretreated Advanced Breast Cancer: A Phase II Study
<p>Supplementary Table S8</p>
<p>Supplementary Methods</p>
<p>Supplementary Figures</p>
<p>Supplementary Table S6</p>
<p>Supplementary Table S9</p>
<p>Supplementary Table S7</p>
<p>Supplementary Table S8</p>
<p>Supplementary Table S7</p>
<p>Supplementary Methods</p>
<p>Supplementary Figures</p>
<p>Supplementary Table S6</p>