Sarah Parackal
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Research Interests
Sarah Parackal has a total of 119 co-authors. Here are the top co-authors by number of shared publications:
- Jason E. Cain
Centre for Cancer Research, Hudson Institute of Medical Research, Clayton, VIC 3168, Australia
18 shared publications - Abdul Mannan
Cancer Signalling Research Group, School of Biomedical Sciences and Pharmacy, College of Health, Medicine and Wellbeing, University of Newcastle, Callaghan, New South Wales, Australia
17 shared publications - Brett Nixon
University of Newcastle
17 shared publications - David A. Skerrett-Byrne
Centre for Reproductive Science, College of Engineering, Science and Environment, The University of Newcastle, Callaghan, NSW, 2308, Australia
17 shared publications - David D. Eisenstat
Stem Cell Medicine, Murdoch Children’s Research Institute
17 shared publications - Dilana E. Staudt
Cancer Signalling Research Group, School of Biomedical Sciences and Pharmacy, College of Health, Medicine and Wellbeing, University of Newcastle, Callaghan, New South Wales, Australia
17 shared publications
Latest Publications
- Open Access
- 24 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Data from ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma
All Supplementary Figures and their captions.
- 24 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data from ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma
All Supplementary Figures and their captions.
- Open Access
- 24 November 2025
- Published by American Association for Cancer Research (AACR)
Supplementary Data from ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma
- 24 November 2025
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data from ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma
- Open Access
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Data from ONC201 in combination with paxalisib for the treatment of H3K27-altered diffuse midline glioma
Supplementary Data from ONC201 in combination with paxalisib for the treatment of H3K27-altered diffuse midline glioma
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data from ONC201 in combination with paxalisib for the treatment of H3K27-altered diffuse midline glioma
Supplementary Data from ONC201 in combination with paxalisib for the treatment of H3K27-altered diffuse midline glioma
- Open Access
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Data from ONC201 in combination with paxalisib for the treatment of H3K27-altered diffuse midline glioma
All Supplementary Figures and their captions.
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data from ONC201 in combination with paxalisib for the treatment of H3K27-altered diffuse midline glioma
All Supplementary Figures and their captions.
- Open Access
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Data from ONC201 in combination with paxalisib for the treatment of H3K27-altered diffuse midline glioma
All Supplementary Figures and their captions.
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data from ONC201 in combination with paxalisib for the treatment of H3K27-altered diffuse midline glioma
All Supplementary Figures and their captions.
- Open Access
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Supplementary Data from ONC201 in combination with paxalisib for the treatment of H3K27-altered diffuse midline glioma
Supplementary Data from ONC201 in combination with paxalisib for the treatment of H3K27-altered diffuse midline glioma
- 16 September 2024
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data from ONC201 in combination with paxalisib for the treatment of H3K27-altered diffuse midline glioma
Supplementary Data from ONC201 in combination with paxalisib for the treatment of H3K27-altered diffuse midline glioma
- Top Cited PapersOpen Access
- 16 January 2024
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 134 (6)
PI3K/mTOR is a therapeutically targetable genetic dependency in diffuse intrinsic pontine glioma
Diffuse midline glioma (DMG), including tumors diagnosed in the brainstem (diffuse intrinsic pontine glioma; DIPG), are uniformly fatal brain tumors that lack effective treatment. Analysis of CRISPR/Cas9 loss-of-function gene deletion screens identified PIK3CA and MTOR as targetable molecular dependencies across patient derived models of DIPG, highlighting the therapeutic potential of the blood-brain barrier–penetrant PI3K/Akt/mTOR inhibitor, paxalisib. At the human-equivalent maximum tolerated dose, mice treated with paxalisib experienced systemic glucose feedback and increased insulin levels commensurate with patients using PI3K inhibitors. To exploit genetic dependence and overcome resistance while maintaining compliance and therapeutic benefit, we combined paxalisib with the antihyperglycemic drug metformin. Metformin restored glucose homeostasis and decreased phosphorylation of the insulin receptor in vivo, a common mechanism of PI3K-inhibitor resistance, extending survival of orthotopic models. DIPG models treated with paxalisib increased calcium-activated PKC signaling. The brain penetrant PKC inhibitor enzastaurin, in combination with paxalisib, synergistically extended the survival of multiple orthotopic patient-derived and immunocompetent syngeneic allograft models; benefits potentiated in combination with metformin and standard-of-care radiotherapy. Therapeutic adaptation was assessed using spatial transcriptomics and ATAC-Seq, identifying changes in myelination and tumor immune microenvironment crosstalk. Collectively, this study has identified what we believe to be a clinically relevant DIPG therapeutic combinational strategy.
- 16 January 2024
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 134 (6)
Top Cited PapersOpen AccessPI3K/mTOR is a therapeutically targetable genetic dependency in diffuse intrinsic pontine glioma
Diffuse midline glioma (DMG), including tumors diagnosed in the brainstem (diffuse intrinsic pontine glioma; DIPG), are uniformly fatal brain tumors that lack effective treatment. Analysis of CRISPR/Cas9 loss-of-function gene deletion screens identified PIK3CA and MTOR as targetable molecular dependencies across patient derived models of DIPG, highlighting the therapeutic potential of the blood-brain barrier–penetrant PI3K/Akt/mTOR inhibitor, paxalisib. At the human-equivalent maximum tolerated dose, mice treated with paxalisib experienced systemic glucose feedback and increased insulin levels commensurate with patients using PI3K inhibitors. To exploit genetic dependence and overcome resistance while maintaining compliance and therapeutic benefit, we combined paxalisib with the antihyperglycemic drug metformin. Metformin restored glucose homeostasis and decreased phosphorylation of the insulin receptor in vivo, a common mechanism of PI3K-inhibitor resistance, extending survival of orthotopic models. DIPG models treated with paxalisib increased calcium-activated PKC signaling. The brain penetrant PKC inhibitor enzastaurin, in combination with paxalisib, synergistically extended the survival of multiple orthotopic patient-derived and immunocompetent syngeneic allograft models; benefits potentiated in combination with metformin and standard-of-care radiotherapy. Therapeutic adaptation was assessed using spatial transcriptomics and ATAC-Seq, identifying changes in myelination and tumor immune microenvironment crosstalk. Collectively, this study has identified what we believe to be a clinically relevant DIPG therapeutic combinational strategy.
- Open Access
- 14 July 2023
- Published by American Association for Cancer Research (AACR)
Supplementary Data from ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma
All Supplementary Figures and their captions.
- 14 July 2023
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data from ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma
All Supplementary Figures and their captions.
- Open Access
- 14 July 2023
- Published by American Association for Cancer Research (AACR)
Supplementary Data from ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma
Supplementary Data from ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma
- 14 July 2023
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data from ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma
Supplementary Data from ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma
- Open Access
- 14 July 2023
- Published by American Association for Cancer Research (AACR)
Supplementary Data from ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma
All Supplementary Figures and their captions.
- 14 July 2023
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Data from ONC201 in Combination with Paxalisib for the Treatment of H3K27-Altered Diffuse Midline Glioma
All Supplementary Figures and their captions.