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Michelle Melino
QIMR Berghofer Medical Research Institute, Queensland University of Technology, The University of Queensland
Research areas: Biochemistry, Genetics and Molecular Biology · Molecular Biology · PI3K/AKT/mTOR signaling in cancer · Liver physiology and pathology · Breast Cancer Treatment Studies
0000-0001-6962-9016
Employment
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QIMR Berghofer Medical Research Institute Post-doctoral research fellow2020 - Present
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Queensland University of Technology Post-doctoral research fellow2018 - 2020
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QIMR Berghofer Medical Research Institute Post-doctoral research fellow2014 - 2017
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University of Queensland Post-doctoral research fellow2009 - 2014
Education
Education history is unavailable.
Projects & Funding
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GESA Project Grant Gastroenterological Society of Australia2019 - 2020
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Queensland University of Technology Innovation Grant Queensland University of Technology2018 - 2019
Publications (26)
- Data from Depleting the Action of EZH2 through PI3K–mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer Save
- Depleting the Action of EZH2 through PI3K–mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer Save
- Supplementary Figure 1 from Depleting the Action of EZH2 through PI3K–mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer Save
- Supplementary Figure 2 from Depleting the Action of EZH2 through PI3K–mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer Save
- Supplementary Figure 3 from Depleting the Action of EZH2 through PI3K–mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer Save
- Supplementary Figure 4 from Depleting the Action of EZH2 through PI3K–mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer Save
- Supplementary Figure 5 from Depleting the Action of EZH2 through PI3K–mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer Save
- Supplementary Figure 6 from Depleting the Action of EZH2 through PI3K–mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer Save
- Supplementary Figure 7 from Depleting the Action of EZH2 through PI3K–mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer Save
- Supplementary Methods from Depleting the Action of EZH2 through PI3K–mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer Save
- Supplementary Results from Depleting the Action of EZH2 through PI3K–mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer Save
- Supplementary Table S1 from Depleting the Action of EZH2 through PI3K–mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer Save
- Supplementary Table S2 from Depleting the Action of EZH2 through PI3K–mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer Save
- Supplementary Table S3 from Depleting the Action of EZH2 through PI3K–mTOR Inhibition to Overcome Metastasis and Immunotherapy Resistance in Triple-Negative Breast Cancer Save
- A Liver Capsular Network of Monocyte-Derived Macrophages Restricts Hepatic Dissemination of Intraperitoneal Bacteria by Neutrophil Recruitment. Save
- Autophagy-dependent regulatory T cells are critical for the control of graft-versus-host disease. Save
- Spatiotemporal Characterization of the Cellular and Molecular Contributors to Liver Fibrosis in a Murine Hepatotoxic-Injury Model. Save
- Deletion of Wntless in myeloid cells exacerbates liver fibrosis and the ductular reaction in chronic liver injury. Save
- Ascites bacterial burden and immune cell profile are associated with poor clinical outcomes in the absence of overt infection. Save
- ELF score ≥9.8 indicates advanced hepatic fibrosis and is influenced by age, steatosis and histological activity. Save