Bruedigam Group - AML Therapeutics
Research goal | Research overview | Our people | Projects | Funding | Publications
Research goal
The Bruedigam Group investigates fundamental biological mechanisms that determine how cells respond to metabolic and genomic stress. Our research focuses on how lipid metabolism and genome structure regulate susceptibility to ferroptosis, a form of regulated cell death that plays important roles in cancer and ageing. By combining functional genomics, multi-omics profiling and in vivo experimental models of normal and malignant blood formation, we aim to uncover biological principles governing cellular stress adaptation and vulnerability.
Understanding these processes provides new insights into the mechanisms that drive acute myeloid leukaemia and other ageing-related diseases, and may ultimately reveal new biological vulnerabilities that can be therapeutically exploited.
Research themes
Ferroptosis and regulated cell death:
We study the molecular mechanisms that control ferroptosis and other stress-induced cell death pathways, with a particular focus on how metabolic and redox processes regulate cellular vulnerability.
Lipid metabolism and oxidative stress:
Our work investigates how lipid metabolism and redox homeostasis influence cellular responses to metabolic stress in cancer and ageing.
Genome structure and G-quadruplex biology:
We explore how DNA and RNA secondary structures such as G-quadruplexes influence genome regulation, cellular stress responses and ferroptotic susceptibility.
Experimental systems
Our laboratory integrates molecular and genomic technologies with in vivo experimental models of normal and malignant blood formation. We combine functional genomics, multi-omics profiling and advanced molecular approaches at single cell level to study how metabolic and genomic stress pathways shape cellular survival and disease evolution.
Training environment
The Bruedigam Group provides an interdisciplinary training environment for students and researchers interested in cancer biology, metabolism, genome regulation and cell death pathways. We are committed to mentoring the next generation of scientists and fostering curiosity-driven research into fundamental biological mechanisms.
For student research project details, please use the Supervisor Connect link above or contact Dr Claudia Bruedigam at Claudia.Bruedigam@monash.edu
Our people
Group Leader
Projects and Opportunities
- Targeting Lipid Droplet Homeostasis to Develop Therapies for Acute Myeloid Leukaemia
Funding
- NHMRC Ideas Grant (2024-2027)
- The NB Gantner Family Trust (2025-)
Publications
Selected publications
Bruedigam C, Porter AH, Song A, Vroeg In de Wei G, Stoll T, Straube J, Cooper L, Cheng G, Kahl VFS, Sobinoff AP, Ling VY, Jebaraj BMC, Janardhanan Y, Haldar R, Bray LJ, Bullinger L, Heidel FH, Kennedy GA, Hill MM, Pickett HA, Abdel-Wahab O, Hartel G, Lane SW. Imetelstat-mediated alterations in fatty acid metabolism to induce ferroptosis as a therapeutic strategy for acute myeloid leukemia. Nat Cancer. 2024 Jan;5(1):47-65. doi: 10.1038/s43018-023-00653-5. Epub 2023 Oct 30. PMID: 37904045; PMCID: PMC10824665.
Waksal JA, Bruedigam C, Komrokji RS, Jamieson CHM, Mascarenhas JO. Telomerase-targeted therapies in myeloid malignancies. Blood Adv. 2023 Aug 22;7(16):4302-4314. doi: 10.1182/bloodadvances.2023009903. PMID: 37216228; PMCID: PMC10424149.
Austin RJ, Straube J, Halder R, Janardhanan Y, Bruedigam C, Witkowski M, Cooper L, Porter A, Braun M, Souza-Fonseca-Guimaraes F, Minnie SA, Cooper E, Jacquelin S, Song A, Bald T, Nakamura K, Hill GR, Aifantis I, Lane SW, Bywater MJ. Oncogenic drivers dictate immune control of acute myeloid leukemia. Nat Commun. 2023 Apr 14;14(1):2155. doi: 10.1038/s41467-023-37592-9. PMID: 37059710; PMCID: PMC10104832.
Salmon JM, Todorovski I, Stanley KL, Bruedigam C, Kearney CJ, Martelotto LG, Rossello F, Semple T, Arnau GM, Zethoven M, Bots M, Bjelosevic S, Cluse LA, Fraser PJ, Litalien V, Vidacs E, McArthur K, Matthews AY, Gressier E, de Weerd NA, Lichte J, Kelly MJ, Hogg SJ, Hertzog PJ, Kats LM, Vervoort SJ, De Carvalho DD, Scheu S, Bedoui S, Kile BT, Lane SW, Perkins AC, Wei AH, Dominguez PM, Johnstone RW. Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML. Cancer Discov. 2022 Jun 2;12(6):1560-1579. doi: 10.1158/2159-8290.CD-20-1145. PMID: 35311997; PMCID: PMC9355625.
Thijssen R, Diepstraten ST, Moujalled D, Chew E, Flensburg C, Shi MX, Dengler MA, Litalien V, MacRaild S, Chen M, Anstee NS, Reljić B, Gabriel SS, Djajawi TM, Riffkin CD, Aubrey BJ, Chang C, Tai L, Xu Z, Morley T, Pomilio G, Bruedigam C, Kallies A, Stroud DA, Bajel A, Kluck RM, Lane SW, Schoumacher M, Banquet S, Majewski IJ, Strasser A, Roberts AW, Huang DCS, Brown FC, Kelly GL, Wei AH. Intact TP-53 function is essential for sustaining durable responses to BH3-mimetic drugs in leukemias. Blood. 2021 May 20;137(20):2721-2735. doi: 10.1182/blood.2020010167. PMID: 33824975; PMCID: PMC8138548.
Porter AH, Leveque-El Mouttie L, Vu T, Bruedigam C, Sutton J, Jacquelin S, Hill GR, MacDonald KPA, Lane SW. Acute myeloid leukemia stem cell function is preserved in the absence of autophagy. Haematologica. 2017 Sep;102(9):e344-e347. doi: 10.3324/haematol.2017.166389. Epub 2017 May 26. PMID: 28550181; PMCID: PMC5685233.
Bruedigam C, Lane SW. Telomerase in hematologic malignancies. Curr Opin Hematol. 2016 Jul;23(4):346-53. doi: 10.1097/MOH.0000000000000252. PMID: 27213497.
Leveque-El Mouttie L, Vu T, Lineburg KE, Kuns RD, Bagger FO, Teal BE, Lor M, Boyle GM, Bruedigam C, Mintern JD, Hill GR, MacDonald KP, Lane SW. Autophagy is required for stem cell mobilization by G-CSF. Blood. 2015 May 7;125(19):2933-6. doi: 10.1182/blood-2014-03-562660. Epub 2015 Mar 18. PMID: 25788702.
Bruedigam C, Bagger FO, Heidel FH, Paine Kuhn C, Guignes S, Song A, Austin R, Vu T, Lee E, Riyat S, Moore AS, Lock RB, Bullinger L, Hill GR, Armstrong SA, Williams DA, Lane SW. Telomerase inhibition effectively targets mouse and human AML stem cells and delays relapse following chemotherapy. Cell Stem Cell. 2014 Dec 4;15(6):775-90. doi: 10.1016/j.stem.2014.11.010. PMID: 25479751; PMCID: PMC4317339.
Mullally A, Bruedigam C, Poveromo L, Heidel FH, Purdon A, Vu T, Austin R, Heckl D, Breyfogle LJ, Kuhn CP, Kalaitzidis D, Armstrong SA, Williams DA, Hill GR, Ebert BL, Lane SW. Depletion of Jak2V617F myeloproliferative neoplasm-propagating stem cells by interferon-α in a murine model of polycythemia vera. Blood. 2013 May 2;121(18):3692-702. doi: 10.1182/blood-2012-05-432989. Epub 2013 Mar 13. PMID: 23487027; PMCID: PMC3643767.
