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YC

Yih-Chih Chan

University of Melbourne

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Mark A. Dawson

Peter MacCallum Cancer Centre

Laura MacPherson

Peter MacCallum Cancer Centre

Andrew A. Guirguis

Olivia Newton-John Cancer Wellness & Research Centre

Ali Motazedian

Murdoch Children's Research Institute

Brian Liddicoat

University of Melbourne

Dane Vassiliadis

Peter MacCallum Cancer Centre

Kathy Knezevic

Peter MacCallum Cancer Centre

Andrea Gillespie

Peter MacCallum Cancer Centre

Elanor N. Wainwright

Peter MacCallum Cancer Centre

Benjamin J. Blyth

University of Melbourne

Cooperative Institutions

University of Melbourne

Peter MacCallum Cancer Centre

Walter and Eliza Hall Institute of Medical Research

Monash University

The Royal Melbourne Hospital

University of Cambridge

Australian Regenerative Medicine Institute

Harvard University

Victorian Comprehensive Cancer Centre

Commonwealth Scientific and Industrial Research Organisation

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Figure S5 from Inhibition of METTL3 results in a cell-intrinsic interferon response that enhances anti-tumour immunity

Andrew A. Guirguis Yaara Ofir-Rosenfeld Kathy Knezevic Wesley Blackaby David Hardick

<p>Co-culture assays + human PBMC data</p>

10.1158/2159-8290.27026033.v1

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Figure S7 from Inhibition of METTL3 results in a cell-intrinsic interferon response that enhances anti-tumour immunity

Andrew A. Guirguis Yaara Ofir-Rosenfeld Kathy Knezevic Wesley Blackaby David Hardick

<p>A20 lymphoma model data</p>

Cell mediated immunity

10.1158/2159-8290.27026027

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Figure S3 from Inhibition of METTL3 results in a cell-intrinsic interferon response that enhances anti-tumour immunity

Andrew A. Guirguis Yaara Ofir-Rosenfeld Kathy Knezevic Wesley Blackaby David Hardick

<p>METTL3 KD in B16 cell line</p>

10.1158/2159-8290.27026039.v1

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Identification of resistance mechanisms to small-molecule inhibition of TEAD-regulated transcription

EMBO Reports (2024)

Aishwarya Kulkarni Varshini Mohan Tracy T. Tang Leonard Post Yih-Chih Chan

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10.1038/s44319-024-00217-3

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Supplementary Figure from Pharmacologic Reduction of Mitochondrial Iron Triggers a Noncanonical BAX/BAK-Dependent Cell Death

Sylvain Garciaz Andrew A. Guirguis Sebastian Müller Fiona C. Brown Yih-Chih Chan

Supplementary Figure from Pharmacologic Reduction of Mitochondrial Iron Triggers a Noncanonical BAX/BAK-Dependent Cell Death

10.1158/2159-8290.22540933

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Supplementary table from Pharmacologic Reduction of Mitochondrial Iron Triggers a Noncanonical BAX/BAK-Dependent Cell Death

Sylvain Garciaz Andrew A. Guirguis Sebastian Müller Fiona C. Brown Yih-Chih Chan

Supplementary table from Pharmacologic Reduction of Mitochondrial Iron Triggers a Noncanonical BAX/BAK-Dependent Cell Death

Table (database)

10.1158/2159-8290.22540915.v1

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Table S1 from Inhibition of METTL3 Results in a Cell-Intrinsic Interferon Response That Enhances Antitumor Immunity

Andrew A. Guirguis Yaara Ofir-Rosenfeld Kathy Knezevic Wesley Blackaby David Hardick

<p>STM3006 properties</p>

Table (database)

10.1158/2159-8290.24249105.v1

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Tables S4-S5 from Inhibition of METTL3 Results in a Cell-Intrinsic Interferon Response That Enhances Antitumor Immunity

Andrew A. Guirguis Yaara Ofir-Rosenfeld Kathy Knezevic Wesley Blackaby David Hardick

<p>Primer + shRNA + Taqman probe sequences</p>

TaqMan

Primer (cosmetics)

10.1158/2159-8290.24249093

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Non-genetic determinants of malignant clonal fitness at single-cell resolution

Katie Fennell Dane Vassiliadis Enid Y.N. Lam Luciano G. Martelotto Jesse J. Balic

clone (Java method)

10.1038/s41586-021-04206-7

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An Evolutionarily Conserved Function of Polycomb Silences the MHC Class I Antigen Presentation Pathway and Enables Immune Evasion in Cancer

Cancer Cell (2019)

Marian L. Burr Christina E. Sparbier Kah Lok Chan Yih-Chih Chan Ariena Kersbergen

Loss of MHC class I (MHC-I) antigen presentation in cancer cells can elicit immunotherapy resistance. A genome-wide CRISPR/Cas9 screen identified an evolutionarily conserved function of polycomb repressive complex 2 (PRC2) that mediates coordinated transcriptional silencing of the MHC-I antigen processing pathway (MHC-I APP), promoting evasion of T cell-mediated immunity. MHC-I APP gene promoters in MHC-I low cancers harbor bivalent activating H3K4me3 and repressive H3K27me3 histone modifications, silencing basal MHC-I expression and restricting cytokine-induced upregulation. Bivalent chromatin at MHC-I APP genes is a normal developmental process active in embryonic stem cells and maintained during neural progenitor differentiation. This physiological MHC-I silencing highlights a conserved mechanism by which cancers arising from these primitive tissues exploit PRC2 activity to enable immune evasion.

PRC2

Bivalent chromatin

Antigen processing

10.1016/j.ccell.2019.08.008

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