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Andrew Wakeham

As seen in: Nature, Cell Press
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Articles by Andrew Wakeham

Identification of broadly tumour-reactive γδ TCRs from multiple myeloma

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By Michael St. Paul, Liam D Hendrikse, Fan Ying, Bryan Snow, Ping Luo, Simone Helke, Logan Smith, Arwa Hilal, Dor D Abelman, Matthew J Gold, Chantal Tobin, Scott Lien, Yi Liu, Wenjing Zhou, Xin Zhang, Dat Nguyen, Stephanie Pedersen Verified, Mary Saunders, Thorsten Berger, Andrew Wakeham, David Scott, Dalam Ly, Cecilia Bonolo de Campos, Guanghao Liang, Chunxing Zheng, Wesley Wilson, Esther Masih-Khan, Darrell White, Arleigh McCurdy, Martha Louzada, Rami Kotb, Michael Chu, Stephen Parkin, Donna E Reece, Engin Gul, Rodger E. Tiedemann, Trevor J. Pugh, Naoto Hirano, Pamela S Ohashi, A. Stewart, Suzanne Trudel, Tak W. Mak, Nisha Ramamurthy, Hayley Nault, Ellen N. Wei, Oluwatobi Agbede, Jenna Eagles
| Nature Verified
Abstract γδ T cells are becoming increasingly appreciated for their antitumour capacity and role in mediating responses to immune checkpoint blockade1,2,3. Unlike classical αβ T cells, the degree to which γδ T cells rely on their T cell receptors (TCRs) to induce antitumour responses remains unclear.
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Lymphocyte-derived cholinergic circuits modulate germinal center output and B cell activation - Nature Immunology

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By Duygu Nechanitzky, Logan Smith, Robert Nechanitzky, Soode Moghadas Jafari, Jillian Haight, Christophe Bontoux, Parameswaran Ramachandran, Matthew J Gold, Andrew Wakeham, Mary Saunders, Justin F. Deniset, Tak W. Mak
| Nature Verified
Abstract Germinal centers (GCs) are specialized lymphoid structures in which activated B cells undergo clonal selection and B cell receptor (BCR) somatic hypermutation to generate high-affinity antibodies. Previous work has shown that T cells expressing choline acetyltransferase (ChAT), the enzyme that synthesizes acetylcholine (ACh), are linked to the production of high-affinity antibodies in the GC response.
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B cell-derived acetylcholine promotes liver regeneration by regulating Kupffer cell and hepatic CD8+ T cell function

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By Nastaran Fazel Modares, Liam D Hendrikse, Logan Smith, Michael St. Paul, Jillian Haight, Ping Luo, Shaofeng Liu, Jérôme Fortin, Andrew Wakeham, Chunxing Zheng, Robert Flick, Frances K. Tong, Soode Moghadas Jafari, Mackenzie Buckland, Jennifer Silve
| Cell Press Verified
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The PTEN and ATM axis controls the G1/S cell cycle checkpoint and tumorigenesis in HER2-positive breast cancer - Cell Death & Differentiation

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By Christian Bassi, Jérôme Fortin, Bryan Snow, Andrew Wakeham
| Nature Verified
Abstract The tumor suppressor PTEN is disrupted in a large proportion of cancers, including in HER2-positive breast cancer, where its loss is associated with resistance to therapy. Upon genotoxic stress, ataxia telangiectasia mutated (ATM) is activated and phosphorylates PTEN on residue 398. To elucidate the physiological role of this molecular event, we generated and analyzed knock-in mice expressing a mutant form of PTEN that cannot be phosphorylated by ATM (PTEN-398A).
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