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Articles by Phil Cheng
Peripheral glia drive the initiation of cutaneous squamous cell carcinoma
Abstract Although tumor innervation is known to promote cancer progression, underlying mechanisms remain poorly understood and have mostly been linked to axonal signaling. Here, we identify peripheral glia as critical drivers of cutaneous squamous cell carcinoma (cSCC), the second most common skin cancer in humans.
Targeting ABL kinases overcomes melanoma immune evasion following resistance to MAPK inhibition
Abstract MAPK inhibitors (MAPKi) are important treatment options for some patients with metastatic melanoma; however, resistance inevitably develops in the vast majority of cases (>70%).
The Virtual Tissues foundation model resolves spatial proteomics across scales
Abstract Spatial proteomics technologies have transformed our understanding of complex tissue architecture in cancer but present unique challenges for computational analysis1. Each study uses a different marker panel and protocol, and most methods are tailored to single cohorts, which limits knowledge transfer and robust biomarker discovery.
NLRP1 inflammasome activation in skin equivalents reveals mechanistic insights into the roles of keratinocytes in psoriasis
Abstract The pro-inflammatory cytokines interleukin(IL)-1β and IL-36γ are key drivers of psoriasis, an inflammatory skin disease for which a causal therapy is not available. However, the mechanisms underlying regulation of these cytokines in psoriasis remain poorly understood. Generation of IL-1β activity is regulated by inflammasomes. We activated the NLRP1 inflammasome in human keratinocytes cultivated in three-dimensional skin equivalents.
Positioning and reversible suppression of CCR7+ dendritic cells in perivascular tumor niches shape cancer immunity
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Keywords cancer immunity dendritic cells immunotherapy cancer immunity cycle regulatory T cells chemokines Introduction The cancer immunity cycle comprises a series of rate-limiting events that collectively drive antitumor immune responses.1 Conventional dendritic cells (cDCs) are critical to this cycle, as their presence and function in different tissues determine T cell activation and effector responses.
By Beatrice Zitti, Florent Duval, Pratyaksha Wirapati, Mehdi Hicham, Yuxuan Xie, Juhyun Oh, Jan Hoelzl, Philippa Meiser, Marco Varrone, Hannah Peterson, Chiara Cianciaruso, Ruben Bill, Felix Bayerl, Evangelia Bolli, Anne-Gaëlle Goubet, Máté G. Kiss, Sheri McDowell, Phil Cheng, Julie Terzic, Nagham Alouche, David Tarussio, Stephanie Tissot, Paula Nunes-Hasler, Mari Mino-Kenudson, Michael Lanuti, William C. Faquin, Peter M. Sadow, Jean-Christophe Tille, Sana Intidhar Labidi-Galy, Christopher Garris, Stéphanie Hugues, Tatiana V. Petrova, Burkhard Ludewig, Sergio A Quezada, Sanjiv A. Luther, Thorsten R. Mempel, Giovanni Ciriello, Sara I Pai, Olivier Michielin, Jan P. Böttcher, Ralph Weissleder, Mikael J. Pittet, Dan Celestini, Thomas Zwahlen, Nawel Zouggari
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Cell Press
Verified
Protein Kinase C Inhibition Overcomes Targeted Therapy Resistance in Cutaneous Melanoma
Conflicts of Interest The authors declare no conflicts of interest. Supporting Information Filename Description exd70093-sup-0001-DataS1.docxWord 2007 document , 272.9 KB Data S1. PKC and MAPK pathway inhibitor combination treatment reduces proliferation in MAPK pathway inhibitor resistant cutaneous melanoma cell cultures in 3D spheroids. exd70093-sup-0002-FigureS1.pdfPDF document, 272.9 KB Figure S1.
A targetable type III immune response with increase of IL-17A expressing CD4+ T cells is associated with immunotherapy-induced toxicity in melanoma - Nature Cancer
Abstract Immune checkpoint inhibitors are standard-of-care for the treatment of advanced melanoma, but their use is limited by immune-related adverse events. Proteomic analyses and multiplex cytokine and chemokine assays from serum at baseline and at the adverse event onset indicated aberrant T cell activity with differential expression of type I and III immune signatures.
Monitoring melanoma patients on treatment reveals a distinct macrophage population driving targeted therapy resistance
Highlights • Targeted therapy resistance is associated with high expression of POSTN in melanoma • POSTN induces a targeted therapy resistance (TTR)-associated macrophage phenotype • POSTN promotes therapy resistance in a mouse melanoma model • TTR macrophages orchestrate melanoma resistance formation via CD44 signaling Summary Resistance to targeted therapy remains a major clinical challenge in melanoma.
Tumor-derived GDF-15 blocks LFA-1 dependent T cell recruitment and suppresses responses to anti-PD-1 treatment - Nature Communications
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Proteins and antibodies HIS-tagged recombinant human Growth and Differentiation Factor-15 was produced in HEK293T cells (Invigate GmbH, Jena). The anti-human GDF-15 antibody used in this manuscript was generated in female C57BL/6J GDF-15-/–mice kindly provided by Dr. Jens Strelau (Heidelberg, Germany) and validated for binding affinity by surface plasmon resonance at NMI (Reutlingen, Germany). Specificity was tested by tissue cross-reactivity studies.
By Carmen Reitinger, Kilian Wistuba-Hamprecht, Hubert Hackl, Hemant R. Joshi, Phil Cheng, Mitchell Levesque, Matthias Goebeler, Markus Sauer, Falk Nimmerjahn, Stefanie von Felten, Michel Mittelbronn, Andreas Beilhack, Reinhard Dummer, Markus Haake, Lena Sorger, Jacob Späth, Rudi Beschorner, Alexander Thiem, Manfred Rüdiger
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Nature
Verified
Highlights • Co-infection of M. bovis and H. pylori boosts gastric Th1 responses and immunopathology • Gastric presence of H. pylori compromises immune control of M. bovis • Both mutual effects result from redirection of Treg cells to sites of M. bovis infection • CXCR3 blockade restores M. bovis control, even if H. pylori is present Summary The two human pathogens Helicobacter pylori and Mycobacterium tuberculosis (Mtb) co-exist in many geographical areas of the world.
Targeting complex, adaptive responses in melanoma therapy
Highlights • Future targeted therapies require knowledge of complex adaptive drug responses. • Drug combinations should target diverse mechanisms such as metabolism or signaling. • Combined targeted/immune therapies show promise, but tolerability is problematic. Abstract Our understanding of the complex, adaptive mechanisms of response to targeted therapies in metastatic melanoma is now leading to more effective combination treatments.
CSS City Greeting Postcard
$shadow-color: #C03820; .container { display: flex; justify-content: center; min-width: 800px; margin-top: 50px; } .card-wrapper { overflow: hidden; box-shadow: 0px 5px 30px rgba(0,0,0,0.25); border: 20px solid #ffffff; width: 800px; height: 500px; background: linear-gradient(172deg, #FFE3EF 64%, #6dd5ed 100%); } .greeting { margin: 10px 0 0 20px; font-size: 60px; font-family: 'Yellowtail', cursive; letter-spacing: 3px; color: #222222; } .city { position: relative; } .city-title,...
Correction: In Vivo E2F Reporting Reveals Efficacious Schedules of MEK1/2-CDK4/6 Targeting and mTOR-S6 Resistance Mechanisms
Correction: In Vivo E2F Reporting Reveals Efficacious Schedules of MEK1/2–CDK4/6 Targeting and mTOR–S6 Resistance Mechanisms Jessica L.F. Teh, Phil F. Cheng, Timothy J. Purwin, Neda Nikbakht, Prem Patel, Inna Chervoneva, Adam Ertel, Paolo M. Fortina, Ines Kleiber, Kim HooKim, Michael A. Davies, Lawrence N. Kwong, Mitch P. Levesque, Reinhard Dummer and Andrew E. Aplin Cancer Discov December 1 2018 (8) (12) 1654; DOI: 10.1158/2159-8290.CD-18-1291
In Vivo E2F Reporting Reveals Efficacious Schedules of MEK1/2-CDK4/6 Targeting and mTOR-S6 Resistance Mechanisms
Research Articles In Vivo E2F Reporting Reveals Efficacious Schedules of MEK1/2–CDK4/6 Targeting and mTOR–S6 Resistance Mechanisms Jessica L.F. Teh, Phil F. Cheng, Timothy J. Purwin, Neda Nikbakht, Prem Patel, Inna Chervoneva, Adam Ertel, Paolo M. Fortina, Ines Kleiber, Kim HooKim, Michael A. Davies, Lawrence N. Kwong, Mitch P. Levesque, Reinhard Dummer and Andrew E. Aplin
In vivo E2F reporting reveals efficacious schedules of MEK1/2-CDK4/6 targeting and mTOR-S6 resistance mechanisms
In vivo E2F reporting reveals efficacious schedules of MEK1/2-CDK4/6 targeting and mTOR-S6 resistance mechanisms Jessica L.F. Teh, Phil F. Cheng, Timothy J. Purwin, Neda Nikbakht, Prem Patel, Inna Chervoneva, Adam Ertel, Paolo M. Fortina, Ines Kleiber, Kim HooKim, Michael A. Davies, Lawrence N. Kwong, Mitch P. Levesque, Reinhard Dummer and Andrew E. Aplin Cancer Discov March 1 2018 DOI: 10.1158/2159-8290.CD-17-0699
Publisher Correction: The low affinity neurotrophin receptor CD271 regulates phenotype switching in melanoma
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
low neurotrophin receptor CD271 regulates phenotype switching in melanoma
To characterize CD271-expressing melanoma cells in vivo, we first determined the genetic signature of this subpopulation of cells at the time of invasion. To do so, we used an orthotopic in vivo model established in our laboratory that is able to recapitulate early events in melanoma progression, including the break out of cells from the primary tumor22.
CSS animated cheese sandwich bite
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CSS Lego Brick
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