Scientist working on Cancer Epigenomics, Immunology, Liquid Biopsy, and Transposable Elements. Faculty @pmcancercentre and @UofTmedicine. Founder, https://xitter.cf/t.co/FJYiJmIpBX

Toronto
Joined February 2014
Ten years ago, we discovered that reactivating transposable elements triggers an antiviral state in cancer cells, a process we named viral mimicry, unmasking tumors to the immune system (Roulois, Cell 2015). Now this idea finally reached patients with some impressive results:
Now online in @CD_AACR: Priming with DNMT Inhibitors Potentiates PD-1 Immunotherapy by Triggering Viral Mimicry in Relapsed/Refractory NK/T-cell Lymphoma - by Cheng Huang, Yan Gao, Jianfeng Chen, Choon Kiat Ong, Huiqiang Huang, and Jing Tan doi.org/10.1158/2159-8290.CD…
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Daniel De Carvalho retweeted
One of the hardest questions after cancer treatment: is it truly gone? SHERLOCK, from @UHN @pmcancercentre, follows 7,000 patients with blood tests for molecular residual disease — so relapse can be caught earlier. Led by Dr Lillian Siu.
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Daniel De Carvalho retweeted
#Review🚨 Viral mimicry activates antiviral immune responses through endogenous nucleic acids in the cytosol. Chen et al. discuss how tumours suppress these responses and why escape from #ViralMimicry may be a key feature of tumour evolution. 📖⬇️ dlvr.it/TVf72T
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Excited to share our new collaborative study, led by Nicholas Cheng and Philip Awadalla in @CellGenomics, exploring the potential of cell-free DNA methylation to identify cancer risk years before diagnosis.
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These applications will require studies demonstrating that decisions guided by molecular risk improve outcomes, including whether screening can safely be reduced for those classified as lower risk. This study provides a foundation for pursuing that goal
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Daniel De Carvalho retweeted
NEW content online! Viral mimicry escape as a necessary feature of malignant transformation dlvr.it/TVTzMM
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Excited to share our newest work in Nature Reviews Cancer, “Viral mimicry escape as a necessary feature of malignant transformation,” in which we propose that escaping viral mimicry is a new hallmark of cancer.
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Understanding how individual tumours escape this surveillance could help us target their dependencies and improve responses to immunotherapy. Matching treatment to each tumour’s viral mimicry and escape state will be essential
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