Jennifer Cain

ORCID: 0009-0006-4246-0170
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About
Contact & Profiles
Research Areas
  • interferon and immune responses
  • Cytokine Signaling Pathways and Interactions
  • Intelligence, Security, War Strategy
  • Religion, Society, and Development
  • Religious Education and Schools
  • Biblical Studies and Interpretation
  • ICT in Developing Communities
  • Cancer-related gene regulation
  • Religion, Ecology, and Ethics
  • Media, Religion, Digital Communication
  • Language, Linguistics, Cultural Analysis
  • Research on Leishmaniasis Studies
  • Biomedical Ethics and Regulation
  • HER2/EGFR in Cancer Research
  • Cancer, Hypoxia, and Metabolism
  • Developmental Biology and Gene Regulation
  • Lung Cancer Treatments and Mutations
  • Learning Styles and Cognitive Differences
  • Experimental and Theoretical Physics Studies
  • Mobile Learning in Education
  • Web and Library Services
  • Religious Tourism and Spaces
  • Religion, Spirituality, and Psychology
  • Open Education and E-Learning
  • Sustainable Design and Development

Gilead Sciences (United States)
2022-2024

Centre de Recherche en Neurobiologie - Neurophysiologie de Marseille
2010

Abstract A substantial fraction of cancers evade immune detection by silencing Stimulator Interferon Genes (STING)-Interferon (IFN) signaling. Therapeutic reactivation this program via STING agonists, epigenetic, or DNA-damaging therapies can restore antitumor immunity in multiple preclinical models. Here we show that adaptive induction three prime exonuclease 1 (TREX1) restrains STING-dependent nucleic acid sensing cancer cells its catalytic function degrading cytosolic DNA. Cancer cell...

10.1158/2159-8290.cd-23-0700 article EN Cancer Discovery 2024-01-10

<div>Abstract<p>A substantial fraction of cancers evade immune detection by silencing Stimulator Interferon Genes (STING)-Interferon (IFN) signaling. Therapeutic reactivation this program via STING agonists, epigenetic, or DNA-damaging therapies can restore antitumor immunity in multiple preclinical models. Here we show that adaptive induction three prime exonuclease 1 (TREX1) restrains STING-dependent nucleic acid sensing cancer cells its catalytic function degrading cytosolic...

10.1158/2159-8290.c.7209207.v1 preprint EN 2024-05-01

<div>Abstract<p>A substantial fraction of cancers evade immune detection by silencing Stimulator Interferon Genes (STING)-Interferon (IFN) signaling. Therapeutic reactivation this program via STING agonists, epigenetic, or DNA-damaging therapies can restore antitumor immunity in multiple preclinical models. Here we show that adaptive induction three prime exonuclease 1 (TREX1) restrains STING-dependent nucleic acid sensing cancer cells its catalytic function degrading cytosolic...

10.1158/2159-8290.c.7209207 preprint EN 2024-05-01
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