A5027272360- Hippo pathway signaling and YAP/TAZ
- Cancer Research and Treatments
- Cancer, Hypoxia, and Metabolism
- Cancer Immunotherapy and Biomarkers
- Immune Cell Function and Interaction
- Immune cells in cancer
- Pancreatic and Hepatic Oncology Research
- Law, logistics, and international trade
- Phagocytosis and Immune Regulation
- Fibroblast Growth Factor Research
- Food Industry and Aquatic Biology
- Ubiquitin and proteasome pathways
- FOXO transcription factor regulation
- Lipid metabolism and biosynthesis
- PI3K/AKT/mTOR signaling in cancer
- Neuroinflammation and Neurodegeneration Mechanisms
- Autophagy in Disease and Therapy
- Cancer, Lipids, and Metabolism
- CAR-T cell therapy research
- Immunotherapy and Immune Responses
- Cancer-related gene regulation
University of Lausanne
2022-2025
Ludwig Cancer Research
2023
Korea Advanced Institute of Science and Technology
2018-2020
Abstract YAP and TAZ play oncogenic roles in various organs, but the role of YAP/TAZ gastric cancer remains unclear. Here, we show that activation initiates tumorigenesis vivo verify its significance human cancer. In mice, pyloric stem cell led to step-wise tumorigenesis. RNA sequencing identified MYC as a decisive target YAP, which controls at transcriptional posttranscriptional levels. These mechanisms tightly regulated homeostatic conditions, altered this balance by impeding miRNA...
Mitophagy, a central process guarding mitochondrial quality, is commonly impaired in human diseases such as Parkinson's disease, but its impact adaptive immunity remains unclear. The differentiation and survival of memory CD8+ T cells rely on oxidative metabolism, that requires robust quality control. Here, we found disease patients have reduced frequency compared with healthy donors failed to form upon vaccination against COVID-19, highlighting the importance control for cell formation. We...
The development of pancreatic cancer is heavily dependent upon the aberrant activation KRAS signaling. Among downstream targets KRAS, effectors Hippo pathway YAP and TAZ (YAP/TAZ) are crucial during initiation progression. However, little known about cell type-specific effects YAP/TAZ on cancer. Here we clarify unique consequences in ductal population pancreas by generating mice with duct cell-specific, inducible knockouts Lats1 Lats2, main kinases upstream YAP/TAZ. Oncogenic deletion...
Abstract Tumor cells employ various mechanisms to evade immune surveillance, including metabolic modulation of the tumor microenvironment (TME). Lipid stress in TME leads upregulation CD36 tumor-infiltrating cells, impairing anti-tumor immunity by enhancing survival and suppressive activity regulatory T (Tregs) promoting ferroptosis exhaustion CD8+ cells. Here, we developed PLT012, a humanized anti-CD36 IgG4 antibody targeting lipid-binding domain CD36, with remarkable safety profile...
Abstract Tumor cells develop various strategies to evade immune surveillance, one of which involves altering the metabolic state tumor microenvironment. In response stress in microenvironment, several tumor-infiltrating subsets upregulate CD36 take up lipids. This leads impaired antitumor immunity, as intratumoral regulatory T exhibit increased survival and suppressive activity, whereas CD8+ become more susceptible ferroptosis exhaustion. this study, we a humanized anti-CD36 IgG4 antibody,...
Hippo signaling acts as a tumor suppressor pathway by inhibiting the proliferation of adult stem cells and progenitor in various organs. Liver-specific deletion components mice induces liver cancer development through activation transcriptional coactivators, YAP TAZ, which exhibit nuclear enrichment are activated numerous types cancer. The upstream-most regulators Warts,
Abstract The accumulation of lipid metabolic products in the TME has been extensively documented to exacerbate cancer malignancy by suppressing anti-tumor immunity. This phenomenon is characterized induction immunosuppressive features various immune cells and development exhausted phenotypes T cells, creating formidable obstacles for effective immunotherapies. Notably, CD36, a fatty acid transporter, identified as up-regulated both malignant tumor-associated including regulatory macrophages,...
<h3>Background</h3> Accumulation of lipid metabolic products in tumor microenvironment (TME) has been documented to augment the malignancy cancer by dampening anti-tumor immunity, including increased immunosuppressive features various immune cells and development exhausted phenotypes T cells, which further orchestrates hurdles for immunotherapies. Previously, CD36, a fatty acid transporter, reported be up-regulated both malignant tumor-associated regulatory macrophages CD8<sup>+</sup> adjust...
<p>Supplementary materials and methods</p>
<p>Figure S6</p>
<p>Knockout of Lats1 and Lats2 in Lgr5+ stem cells causes dysplasia the pyloric stomach</p>
<p>YAP/TAZ overexpression causes transformation of normal gastric epithelial cells</p>
<p>YAP/TAZ overexpression causes transformation of normal gastric epithelial cells</p>
<p>Supplementary Table S1-4</p>
<p>Supplementary materials and methods</p>
<p>Figure S6</p>
<p>Supplementary Figure S7</p>
<div>Abstract<p>The development of pancreatic cancer is heavily dependent upon the aberrant activation KRAS signaling. Among downstream targets KRAS, effectors Hippo pathway YAP and TAZ (YAP/TAZ) are crucial during initiation progression. However, little known about cell type-specific effects YAP/TAZ on cancer. Here we clarify unique consequences in ductal population pancreas by generating mice with duct cell-specific, inducible knockouts <i>Lats1</i>...
<p>Supplementary Table S1-4</p>
<div>Abstract<p>The development of pancreatic cancer is heavily dependent upon the aberrant activation KRAS signaling. Among downstream targets KRAS, effectors Hippo pathway YAP and TAZ (YAP/TAZ) are crucial during initiation progression. However, little known about cell type-specific effects YAP/TAZ on cancer. Here we clarify unique consequences in ductal population pancreas by generating mice with duct cell-specific, inducible knockouts <i>Lats1</i>...
<p>Supplementary Figure S2</p>
<p>Supplementary Figure S5</p>