Adrià Cañellas‐Socias

ORCID: 0000-0002-8373-7803
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About
Contact & Profiles
Research Areas
  • Cancer, Lipids, and Metabolism
  • Colorectal Cancer Treatments and Studies
  • Cancer, Hypoxia, and Metabolism
  • Cancer Cells and Metastasis
  • Eicosanoids and Hypertension Pharmacology
  • Hippo pathway signaling and YAP/TAZ
  • Cancer Immunotherapy and Biomarkers
  • Cellular Mechanics and Interactions
  • Genetic factors in colorectal cancer
  • Melanoma and MAPK Pathways
  • Hepatocellular Carcinoma Treatment and Prognosis
  • Cardiac Fibrosis and Remodeling
  • Cancer Research and Treatments
  • Protein Degradation and Inhibitors
  • Ubiquitin and proteasome pathways
  • 3D Printing in Biomedical Research
  • Endoplasmic Reticulum Stress and Disease
  • Ferroptosis and cancer prognosis
  • Autophagy in Disease and Therapy
  • RNA and protein synthesis mechanisms
  • Genomics and Chromatin Dynamics
  • Genetics, Aging, and Longevity in Model Organisms
  • Phagocytosis and Immune Regulation
  • FOXO transcription factor regulation
  • CRISPR and Genetic Engineering

Institute for Research in Biomedicine
2018-2024

Centro de Investigación Biomédica en Red de Cáncer
2020-2024

Stanford University
2024

MRC London Institute of Medical Sciences
2022

Imperial College London
2022

Abstract A substantial proportion of cancer patients do not benefit from platinum-based chemotherapy (CT) due to the emergence drug resistance. Here, we apply elemental imaging mapping CT biodistribution after therapy in residual colorectal and achieve a comprehensive analysis genetic program induced by oxaliplatin-based tumor microenvironment. We show that oxaliplatin is largely retained cancer-associated fibroblasts (CAFs) long time treatment ceased. determine accumulation CAFs intensifies...

10.1038/s41467-023-36334-1 article EN cc-by Nature Communications 2023-02-10

Abstract Colorectal cancer (CRC) tumors are composed of heterogeneous and plastic cell populations, including a pool stem cells that express LGR5. Whether these distinct populations display different mechanical properties, how properties might contribute to metastasis is poorly understood. Using CRC patient derived organoids (PDOs), we find compared LGR5- cells, LGR5+ stiffer, adhere better the extracellular matrix (ECM), move slower both as single clusters, higher nuclear YAP, show survival...

10.1038/s41467-024-47227-2 article EN cc-by Nature Communications 2024-04-18

Carcinoma development in colorectal cancer is driven by genetic alterations numerous signaling pathways. Alterations the RAS-ERK1/2 pathway are associated with shortest overall survival for patients after diagnosis of metastatic disease, yet how RAS-ERK regulates metastasis remains unknown. In this study, we used an unbiased screening approach based on selection highly liver cells vivo to determine genes metastasis. From this, ERK1/2-controlled gene set (EMGS) was defined. EMGS increased...

10.1158/0008-5472.can-19-4028 article EN Cancer Research 2020-08-19

Innate immune responses rely on inducible gene expression programmes which, in contrast to steady-state transcription, are highly dependent cohesin. Here we address transcriptional parameters underlying this cohesin-dependence by single-molecule RNA-FISH and single-cell RNA-sequencing. We show that innate genes regulated predominantly an increase the probability of active probabilities enhancer promoter transcription coordinated. Cohesin has no major impact fraction transcribed enhancers, or...

10.1038/s41467-022-31192-9 article EN cc-by Nature Communications 2022-07-27

<div>Abstract<p>Carcinoma development in colorectal cancer is driven by genetic alterations numerous signaling pathways. Alterations the RAS-ERK1/2 pathway are associated with shortest overall survival for patients after diagnosis of metastatic disease, yet how RAS–ERK regulates metastasis remains unknown. In this study, we used an unbiased screening approach based on selection highly liver cells <i>in vivo</i> to determine genes metastasis. From this,...

10.1158/0008-5472.c.6512596.v1 preprint EN 2023-03-31

<p>SF1: The expression of ANGPT2 and CXCR4 in CRC; SF2: Expression levels ANGPT2, CXCR4, CXCL12, TEK VEGFA SW620_P SW620_LiM2 cells; SF3: upon downregulation upregulation.; SF4: CXCL1 IL10 is controlled by RAS-ERK signaling pathway; SF5: Correlation various genes BRAF-signature or CRIS subtypes across CRC tumors; ST1: mRNA comparisons; ST2: Hypergeometric test for Signature FC-1.75.up ( 15 genes) - KEGG.</p>

10.1158/0008-5472.22427224 preprint EN cc-by 2023-03-31

<p>SF1: The expression of ANGPT2 and CXCR4 in CRC; SF2: Expression levels ANGPT2, CXCR4, CXCL12, TEK VEGFA SW620_P SW620_LiM2 cells; SF3: upon downregulation upregulation.; SF4: CXCL1 IL10 is controlled by RAS-ERK signaling pathway; SF5: Correlation various genes BRAF-signature or CRIS subtypes across CRC tumors; ST1: mRNA comparisons; ST2: Hypergeometric test for Signature FC-1.75.up ( 15 genes) - KEGG.</p>

10.1158/0008-5472.22427224.v1 preprint EN cc-by 2023-03-31

Colorectal cancer tumors are composed of heterogeneous and plastic cell populations, including a pool stem cells that express LGR5. Whether these distinct populations display different mechanical properties, how properties might contribute to metastasis is unknown. Using CRC patient derived organoids (PDOs), we found compared LGR5- cells, LGR5+ stiffer, adhere better the extracellular matrix (ECM), move slower both as single clusters, higher nuclear YAP, show survival rate in response...

10.1101/2023.12.04.569244 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-12-05

<div>Abstract<p>Carcinoma development in colorectal cancer is driven by genetic alterations numerous signaling pathways. Alterations the RAS-ERK1/2 pathway are associated with shortest overall survival for patients after diagnosis of metastatic disease, yet how RAS–ERK regulates metastasis remains unknown. In this study, we used an unbiased screening approach based on selection highly liver cells <i>in vivo</i> to determine genes metastasis. From this,...

10.1158/0008-5472.c.6512596 preprint EN 2023-03-31
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