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Video

Cancer neuroscience

Session: Abstract Concurrent Session: Cancer Neuroscience

CNSC-09 - CHI3L1 is a molecular marker for glioblastoma network connectivity and functionally orchestrates tumor microtube formation

Saturday, November 18, 2023
8:35 AM – 8:40 AM PT
Location: Room 118-120
Non-CME

    Oral Abstract Presenter(s)

  • Dirk C. Hoffmann

    German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

    • Author(s)

  • LH

    Ling Hai

    German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

  • RW

    Robin J. Wagener

    German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

  • David Hausmann

    German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

  • DD

    Daniel D. Domínguez Azorín

    German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

  • RX

    Ruifan Xie

    German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

  • MH

    Magnus-Carsten Huppertz

    Max Planck Institute for Medical Research
    Heidelberg, Baden-Wurttemberg, Germany

  • JH

    Julien Hiblot

    Max Planck Institute for Medical Research
    Heidelberg, Baden-Wurttemberg, Germany

  • PS

    Philipp Sievers

    University Hospital Heidelberg
    Heidelberg, Baden-Wurttemberg, Germany

  • JI

    Jakob Ito

    German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

  • Sophie Heuer

    Neurology Clinic University Hospital Heidelberg & German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

  • GC

    Gina Cebulla

    German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

  • HM

    Henriette Mandelbaum

    German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

  • EJ

    Erik Jung

    Heidelberg University Hospital and National Center for Tumor Diseases (NCT)
    Heidelberg, Baden-Wurttemberg, Germany

  • AK

    Alexandros Kourtesakis

    German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

  • KE

    Kati Ernst

    German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

  • DR

    Denise Reibold

    German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

  • UW

    Uwe Warnken

    German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

  • Varun Venkataramani

    Neurology Clinic and National Center for Tumor Diseases, University Hospital Heidelberg, INF 400, 69120 Heidelberg
    Heidelberg, Baden-Wurttemberg, Germany

  • RW

    Rainer Will

    German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

  • Mario Suva

    Massachusetts General Hospital and Harvard Medical School
    Boston, Massachusetts, United States

  • Christel C. Herold-Mende

    Division of Experimental Neurosurgery, Dept. of Neurosurgery, Heidelberg University Hospital,
    Heidelberg, Baden-Wurttemberg, Germany

  • Felix Sahm

    University Hospital Heidelberg
    Heidelberg, Baden-Wurttemberg, Germany

  • Frank Winkler

    German Cancer Research Center
    Heidelberg, Baden-Wurttemberg, Germany

  • MS

    Matthias Schlesner

    University of Augsburg
    Augsburg, Bayern, Germany

  • Wolfgang Wick

    Universitatsklinikum Heidelberg
    Heidelberg, Baden-Wurttemberg, Germany

  • TK

    Tobias Kessler

    Dept. of Neurology, Heidelberg University Hospital, Heidelberg University,
    Heidelberg, Baden-Wurttemberg, Germany

Chitinase 3-like 1 (CHI3L1) is a secreted glycoprotein and its RNA expression elevated in glioblastoma (GB) compared to other tumor types and related normal tissues. Furthermore, transcript levels in GB dictate aggressiveness through modulating stemness, proliferation and tumor microenvironment. This ultimately influences patient survival. We here provide evidence that the pathogenic relevance of CHI3L1 expression is associated with the extent of tumor microtubes (TMs) - ultralong membrane tubes that connect GB cells (GBCs) to a network with considerable relevance for tumor progression and therapy resistance. Single cell RNA profiling of xenografted GBCs with different degrees of morphological and functional TMs identified CHI3L1 as a prognostic marker for TM network extent. We demonstrate that both RNA and protein expression levels are suitable markers in preclinical in vitro systems modeling TM connectivity as well as in clinical specimens. Genetic perturbation of CHI3L1 influenced GBC network integration, caused a shift of the dominant cell state and altered the phosphorylation status of the TM-driver GAP43. Pharmacological blocking of CHI3L1 with an antibody reduced TM networks, thus providing a handle for future clinical translation. Together, these data identify a functional and upstream role of CHI3L1 in governing tumor cell connectivity, CHI3L1 RNA and protein expression as a novel way to determine overall GBC connectivity for future trials, and finally a new therapeutic target for tumor network-disrupting strategies.