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Csiszar Lab

  1. Center for Cancer Research
  2. Research Focuses
  3. Chemical Safety and Cancer Prevention
  4. Agnes Csiszar

Dr.rer.nat. Agnes Csiszar

Research Focus

Metastasis is responsible for more than 80% of cancer-associated deaths, yet the mechanism of dissemination is still poorly understood. Therapy failure eventually leads to metastasis, which is usually refractory to treatment. One major developmental process hijacked by cancer cells for metastatic spreading and treatment escape is the epithelial to mesenchymal transition (EMT), which is the initial step of the metastatic cascade, associated with the acquisition of cancer stem cell properties and resistance to anticancer therapies. 

Interleukin-like EMT inducer (ILEI), also called FAM3C, is one of the secreted factors that regulate tumor progression. Increased secretion and altered subcellular localization of ILEI is associated with unfavorable prognosis.

Using cellular and mouse model systems of EMT and tumor progression, our aim is to understand the molecular mechanisms of ILEI function and regulation in cancer pathogenesis as well as its contribution to drug tolerance and resistance.

Selected Publications

The FAM3C locus that encodes interleukin-like EMT inducer (ILEI) is frequently co-amplified in MET-amplified cancers and contributes to invasiveness
Schmidt U, Heller G, Timelthaler G, Heffeter P, Somodi Z, Schweifer N, Sibilia M, Berger W, Csiszar A*
J Exp Clin Cancer Res. 2021 Feb 17;40(1):69. doi: 10.1186/s13046-021-01862-5.

Covalent dimerization of interleukin-like epithelial-to-mesenchymal transition (EMT) inducer (ILEI) facilitates EMT, invasion, and late aspects of metastasis
Kral M, Klimek C, Kutay B, Timelthaler G, Lendl T, Neuditschko B, Gerner C, Sibilia M, Csiszar A*.
FEBS J. 2017 Oct;284(20):3484-3505. doi: 10.1111/febs.14207. Epub 2017 Sep 14.

The interleukin-like epithelial-mesenchymal transition inducer ILEI exhibits a non-interleukin-like fold and is active as a domain-swapped dimer
Jansson AM, Csiszar A, Maier J, Nyström AC, Axe E, Johansson P, Schiavone LH.
J Biol Chem. 2017 Sep 15;292(37):15501-15511. doi: 10.1074/jbc.M117.782904. Epub 2017 Jul 27.

Interleukin-like epithelial-to-mesenchymal transition inducer activity is controlled by proteolytic processing and plasminogen-urokinase plasminogen activator receptor system-regulated secretion during breast cancer progression
Csiszar A*, Kutay B, Wirth S, Schmidt U, Macho-Maschler S, Schreiber M, Alacakaptan M, Vogel GF, Aumayr K, Huber LA, Beug H.
Breast Cancer Res. 2014 Sep 9;16(5):433. doi: 10.1186/s13058-014-0433-7.

CDK8-mediated STAT1-S727 phosphorylation restrains NK cell cytotoxicity and tumor surveillance
Putz EM, Gotthardt D, Hörmann G, Csiszar A, Wirth S, Berger A, Straka E, Rigler D, Wallner B, Jamieson AM, Pickl WF, Zebedin-Brandl EM, Müller M, Decker T, Sexl V.
Cell Rep. 2013 Aug 15;4(3):437-44. doi: 10.1016/j.celrep.2013.07.012. Epub 2013 Aug 8.

All Publications

PubmedDatabase

Master Student (f/m/d)

Actionable targets of cancer plasticity

Are you interested in combating driving mechanisms of cancer resistance and metastasis?

The Csiszar Group is recruiting a master student (f/m/d) interested in applying in vitro and mouse models in cancer plasticity research.

Our team, closely associated with the Szakacs group, at the Center of Cancer Research, Medical University of Vienna, aims to find vulnerabilities of cancer plasticity—the ability of tumor cells to dynamically shift between epithelial, mesenchymal, stem-like, and drug-tolerant states. While plasticity is a major driver of metastasis and therapy resistance, yet its actionable molecular targets remain poorly defined. This project aims to validate candidate targets of cancer plasticity using advanced 3D in vitro and clinically relevant in vivo models of metastatic breast cancer covering both cell intrinsic and systemic mechanisms of actions and therapeutic effects.

Your responsibilities

  • experimental design and scientific methods: extract state-of-the-art methodologies from literature and adapt to our model systems and research questions
  • cell culture and organoid assays: characterize genetic and pharmacological loss- and gain-of-function scenarios of candidate genes/pathways in diverse in vitro drug treatment and invasion assays.
  • live-cell imaging and image analysis: monitor drug-induced cellular plasticity using reporters, morphological and motility changes and develop quantitative measures
  • tissue preparation, histology and AI-assisted digital pathology: mouse tumor model-derived tissue preparation for omics pipelines, histological stainings and quantitative analysis
  • spectral flow cytometry: immune profiling of syngeneic mouse tumor models upon different perturbations
  • documentation: collect, analyze, and summarize data in a structured and accurate manner. Present results at lab meetings and institutional seminar.

Your profile

  • enrolled in a Master's degree in a relevant subject
  • good technical skills with wet-lab experience (mammalian cell culture experience is highly desirable)
  • experience (e.g. internships) in a relevant area and R coding are a plus
  • excellent verbal and written communication skills in English (German not required)
  • self-motivated, enthusiastic and keen to learn, good team player, creativity
  • Independent and scientific mindset with problem-solving attitude

What we offer

  • A master thesis position for 9-12 months, starting in March 2026
  • An exciting project in a stimulating and international environment
  • Access to state-of-the-art infrastructure
  • A monthly allowance of € 440

Your application

  • Motivation letter
  • CV with listing relevant pre-experience
  • Contact of two references

Applications will be reviewed on a rolling basis until the position is filled.

 Mail an Agnes Csiszar

Financial Support

  • EU/Horizont 2020
  • Fonds des Bürgermeisters der Bundeshauptstadt Wien (Agnes Csiszar)
  • DOC-Stipendium der Österreichischen Akademie der Wissenschaften (Silvia Steinbauer)