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Patrick Starlinger
Assoc. Prof. Patrick Starlinger, MD, PhDHead of Research Group: Molecular Aspects of Liver Cancer & Regeneration

Department of General Surgery (Division of Visceral Surgery)
Position: Associate Professor

ORCID: 0000-0002-4666-5337


Abdominal Neoplasms; Blood Platelets; Colorectal Surgery; Liver Diseases; Liver Regeneration; Serotonin; von Willebrand Factor

Research interests

Main research objectives:

a)    Molecular mechanisms of liver regeneration and potential treatment targets:

  • Identification of central regulators and processes involved in the initiation of liver regeneration.
  • Characterization of regulatory mechanisms and thereby identification of novel therapeutic targets to support the regenerative capacity after liver resection as well as to improve our understanding of the pathophysiological processes involved in liver regeneration.

b)    Predictive and prognostic markers for liver regeneration and primary and secondary liver cancer:

  • Identification of clinical and experimental markers of liver regeneration which reflect the prognosis of regenerative capability and therefore the postoperative outcome after liver surgery, to ultimately tailor surgical strategy to each individual patient and thereby avoid potentially fatal complications.
  • Quantification of tumor aggressiveness using clinical and experimental markers to predict early disease recurrence, to spare unnecessary surgery in patients that will not benefit from tumor resection.

c)    Cancer development:

  • Identification of the role of platelets and immune cells and their interaction during the development of liver cancer and progression.

Selected publications

  1. Bivalent role of Intra-Platelet Serotonin in Liver Regeneration and Tumor Recurrence in Humans.
  2. P2X1-regulated IL-22 secretion by innate lymphoid cells is required for efficient liver regeneration.
  3. The profile of platelet α-granule released molecules affects postoperative liver regeneration.
  4. Evidence for serotonin as a relevant inducer of liver regeneration after liver resection in humans.
  5. Neoadjuvant bevacizumab persistently inactivates VEGF at the time of surgery despite preoperative cessation.