Prof. Dr. rer. nat. Natalia S. Pellegata
Head of Division Neuroendocrinology"The goal of my research projects is to improve the clinical management of cancer patients by identifying novel targeted therapies. The latest scientific contributions of my laboratory consists in translational studies that identified novel and druggable therapeutic targets in neuroendocrine tumors (NETs)"
"The goal of my research projects is to improve the clinical management of cancer patients by identifying novel targeted therapies. The latest scientific contributions of my laboratory consists in translational studies that identified novel and druggable therapeutic targets in neuroendocrine tumors (NETs)"
Academic Career and Research Areas
For over 2 decades, Natalia’s research projects focused on the elucidation of the molecular mechanisms involved in neuroendocrine tumors (NETs) development/progression, on the genetic predisposition to NETs and on the identification of novel therapeutic targets for these tumors. Natalia exploited novel and unique animal models in translational studies aimed at evaluating novel therapies against NETs based on their genetic profiles (precision medicine).
Capitalizing on the discovery that mutation of Cdkn1b (encoding p27) causes a Multiple Endocrine Neoplasia (MEN) syndrome in the rat (named MENX), Natalia identified the first patient with multiple endocrine tumors carrying a germline mutation in CDKN1B. These and subsequent studies established CDKN1B as novel tumor susceptibility gene for multiple NETs, and led to the definition of a new MEN syndrome in man (MEN4) cause by p27 mutations (PMID: 17030811; article cited >450 times). Given that animal models recapitulating human NETs and suitable for preclinical studies are scarce, Natalia has endeavored to characterize MENX-associated NETs at various levels (pathological, physiological, molecular) and could show that rat NETs quite faithfully recapitulate their human cognate tumors. Rat pheochromocytomas (PCCs) and nonfunctioning pituitary tumors (NFPTs) share genetic signatures, histomorphological, biochemical and physiological features with their cognate human tumors, attesting that rat NETs can be exploited as to gene discovery. Thus, starting from transcriptome data of the rat tumors, Natalia’s group found a new druggable pathway (BMP signaling) active in both rat and human PCCs. Along the same lines, her group recently demonstrated that the angiopoietin/Tie2 pathway is present in pituitary tumor cells (rat and human) and represents a promising target for therapy, as demonstrated by proof-of-principle in vivo studies. Natalia also exploited the MENX rat model for preclinical therapy-response studies to evaluate new drugs for efficacy against NETs, and provided the rationale for clinical implementation of dual PI3K/mTOR inhibitors and anti-angiogenic drugs in pituitary tumors and PCC. Being part of an SFB focusing on imaging for tumor monitoring for 12 years, she established important collaborations to apply functional imaging modalities to follow tumor response to various drugs in vivo.
Fields of Work and Expertise
Neuroendocrine Tumors Preclinical in vivo Studies Drug Testing
Professional Background
Adjunct Professor, Faculty of Medicine, Technical University Munich
Head of Neuroendocrinology, Institute for Diabetes and Cancer, Helmholtz Munich
Priv-Doz Faculty of Medicine, Technical University Munich
Principal Investigator, Institute of Pathology, Helmholtz Munich
Honors and Awards
2022 - Associate Editor, Special Issue “MEN1” to be published in Frontiers in Endocrinology
2022 - Guest Editor, Special Issue “Translational Research on Neuroendocrine Tumors and Experimental Tumor Therapy” to be published in Cancers
2021 - Editorial Board of Frontiers in Endocrinology
2015 - Eleonore Trefftz Visiting Professorship for Women Scientists, Technical University of Dresden
Highlight Publications
More on PubMedJ Cachexia Sarcopenia Muscle
Trends Cancer
J Cachexia Sarcopenia Muscle
High levels of modified ceramides are a defining feature of murine and human cancer cachexia.