Professor Márta Korbonits
Professor in Endocrinology and Deputy Director of the WHRI
Centre: Endocrinology
Email: m.korbonits@qmul.ac.uk
Telephone: +44(0) 20 7882 6238
Website: https://www.qmul.ac.uk/fipa-patients/
Profile
ORCID iD: 0000-0002-4101-9432
Márta Korbonits graduated in Medicine in Budapest and undertook her early clinical training at the Internal Medicine Department of the Postgraduate Medical School, Budapest. She joined the Department of Endocrinology at St. Bartholomew’s Hospital under the mentorship of Professors Ashley Grossman and Michael Besser. Her MD concentrated on the effects of growth hormone secretagogues on hypothalamic hormone release, while her PhD studies explored the nature and causes of pituitary tumorigenesis.
She was awarded an MRC Clinician Scientist Fellowship, and commenced studies that produced novel insights into ghrelin physiology and genetics. Her findings related to the regulation of the metabolic enzyme AMPK by ghrelin, cannabinoid and glucocorticoid opened a new aspect of hormonal regulation of metabolism. She is working on novel aspects of the genetics of endocrine tumours as well as metabolic consequences of hormonal imbalances.
She is Professor of Endocrinology and Metabolism, Centre Lead of Endocrinology and Deputy Director of the William Harvey Research Institute at Barts and the London School of Medicine, Queen Mary University of London and Honorary Consultant at Barts Health NHS Trust.
Prof Korbonits’s publications and metrics can be found on Google Scholar.
Professor Korbonits continues to integrate human studies alongside with laboratory-based research and has pioneered several projects in translational medicine. Over the last decade her major research focus involves the clinical and scientific aspects of familial isolated pituitary adenomas. In addition to her basic research, she looks after patients with endocrine diseases in St. Bartholomew’s Hospital and undertakes wide-ranging undergraduate and postgraduate teaching activities as well as supervision of MSc and PhD students.
Professor Korbonits has received several awards, including the Nicholas T. Zervas Lectureship in Pituitary and Neuroendocrine Disorders at Massachusetts General Hospital (2010), the Society for Endocrinology Medal (2013), the Endocrine Society’s Delbert Fischer award (2015), the Hadden Lecture Prize, Irish Endocrine Society (2017), the Harrison Lecture Prize, Endocrine Society of Australia (2017) and the Estelle Wolfson award from the Royal College of Physicians (2018). She has been invited Professor at University of Colorado 2019 and had the KROC Visiting Professorship Award, Mayo Clinic in 2020, and is the Royal College of Physicians of Edinburgh keynote lecturer, Edinburgh in 2020.
She supports the endocrine community’s learned societies: served as the Conference Program Secretary for the Society for Endocrinology, was Board member for Pituitary Society and European Neuroendocrine Society and Chair of the Science Committee of the European Society of Endocrinology.
She is a current or past Editorial Board member of the Journal of Clinical Endocrinology and Metabolism, Journal and Neuroendocrinology, Pituitary and Journal of Endocrinology and Associate Editor of Scientific Reports, Annals of Human Genetics and the Journal of the Endocrine Society.
She is a member of the Medical Research Council (MRC) Fellowship Committee and Head of the Society of Endocrinology Leadership program.
Figure 1. AIP Mutations and Gigantism. First panel. 18th century patient with gigantism due to a mutation of AIP (aryl hydrocarbon receptor interacting protein) beside his twin cousins who also had gigantism, in an etching by John Kay (1742–1826) (National Portrait Gallery, London) (Chahal, NEJM, 2011). Middle panel. Ribbon representation of the crystal structure of human AIP (based on data published in Morgan, PlosOne, 2012 and Linnert, Biomol.NMR Assign., 2012) with the stop mutation from the 18th-century patient marked in red. Right-hand panel. A hand of a 4th-year male medical student (172 cm tall) compared to the tracing of the hand of an Irish patient from the 18th century with gigantism (tracing from Frankom, G; Musgrave, J.H. The Irish giant, 1974, Duckworth, London).
Nearly one percent of the general population and 2.5% of those above 70 years of age are on long-term glucocorticoid treatment for a chronic inflammatory disease. Many of these patients develop iatrogenic Cushing syndrome, causing significant metabolic, cardiovascular and musculoskeletal morbidity for which there is a treatment need but no current solution. We conducted a clinical trial exploring a concept arisen from our previous experimental studies (Christ-Crain, Faseb J, 2008, Pubmed 18198220 and Kola JCEM, 2008, Pubmed 18782871): many of the changes seen in glucocorticoid excess correspond to metabolic steps regulated by the enzyme 5’AMP-activated protein kinase (AMPK), a key regulator of energy metabolism and one of the well-recognized mediators of metformin’s mode of action (Pernicova & Korbonits, Nature Rev Endocrinal, 2014). We assessed the effect of metformin in glucocorticoid-treated patients. Despite the relatively short duration of the study, we found, in addition to glucose-related positive outcomes, beneficial effects in several cardiovascular, metabolic, bone and inflammatory parameters. Key findings with significant relevance to healthcare were the lower frequency of pneumonia in the metformin group compared with placebo, reduced overall rate of moderate-to-severe infections and, most significantly, lower all-cause hospital admissions.
Crosstalk between AIPpos tumours and the tumour microenvironment. AIPpos tumours have EMT signatures and increased immune cell contents, cytokines and abundant vascular structures which create a tumour supportive microenvironment to promote aggressive tumour growth. The upregulation of the CCL5 in the AIPpos tumours and the in vitro data presented suggest that CCL5, secreted by the tumour cells, may contribute to the recruitment of macrophages and initiate bidirectional paracrine signalling loops which facilitate increased migratory/invasive potential of the tumour cells. Our findings indicate that AIP deficiency in pituitary cells drives invasion through the induction of EMT and immune cells recruitment.
Pituitary tumour cells release different cytokines, particularly chemokines (including IL-8, CCL2, CCL3, CCL4, CXCL10, CXCL1), directly into the tumour microenvironment promoting the recruitment and infiltration of immune cells, including macrophages, lymphocytes and neutrophils. These infiltrating immune cells increase the growth of the tumour. Fibroblasts within the tumour are also able to secrete cytokines, such as IL-6, into the tumour microenvironment, which leads to increased invasion of pituitary tumour cells or the surrounding tissues.