Professor Ashley Grossman

Profile

ORCID iD: 0000-0003-1176-6186

Ashley Grossman was awarded an Open Exhibition to St Catharine's College, Cambridge, completed a degree in Psychology and Social Anthropology at the University of London, and then entered University College London where he received a First-Class degree in Anatomy, and the University Gold Medal from UCHMS. He started in the Dept. of Endocrinology at St Bartholomew's Hospital and medical school, eventually becoming Professor of Endocrinology at Barts and the London School of Medicine in 1993. He moved to the Oxford Centre for Diabetes, Endocrinology and Metabolism at the Churchill Hospital, in 2011, where he was appointed Professor of Endocrinology at the University of Oxford, and in 2012 Senior Research Fellow of Green-Templeton College, now Emeritus Professor at the University. Most recently, he moved to become Consultant in Neuroendocrine Tumours at the Royal Free Hospital, London, in the ENETS Centre of Excellence, and is also Professor of Endocrinology at Barts and the London School of Medicine and Dentistry, Queen Mary University of London. He has published some 550 peer-reviewed papers and over 450 chapters and reviews, most recently on hypothalamic and pituitary tumours and endocrine oncology. He has been President of the ENEA, the Society for Endocrinology (2012-2014), Chairman of UKINETS (2010-2012), was President of the Pituitary Society (2015-2016), and is President of Endotext. He has an honorary PhD from the University of Athens, and was awarded the Clinical Endocrinology Trust Prize 2004, the Geoffrey Harris Award in Neuroendocrinology, European Society for Endocrinology 2014,  the Iain MacIntye Prize, Barts and the London School of Medicine, July 2017, Outstanding Mentor, American Endocrine Society, March 2020, the Jubilee Lecturer at the British Endocrine Societies meeting in March 2025, the ESE/Endocrine Society Transatlantic Award for 2025, and the Lifetime Achievement Award from ENETs, Krakow, 2026. He is currently Editor-in-Chief of Endcorine Reviews, and Associate Editor of Endocrine Pathology, the Journal of Neuroendocrinology and Endocrine Oncology.

Research

Group members

Prof. Márta Korbonits

Summary

Starting with an on-going interest in pituitary tumours, especially secretory tumours as in acromegaly and Cushing’s disease, my research has extended to all forms of endocrine tumour, focusing on neuroendocrine tumours, phaeochromocytomas and paragangliomas. My research has centred on understating the molecular pathogenesis of these tumours, and translating this into effective medical therapies.

Publications

• Grossman, A., Kruseman, A.C.N., Perry, L., Tomlin, S., Schally, A.V., Coy, D.H., Comaru‑Schally, A.‑M., Rees, L.H. and Besser, G.M. (1982). A new hypothalamic hormone, CRF, specifically stimulates the release of adrenocorticotropin and cortisol in man. Lancet, i, 921 ‑ 922. This was the first use of the releasing factor CRH in humans.
• Grossman, A., Savage, M.O., Wass, J.A.H., Lytras, N., Sueiras‑ Diaz, J., Coy, D.H., and Besser, G.M. (1983). Growth hormone‑ releasing factor in growth hormone deficiency: the demonstration of  a hypothalamic defect in growth hormone release. Lancet, ii, 137‑ 138. We demonstrated that growth hormone deficiency in children was primarily a hypothalamic not a pituitary defect.
• Clark, A.J.L., McLoughlin, L. and Grossman, A. (1993). Familial glucocorticoid deficiency associated with point mutation in the adrenocorticotrophin receptor. Lancet, 341, 461-2. Following the contemporaneous sequencing of the ACTH receptor, this was the first evidence for a clinical syndrome associated with its mutation, defining  the novel field of ‘familial glucocorticoid deficiency’.
• Ur, E., Capstick, L., McLoughlin, L., Checkley, S., Besser, G.M. and Grossman, A. (1995). Continuous infusion of corticotropin-releasing hormone in the absence of corticosteroid feedback in man. Neuroendocrinology, 61, 191-197. We showed in normal volunteers that the circadian rhythmicity in the pituitary-adrenal axis was likely driven by AVP and not CRH.
• Dahia, P.L.M., Ahmed-Shuaib, A., Jacobs, R.A., Chew, S.L., Honegger, J., Fahlbusch, R., Besser, G.M. and Grossman, A. (1996). Vasopressin receptor expression and mutation analysis in corticotropin-secreting tumors. J. Clin. Endocrinol. Metab.,  81, 1768-1771. While mutations in the AVP receptor were unlikely to be responsible for Cushing’s disease, the V2 receptor was expressed in these tumours and not the normal pituitary, underpinning the use of the desmopressin stimulation test.
• Kostoglou-Athanassiou, I., Forsling, M.L., Navarra, P. and Grossman, A.B.  (1996). Oxytocin release is inhibited by the generation of carbon monoxide from the rat hyopothalamus - further evidence for carbon monoxide as a neuromodulator.  Mol. Brain Res., 42, 301-306.
• Carbon monoxide is a significant modulator of AVP, and this may explain the syndrome of SIAD seen in patients with acute intermnittent porphyria
• Dahia, P.M.L., Aguiar, R.C.T., Honegger, J., Fahlbusch, R., Jordan, S., Lowe, D.L., Lu, X., Besser, G.M. and Grossman, A.B. (1998). Mutation and expression analysis of the P27/Kip gene in corticotrophin-secreting tumours. Oncogene, 16, 69-76. The cyclin-dependent kinase inhibitor p27 is under-expressed in pituitary tumours leading to enhanced cell proliferation.
• Lidhar, K., Korbonits, M., Jordan, S., Khalimova, Kaltsas, G., Lu, X., Jenkins, P.J., Monson, J.P., Besser, G.M., Lowe, D.G. and Grossman, A.B. (1999). Low expression of the cell cycle inhibitor p27^Kip1 in normal corticotroph cells, corticotroph tumors, and malignant pituitary tumors. J. Clin. Endocrinol. Metab., 84, 3823-3830. P27 is phosphorylated in pituitary tumours leading to its degradation, which we subsequently demonstrated to be secondary to enhanced Akt and MAPK activities, implicating a cell-surface receptor in pitiuitary tumorigenesis.
• Isidori, A.M., Kaltsas, G.A., Mohammed, S., Morris, D., Jenkins, P.J., Chew, S.L., Monson, J.P., Besser, G.M. and Grossman, A.B. (2003). Discriminatory value of the low-dose dexamethasone suppression test in establishing the diagnosis and differential diagnosis of Cushing’s syndrome. J. Clin. Endocrinol. Metab., 88, 5299-5306. We demonstrated that the low-dose dexamethasone suppression test could be used more safely in place of the high-dose test to discriminate the cause of ACTH-dependent Cushing’s syndrome.
• Larkin, S.J., Preda, V., Karavitaki, N., Grossman, A. and Ansorge, O. (2014). BRAF V600E mutations are characteristic for papillary craniopharyngioma and may coexist with CTNNB1-mutated adamantinomatous craniopharyngioma. Acta Neuropathol., 127, 927-929 Contemporaneously with a group from Harvard, we established that BRAF mutations were the primary driver for papillary craniopharyngiomas.
• Walia, R., Chakraborty, A.M., Pandey, S., Rana, N., Kumar, R., Ahuja, C., Singh, H., Dhandapani, S., Sahoo, S.K., Chhabra, R., Singh, A., Bhadada, S.K., Mittal, B.R., Saikia, U.N., Grossman, A. and Shukla, J. (2025). Unveiling the hidden: A novel molecular imaging technique for localizing tumours in Cushing’s Disease. Eur. J. Med. Mol. Imag., 52(12), 4558-4568. With my colleagues in India, we have shown that radiolabelled desmopressin can differentiate Cushing’s disease from the ectopic ACTH syndrome.
• Pacak, K., Blake, M., Sweeney, A., Jha, A., Imperiale, A., Habbib, Raffaelli, M., Tudos, Z., Timmers, H., Grossman, A., Nolting, S. and Taieb, D. (2025). Adrenal Tumour Imaging: Clinical, Molecular and Radiomics aspects. Lancet Diabet. Endocrinol., in press. A total overview of all types of adrenal imaging and their interpretations and uses.
  
  

Collaborators

• Prof. Martyn Caplin, Royal Free Hospital, London
• Prof. Karel Pacak, Charles University, Prague, Czechia
• Prof. Svenja Nölting, LMU, Munich, Germany
• Prof. Gregory Kaltsas, Kapodistrian University of Athens, Greece

News

Frequent contributor to Guardian and Daily Mail health sections.

Teaching

• Regular input to weekly research meetings, MSc Course in Neuroendocrinology

Disclosures

None.