Rajesh Thakker

Last updated

Rajesh Thakker

FRS FMedSci FRCPath FRCPE FRCP
Professor Rajesh Thakker FMedSci FRS.jpg
Professor Rajesh Thakker in 2014, portrait via the Royal Society
Born
Rajesh Vasantlal Thakker

(1954-08-27) 27 August 1954 (age 69) [1]
Alma mater University of Cambridge (MA, MB BChir, MD, ScD)
SpouseJulie Clare Magee [1]
Awards Raymond Horton-Smith Prize (1994) [2]
Scientific career
Fields
Institutions
Website ocdem.ox.ac.uk/rajesh-thakker

Rajesh Vasantlal Thakker FRS FMedSci FRCPath FRCPE FRCP [3] (born 1954) is May Professor of Medicine in the Nuffield Department of Clinical Medicine at the University of Oxford and a fellow of Somerville College, Oxford. [4] Thakker is also a Consultant physician at the Churchill Hospital and the John Radcliffe Hospital, Principal investigator (PI) at the Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM) and was Chairman of the NIHR/MRC Efficacy and Mechanism Evaluation (EME) Board until Spring 2016. [5] [6] [7] [8] [9] [10] [11] [12]

Contents

Education

Thakker was educated at Pembroke College, Cambridge, where he was awarded his Master of Arts (MA), Bachelor of Medicine, Bachelor of Surgery (MB BChir), Doctor of Medicine (MD) and Doctor of Science (ScD) degrees. He completed his clinical training at Middlesex Hospital Medical School. [1]

Research and career

Thakker's research investigates neuroendocrine tumours such as multiple endocrine neoplasia type 1 (MEN1) [3] [11] [13] [14] and the molecular basis of disorders of calcium homeostasis. [7] He has supervised nine successful Doctor of Philosophy students [15] [16] [17] [18] [19] [20] [21] [22] [23] and his research has been funded by the Medical Research Council (MRC). [24]

Thakker has edited several books including Genetic and Molecular Biological Aspects of Endocrine Disease, [25] Molecular Genetics of Endocrine Disorders, [26] and Genetics of Bone Biology and Skeletal Disease. [27]

Awards and honours

Thakker was elected a Fellow of the Royal Society (FRS) in 2014. His nomination reads:

Thakker has made a sustained series of major contributions to endocrinology, particularly parathyroid and renal disorders affecting calcium homeostasis. His research at the basic-science and clinical interface has resulted in seminal gene discoveries and insights into molecular, cellular and physiological mechanisms. These include: identification of functional pathways of calcium-sensing, through characterisation of mutations of the calcium-sensing-receptor, a G-protein-coupled- receptor (GPCR), and its signalling pathway through G-protein-alpha-11-subunit (Gα11) and adaptor-protein-2-sigma-subunit (AP2σ), which regulates GPCR endocytosis; and defining a molecular-based taxonomy of syndromic and non-syndromic hyperparathyroid and hypoparathyroid disorders that has resulted in new pathophysiological insights and advances in diagnosis and treatment. [28]

Personal life

Thakker is married to Julie Clare Magee and has one daughter, Clare Thakker, who has qualified as a doctor from Clare College, Cambridge. [1] He is a school governor at Oxford High School, Oxford. [29]

Related Research Articles

<span class="mw-page-title-main">Multiple endocrine neoplasia</span> Group of genetic conditions

Multiple endocrine neoplasia is a condition which encompasses several distinct syndromes featuring tumors of endocrine glands, each with its own characteristic pattern. In some cases, the tumors are malignant, in others, benign. Benign or malignant tumors of nonendocrine tissues occur as components of some of these tumor syndromes.

<span class="mw-page-title-main">Zollinger–Ellison syndrome</span> Condition in which tumours stimulate excessive gastric acid production

Zollinger–Ellison syndrome is rare disease in which tumors cause the stomach to produce too much acid, resulting in peptic ulcers. Symptoms include abdominal pain and diarrhea.

<span class="mw-page-title-main">Parathyroid hormone</span> Mammalian protein found in Homo sapiens

Parathyroid hormone (PTH), also called parathormone or parathyrin, is a peptide hormone secreted by the parathyroid glands that regulates the serum calcium concentration through its effects on bone, kidney, and intestine.

Hypercalcemia, also spelled hypercalcaemia, is a high calcium (Ca2+) level in the blood serum. The normal range is 2.1–2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L), with levels greater than 2.6 mmol/L defined as hypercalcemia. Those with a mild increase that has developed slowly typically have no symptoms. In those with greater levels or rapid onset, symptoms may include abdominal pain, bone pain, confusion, depression, weakness, kidney stones or an abnormal heart rhythm including cardiac arrest.

<span class="mw-page-title-main">Hyperparathyroidism</span> Increase in parathyroid hormone levels in the blood

Hyperparathyroidism is an increase in parathyroid hormone (PTH) levels in the blood. This occurs from a disorder either within the parathyroid glands or as response to external stimuli.

<span class="mw-page-title-main">Pituitary adenoma</span> Human disease

Pituitary adenomas are tumors that occur in the pituitary gland. Most pituitary tumors are benign, approximately 35% are invasive and just 0.1% to 0.2% are carcinomas. Pituitary adenomas represent from 10% to 25% of all intracranial neoplasms and the estimated prevalence rate in the general population is approximately 17%.

<span class="mw-page-title-main">Walter Bodmer</span> German-born British human geneticist

Sir Walter Fred Bodmer is a German-born British human geneticist.

<span class="mw-page-title-main">Primary hyperparathyroidism</span> Medical condition

Primary hyperparathyroidism is a medical condition where the parathyroid gland produce excess amounts of parathyroid hormone (PTH). The symptoms of the condition relate to the resulting elevated serum calcium (hypercalcemia), which can cause digestive symptoms, kidney stones, psychiatric abnormalities, and bone disease.

<span class="mw-page-title-main">Multiple endocrine neoplasia type 1</span> Medical condition

Multiple endocrine neoplasia type 1 (MEN-1) is one of a group of disorders, the multiple endocrine neoplasias, that affect the endocrine system through development of neoplastic lesions in pituitary, parathyroid gland and pancreas. Individuals suffering from this disorder are prone to developing multiple endocrine and nonendocrine tumors. It was first described by Paul Wermer in 1954.

<span class="mw-page-title-main">Multiple endocrine neoplasia type 2</span> Medical condition

Multiple endocrine neoplasia type 2 is a group of medical disorders associated with tumors of the endocrine system. The tumors may be benign or malignant (cancer). They generally occur in endocrine organs, but may also occur in endocrine tissues of organs not classically thought of as endocrine. MEN2 is a sub-type of MEN and itself has sub-types, as discussed below. Variants in MEN2A have been associated with Hirschsprung disease. Screening for this condition can begin as young as eight years old for Pheochromocytoma.

<span class="mw-page-title-main">Osteitis fibrosa cystica</span> Medical condition

Osteitis fibrosa cystica is a skeletal disorder resulting in a loss of bone mass, a weakening of the bones as their calcified supporting structures are replaced with fibrous tissue, and the formation of cyst-like brown tumors in and around the bone. Osteitis fibrosis cystica (OFC), also known as osteitis fibrosa, osteodystrophia fibrosa, and von Recklinghausen's disease of bone, is caused by hyperparathyroidism, which is a surplus of parathyroid hormone from over-active parathyroid glands. This surplus stimulates the activity of osteoclasts, cells that break down bone, in a process known as osteoclastic bone resorption. The hyperparathyroidism can be triggered by a parathyroid adenoma, hereditary factors, parathyroid carcinoma, or renal osteodystrophy. Osteoclastic bone resorption releases minerals, including calcium, from the bone into the bloodstream, causing both elevated blood calcium levels, and the structural changes which weaken the bone. The symptoms of the disease are the consequences of both the general softening of the bones and the excess calcium in the blood, and include bone fractures, kidney stones, nausea, moth-eaten appearance in the bones, appetite loss, and weight loss.

<span class="mw-page-title-main">Albright's hereditary osteodystrophy</span> Form of osteodystrophy and a rare human disease

Albright's hereditary osteodystrophy is a form of osteodystrophy, and is classified as the phenotype of pseudohypoparathyroidism type 1A; this is a condition in which the body does not respond to parathyroid hormone.

Pseudohypoparathyroidism is a rare autosomal dominant genetic condition associated primarily with resistance to the parathyroid hormone. Those with the condition have a low serum calcium and high phosphate, but the parathyroid hormone level (PTH) is inappropriately high. Its pathogenesis has been linked to dysfunctional G proteins. Pseudohypoparathyroidism is a very rare disorder, with estimated prevalence between 0.3 and 1.1 cases per 100000 population depending on geographic location.

<span class="mw-page-title-main">Tertiary hyperparathyroidism</span> Medical condition

Tertiary hyperparathyroidism is a condition involving the overproduction of the hormone, parathyroid hormone, produced by the parathyroid glands. The parathyroid glands are involved in monitoring and regulating blood calcium levels and respond by either producing or ceasing to produce parathyroid hormone.

<span class="mw-page-title-main">Endocrine disease</span> Medical condition

Endocrine diseases are disorders of the endocrine system. The branch of medicine associated with endocrine disorders is known as endocrinology.

<span class="mw-page-title-main">RET proto-oncogene</span> Mammalian protein

The RETproto-oncogene encodes a receptor tyrosine kinase for members of the glial cell line-derived neurotrophic factor (GDNF) family of extracellular signalling molecules. RET loss of function mutations are associated with the development of Hirschsprung's disease, while gain of function mutations are associated with the development of various types of human cancer, including medullary thyroid carcinoma, multiple endocrine neoplasias type 2A and 2B, pheochromocytoma and parathyroid hyperplasia.

<span class="mw-page-title-main">MEN1</span> Protein

Menin is a protein that in humans is encoded by the MEN1 gene. Menin is a putative tumor suppressor associated with multiple endocrine neoplasia type 1 and has autosomal dominant inheritance. Variations in the MEN1 gene can cause pituitary adenomas, hyperparathyroidism, pancreatic neuroendocrine tumors, gastrinoma, and adrenocortical cancers.

<span class="mw-page-title-main">Calcium-sensing receptor</span> Mammalian protein found in Homo sapiens

The calcium-sensing receptor (CaSR) is a Class C G-protein coupled receptor which senses extracellular levels of calcium ions. It is primarily expressed in the parathyroid gland, the renal tubules of the kidney and the brain. In the parathyroid gland, it controls calcium homeostasis by regulating the release of parathyroid hormone (PTH). In the kidney it has an inhibitory effect on the reabsorption of calcium, potassium, sodium, and water depending on which segment of the tubule is being activated.

<span class="mw-page-title-main">Adrenal gland disorder</span> Medical condition

Adrenal gland disorders are conditions that interfere with the normal functioning of the adrenal glands. Your body produces too much or too little of one or more hormones when you have an adrenal gland dysfunction. The type of issue you have and the degree to which it affects your body's hormone levels determine the symptoms.

<span class="mw-page-title-main">Annette Dolphin</span> Professor of Pharmacology

Annette Catherine Dolphin is a Professor of Pharmacology in the Department of Neuroscience, Physiology and Pharmacology at University College London (UCL).

References

  1. 1 2 3 4 Anon (2014). "Thakker, Prof. Rajesh Vasantlal" . Who's Who (online edition via Oxford University Press  ed.). A & C Black. doi:10.1093/ww/9780199540884.013.U37302.(Subscription or UK public library membership required.)
  2. ↑ ORCID   0000-0002-1438-3220
  3. 1 2 3 "Professor Rajesh Thakker FRS FMedSci". acmedsci.ac.uk. Academy of Medical Sciences.
  4. ↑ Professor Rajesh Thakker, Somerville College, University of Oxford
  5. ↑ "EME Programme appoint new Chair of Funding Board". www.nihr.ac.uk. Archived from the original on 17 September 2016.
  6. ↑ Prof Rajesh V Thakker, Oxford Centre for Diabetes, Endocrinology and Metabolism OCDEM
  7. 1 2 Rajesh Thakker publications indexed by the Scopus bibliographic database. (subscription required)
  8. ↑ Holmes, David (2013). "Rajesh Thakker: A man of hidden depths". The Lancet Diabetes & Endocrinology. 1 (4): 274. doi: 10.1016/S2213-8587(13)70196-7 . PMID   24622412.
  9. ↑ Lloyd, S. E.; Pearce, S. H.; Fisher, S. E.; Steinmeyer, K; Schwappach, B; Scheinman, S. J.; Harding, B; Bolino, A; Devoto, M; Goodyer, P; Rigden, S. P.; Wrong, O; Jentsch, T. J.; Craig, I. W.; Thakker, R. V. (1996). "A common molecular basis for three inherited kidney stone diseases". Nature. 379 (6564): 445–9. Bibcode:1996Natur.379..445L. doi:10.1038/379445a0. hdl: 11858/00-001M-0000-0012-CBFE-2 . PMID   8559248. S2CID   4364656.
  10. ↑ Modlin, I. M.; Oberg, K.; Chung, D. C.; Jensen, R. T.; De Herder, W. W.; Thakker, R. V.; Caplin, M.; Delle Fave, G.; Kaltsas, G. A.; Krenning, E. P.; Moss, S. F.; Nilsson, O.; Rindi, G.; Salazar, R.; Ruszniewski, P.; Sundin, A. (2008). "Gastroenteropancreatic neuroendocrine tumours". The Lancet Oncology. 9 (1): 61–72. doi:10.1016/S1470-2045(07)70410-2. PMID   18177818. S2CID   46127116.
  11. 1 2 Pearce, S. H.; Williamson, C; Kifor, O; Bai, M; Coulthard, M. G.; Davies, M; Lewis-Barned, N; McCredie, D; Powell, H; Kendall-Taylor, P; Brown, E. M.; Thakker, R. V. (1996). "A familial syndrome of hypocalcemia with hypercalciuria due to mutations in the calcium-sensing receptor". The New England Journal of Medicine. 335 (15): 1115–22. doi: 10.1056/NEJM199610103351505 . PMID   8813042.
  12. ↑ Carpten, J. D.; Robbins, C. M.; Villablanca, A; Forsberg, L; Presciuttini, S; Bailey-Wilson, J; Simonds, W. F.; Gillanders, E. M.; Kennedy, A. M.; Chen, J. D.; Agarwal, S. K.; Sood, R; Jones, M. P.; Moses, T. Y.; Haven, C; Petillo, D; Leotlela, P. D.; Harding, B; Cameron, D; Pannett, A. A.; Höög, A; Heath h, 3rd; James-Newton, L. A.; Robinson, B; Zarbo, R. J.; Cavaco, B. M.; Wassif, W; Perrier, N. D.; Rosen, I. B.; et al. (2002). "HRPT2, encoding parafibromin, is mutated in hyperparathyroidism-jaw tumor syndrome". Nature Genetics. 32 (4): 676–80. doi:10.1038/ng1048. PMID   12434154. S2CID   23713328.{{cite journal}}: CS1 maint: numeric names: authors list (link)
  13. ↑ Brandi, M. L.; Gagel, R. F.; Angeli, A; Bilezikian, J. P.; Beck-Peccoz, P; Bordi, C; Conte-Devolx, B; Falchetti, A; Gheri, R. G.; Libroia, A; Lips, C. J.; Lombardi, G; Mannelli, M; Pacini, F; Ponder, B. A.; Raue, F; Skogseid, B; Tamburrano, G; Thakker, R. V.; Thompson, N. W.; Tomassetti, P; Tonelli, F; Wells Jr, S. A.; Marx, S. J. (2001). "Guidelines for diagnosis and therapy of MEN type 1 and type 2". The Journal of Clinical Endocrinology and Metabolism. 86 (12): 5658–71. doi: 10.1210/jcem.86.12.8070 . PMID   11739416.
  14. ↑ Lemmens, I; Van De Ven, W. J.; Kas, K; Zhang, C. X.; Giraud, S; Wautot, V; Buisson, N; De Witte, K; Salandre, J; Lenoir, G; Pugeat, M; Calender, A; Parente, F; Quincey, D; Gaudray, P; De Wit, M. J.; Lips, C. J.; Höppener, J. W.; Khodaei, S; Grant, A. L.; Weber, G; Kytölä, S; Teh, B. T.; Farnebo, F; Thakker, R. V. (1997). "Identification of the multiple endocrine neoplasia type 1 (MEN1) gene. The European Consortium on MEN1". Human Molecular Genetics. 6 (7): 1177–83. doi: 10.1093/hmg/6.7.1177 . PMID   9215690.
  15. ↑ Bowl, Michael Richard (2003). Molecular genetics of hypoparathyroid disorders (DPhil thesis). University of Oxford. EThOS   uk.bl.ethos.275359.
  16. ↑ Bradley, Karin J. (2006). Molecular genetics of the hyperparathyroidism-jaw tumour syndrome (DPhil thesis). University of Oxford.
  17. ↑ Gaynor, Katherine Ursula (2011). The role of the transcription factor GATA3 in calcium homeostasis and tumourigenesis (DPhil thesis). University of Oxford.
  18. ↑ Leotlela, Poloko D. (2003). Molecular genetics of multiple endocrine neoplasia type 1 and related disorders (DPhil thesis). University of Oxford.
  19. ↑ Loureiro de Lemos, Manuel C. (2007). Genetic and phenotypic studies of the multiple endocrine neoplasia type 1 syndrome (DPhil thesis). University of Oxford. EThOS   uk.bl.ethos.445777.
  20. ↑ Javid, Mahsa (2012). Gene modifiers and novel therapies for multiple endocrine neoplasia type 1 (DPhil thesis). University of Oxford.
  21. ↑ Jeyabalan, Jeshmi (2008). Role of sedlin in spondyloepiphyseal dysplasia tarda (DPhil thesis). University of Oxford. EThOS   uk.bl.ethos.496979.
  22. ↑ Turner, Jeremy James Osborne (2003). Molecular genetics of renal tubular disorders affecting urate transport (DPhil thesis). University of Oxford.
  23. ↑ Wu, Fiona (2014). Dent's disease and the chloride channel, CLC-5 (DPhil thesis). University of Oxford.
  24. ↑ UK Government research grants awarded to Rajesh Thakker, via Research Councils UK
  25. ↑ Thakker, R. V (1995). Genetic and Molecular Biological Aspects of Endocrine Disease. SPCK. ISBN   9780702019456.
  26. ↑ Thakker, R. (4 September 1998). Molecular Genetics of Endocrine Disorders. Taylor & Francis. ISBN   9780412589706.
  27. ↑ Thakker, R. V; Whyte, Michael P; Eisman, John; Igarashi, Takashi (2013). Genetics of Bone Biology and Skeletal Disease. Academic Press. ISBN   9780123878298.
  28. ↑ "Professor Rajesh Thakker FMedSci FRS". London: The Royal Society. Archived from the original on 5 August 2014.
  29. ↑ "Oxford High School GDST School Governors". Archived from the original on 4 July 2014.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.