Professor Ahmad Waseem, BSc, MSc, MPhil, PhD (Biochemistry)
Professor of Molecular and Cellular Oral Biology
Email: email@example.comTelephone: +44 (0) 20 7882 2387Room Number: G81, Blizard Building, Institute of Dentistry
Dr. Ahmad Waseem is a Professor of Molecular and Cellular Oral Biology at the Centre for Immunobiology and Regenerative Medicine, Institute of Dentistry.
He obtained his PhD from the Department of Biochemistry, Jawaharlal Nehru Medical College, Aligarh Muslim University, India, in 1983 and spent 4 years as a post-doctoral research fellow at the University of Chicago, USA. In 1987 he came to the United Kingdom and joined Clare Hall Laboratories, Imperial Cancer Research Fund (now part of CRUK) to work on a three-year post-doctoral research associate position. After spending a year in the University of Dundee, Scotland, Dr Waseem joined King’s College London (then United Medical and Dental Schools of Guy’s and St Thomas’s Hospitals, UMDS) in 1992 as a Lecturer in Oral Biology. In 1998 he spent six months at the Department of Biochemistry, NYU Medical Centre, New York, USA on a sabbatical. He then joined the Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, in May 2003 as a Reader in Oral Biology. The title of Professor of Molecular and Cellular Oral Biology was conferred upon him in 2015. He received Queen Mary ADEPT Fellowship in 2017 for his extensive experience of teaching Biochemistry, Cell and Molecular Biology at both undergraduate and post-graduate levels.
Professor Waseem has supervised more than 40 researchers including 13 PhDs all of whom have gone on to hold high academic/industry positions both in this country and abroad. He has also examined several PhD theses from Universities both from in and outside the UK. He has collaborations with national and international research groups on both basic and clinical aspects of his research. He is on the editorial board of a number of International journals and regularly provides his expert opinion on submitted manuscripts and grant proposals. He publishes his research in high impact peer-reviewed international journals.
Professor Waseem teaches Biochemistry to 1st year BDS and Cell and Molecular Biology to 3rd year Biomed students. He also teaches Cell and Molecular Biology to MSc Experimental Oral Pathology and MSc Oral Biology students. He is the lead for “Oral Biology for Biomedical Sciences” Module BMD357, an optional module available to 3rd year Biomed students. This is the only dentally oriented optional module offered to the Biomed students.
Professor Waseem started his research career in Biochemistry as a PhD student during which he studied interaction of proteins with multi-valent ligands in order to understand the mechanism that leads to the formation of large insoluble complexes such as blood clots. These studies led him to publish 6 papers in national and international journals.
As a post-doctoral research fellow at the University of Chicago (USA) he was interested in protein associations in the cytoskeleton of human red blood cells (HRBC). He discovered that glycolytic enzymes, such as glyceraldehyde 3-phosphate dehydrogenase, can associate with the plasma membrane in intact cells leading to suppression of the enzyme activity and regulation of glycolytic pathway. He also discovered protein kinase C (PKC) activity in HRBC, which translocated to plasma membrane in response to phorbol ester treatment exactly the same way as was reported for the brain enzyme. His most notable achievement was the identification of a novel protein complex in HRBC cytoskeleton, which was an excellent substrate for PKC and was later named as ‘Adducin’. He also identified similar protein complexes in non-erythroid cells such as fibroblasts. These proteins have since been shown by others as a component of actin cytoskeleton and play vital roles in cell motility.
He continued his research interest in cytoskeletal proteins especially of Intermediate Filament types at Clare Hall Laboratories, Imperial Cancer Research Fund (now part of CRUK). He made an Important discovery related to the chromosomal localisation of keratin genes. He found that a type I keratin gene, KRT18, was located on chromosome 12 instead of chromosome 17, where rest of the type I genes were located. This is the first and the only exception ever reported for this family of genes. This discovery had important implication for the evolutionary relationship of KRT18 with other members of this gene family.
At King’s College London he started his research as an independent researcher where initially he focussed on characterisation of keratin antibody epitopes and their involvement in filament assembly. He showed that certain keratin antibody epitopes were discontinuous and were shared between two different polypeptides. An important finding was that the heterotypic associations between complementary keratin polypeptides induced conformational changes essential for the filament assembly. Most of his research during this period was directed on identifying the role of anomalous keratinocyte differentiation in several cutaneous diseases manifested by changes in keratin protein expression.
At the Institute of Dentistry, Queen Mary University of London, Professor Waseem further explored the keratin expression as a biomarker for keratinocyte differentiation in health and disease. He showed that keratin K15 expression was a reliable biomarker for stem cells located in the basal layer of follicular and interfollicular epidermis and the expression is downregulated in response to inflammatory signals associated with skin conditions such as psoriasis and hypertropic scar. His more recent research has focussed on understanding the molecular mechanisms that regulate keratinocyte differentiation and growth. The alterations in keratin expression provide a reliable diagnostic and prognostic tools for squamous cell carcinoma (SCC) of skin and oral cavity. His group is evaluating expression of specific keratin as biomarkers for head and neck squamous cell carcinoma (HNSCC) associated with HPV16 infection for patient stratification and personalised treatment. He is also interested in understanding the mechanism(s) that allows expression of differentiation-specific keratins to be suppressed in SCCs. A related aspect of his research is to decipher the mechanism of suppression of epithelial phenotype and induction of mesenchymal features during epithelial-mesenchymal transition that allows solid tumours to metastasise and become life threatening. His group is testing a novel hypothesis that molecular changes that induce expression of vimentin, a type III intermediate filament protein, during oncogenesis is responsible for transcriptionally suppressing keratin expression and other epithelial specific genes.
Lallia A, Aldehlawi H, Buchanan JAG, Seoudi N, Fortune F, Waseem A (2020) Screening for oral cancer utilising risk-factor analysis is ineffective in high - risk populations. Brit J Oral Max Surg (in press).
Waseem NH, Low S, Shah AZ, Avisetti D, Ostergaard P, Simpson M, Niemiec KA, Martin-Martin B, Aldehlawi H, Usman S, Lee PS, Khawaja AP, Ruddle JB, Shah A, Sackey E, Day A, Jiang Y, Swinfield G, Viswanathan A, Alfano G, Chakarova C, Cordell HJ, Garway-Heath DF, Khaw PT, Bhattacharya SS, Waseem A, Foster PJ (2020) Mutations in SPATA13/ASEF2 cause primary angle closure glaucoma. PLoS Genet. 16:e1008721. doi: 10.1371/journal.pgen.1008721
Aldehlawi H, Usman S, Lalli A, Ahmad F, Williams G, Teh MT, Waseem A. (2020) Serum lipids, retinoic acid and phenol red differentially regulate expression of keratins K1, K10 and K2 in cultured keratinocytes. Sci Rep. 10:e4829. doi: 10.1038/s41598-020-61640-9.
Haider A, Waseem A, Karpukhina N, Mohsin S (2020) Strontium- and zinc-containing bioactive glass and alginates scaffolds. Bioengineering (Basel). 7: e10. doi: 10.3390/bioengineering7010010.
Qadir F, Lalli A, Dar HH, Hwang S, Aldehlawi H, Ma H, Dai H, Waseem A, Teh MT. (2019) Clinical correlation of opposing molecular signatures in head and neck squamous cell carcinoma. BMC Cancer. 19:830. doi: 10.1186/s12885-019-6059-5.
Aldehlawi H, Niemiec KA, Avisetti DR, Lalli A, Teh MT, Waseem A. (2019) The monoclonal antibody EPR1614Y against the stem cell biomarker keratin K15 lacks specificity and reacts with other keratins. Sci Rep. 9:e1943. doi: 10.1038/s41598-018-38163-5.
Qadir F, Aziz MA, Sari CP, Ma H, Dai H, Wang X, Raithatha D, Da Silva LGL, Hussain M, Poorkasreiy SP, Hutchison IL, Waseem A, Teh MT. (2018) Transcriptome reprogramming by cancer exosomes: identification of novel molecular targets in matrix and immune modulation. Mol Cancer. 17:97. doi: 10.1186/s12943-018-0846-5.
Maruthappu T, Chikh A, Fell B, Delaney PJ, Brooke MA, Levet C, Moncada-Pazos A, Ishida-Yamamoto A, Blaydon D, Waseem A, Leigh IM, Freeman M, Kelsell DP (2017) Rhomboid family member 2 regulates cytoskeletal stress-associated keratin 16. Nat Commun. 8:e14174. doi: 10.1038/ncomms14174.
Brown L, Waseem A, Cruz IN, Szary J, Gunic E, Mannan T, Unadkat M, Yang M, Valderrama F, O′Toole EA and Wan H (2014) Desmoglein 3 promotes cancer cell migration and invasion by regulating activator protein 1 and protein kinase C-dependent-ezrin activation. Oncogene 33: 2363. doi: 10.1038/onc.2013.186
Bose A, Teh MT, Mackenzie IC, Waseem A (2013) Keratin K15 as a biomarker of epidermal stem cells Int J Mol Sci. 14: e19385. doi: 10.3390/ijms141019385
Hwang S, Mahadevan S, Qadir F, Hutchison IL, Costea DE, Neppelberg E, Liavaag PG, Waseem A, The MT (2013) Identification of FOXM1‐induced epigenetic markers for head and neck squamous cell carcinomas. Cancer 119:4249.
Teh MT, Hutchison IL, Costea DE, Neppelberg E, Liavaag PG, Purdie K, Harwood C, Hong Wan, EW, Hackshaw A, Waseem A (2013) Exploiting FOXM1‐orchestrated molecular network for early squamous cell carcinoma diagnosis and prognosis. Intl J Cancer 132:2095.
Bose A, The MT, Hutchison IL, Wan H, Leigh IM, Waseem A (2012) Two mechanisms regulate keratin K15 expression in keratinocytes: role of PKC/AP-1 and FOXM1 mediated signalling. PLoS One 7: e38599. doi: 10.1371/journal.pone.0038599
Teh MT, Gemenetzidis E, Patel D, Tariq R, Nadir A, Bahta AW, Waseem A, Hutchison IL (2012) FOXM1 induces a global methylation signature that mimics the cancer epigenome in head and neck squamous cell carcinoma. PLoS One 7: e34329. doi: 10.1371/journal.pone.0034329
Waseem A, Ali M, Odell EW, Fortune F and The MT (2010) Downstream targets of FOXM1: CEP55 and HELLS are cancer progression markers of head and neck squamous cell carcinoma. Oral Oncology 46: 536. doi: 10.1016/j.oraloncology.2010.03.022