Who invented qMIDS?
Dr Muy-Teck Teh pursued his Biomedical Science degree (B.Sc. Hons, 1996) followed by PhD in Physiology (2000) at King’s College London. Following two postdoctoral training positions funded by Wellcome Trust and Cancer Research UK, he is currently a tenured Senior Lecturer (Associate Professor) in Head and Neck Cancer at the Barts & the London School of Medicine & Dentistry, Queen Mary University of London, leading a transnational research group investigating cancer biomarker discovery, molecular diagnostics and prognostics. He aims to translate basic science into clinical applications and towards personalised medicine based on molecular signatures. Dr Teh has international collaborators from USA, Norway, Switzerland, India, Pakistan, Sri Lanka, Malaysia and China on clinical translation of the world’s first FOXM1-based digital squamous cancer test – “qMIDS” for quantitative cancer diagnosis and prognosis. A second generation qMIDSV2 with significantly improved performance, validated in over 535 patients from UK, China and India, has been shown to be able to detect high-risk oral lesions.
Current Research
Dr Teh identified and delineated the mechanism of a key driver oncogene FOXM1 in human cancer1-11 which subsequently led to the Molecule of the Year 2010 Award12. He later pioneered the world first FOXM1-based digital molecular cancer test - "quantitative malignancy diagnostic system (qMIDS)" for early detection oral cancer risk21. The qMIDS test has been validated on several hundreds of oral cancer patients from UK, Norway, China and India with highly accurate results (>90%) compared to conventional histopathology13,14,21. The qMIDS test requires only a tiny 1 mm (a grain of rice) tissue biopsy and test results could be obtained within 90 mins by measuring 16 genes to produce a malignancy index via an algorithm13. The qMIDS test may potentially revolutionise oral cancer diagnosis in the future by providing a cost-effective, fully automated, high-throughput, rapid, quantitative, digital diagnostic system for managing ever increasing population of patients with oral lesions. Rapid segregation and release of majority (>90%) of low risk patients from surveillance whilst channelling funding and resources to treat high-risk patients will result in long-term benefits for both the patients and healthcare establishments.
Lay articles of Dr Teh's qMIDS research:
Animated video summary [YouTube] [Chinese subtitled version 中文字幕版]
Executive research summary on Scientia (21 Oct 2020): [webpage] [PDF]
Profile article on Open Access Government (13 Nov 2020): [webpage]
A brief overview of Dr Teh's other research areas:
Identification of exosome biomarkers for developing non-invasive salivary or blood-based diagnostic tests15.
New molecular signatures were found to characterise a clinically distinct UK population of oral cancer patients that may be predisposed to therapeutic resistance16.
Using a three-dimensional (3D) culture and xenograft tumour models, a novel mechanism regulated by FOXM1 was found to promote aberrant differentiation in squamous differentiation17.
He further discovered the squamous differentiation mechanism could be perturbed by serum lipids, retinoic acid and phenol red, raised important issues with using cell culture models18.
Using in vitro and in vivo mouse models, a new target tumour suppressor gene RASSF1A was found to be regulated via a YAP pathway in nasopharyngeal carcinoma cells19.
Tobacco is a risk factor for oral cancer, recent discovery using a zebrafish model identified a genetic locus (Slit3) regulates nicotine addiction in human20 could lead to new ways to prevent or treat tobacco addiction thereby eliminating a key risk factor for many cancers including oral cancer.
Role and mechanism of vimentin in cancer metastasis22,23,24.
Receptors for SARS-CoV-2 entry in oral mucosa and OSCC25.
Mouthwashes on salivary SARS-CoV-2 viral load randomised controlled pilot study26.
Identification of two multidrug chemoresistant genes (NEK2 and INHBA) and found a naturally occurring fungal derivative Sirodesmin A and a licensed anticancer drug Carfilzomib, both targeting NEK2 and INHBA, could re-sensitise resistant HNSCC cells to cisplatin27.
Molecular Pattern Recognition
in Pre-Cancer Cells
in Pre-Cancer Cells
All cellular processes are tightly regulated by a complex network of interacting biomolecules. Given that mRNA transcription precedes protein translation, change in gene expression levels often precedes visible pathological manifestation. Hence, transcriptome instability in the form of gene expression alterations serves as key signals for subsequent disease initiation and manifestation. Dr Teh hypothesised that if we could recognise and measure cancer-associated transcriptome instability, this could enable better understanding of cancer initiation and smarter way to predict cancer risk13,14 in otherwise asymptomatic patients7-9. With the help of Artificial Intelligence (AI), this study could be translated into a clinically useful clinical AI tool for risk prediction before disease manifestation.
Molecular Patterns of Therapeutic Resistance
in Cancer Cells
in Cancer Cells
Multidrug resistance renders chemotherapeutic treatment failure in large proportion of head and neck squamous cell carcinoma (HNSCC) patients requiring multimodal therapy involving chemotherapy in conjunction with surgery and/or radiotherapy. Molecular events conferring chemoresistance remain unclear. This project investigates a number of chemical, biological and physical strategies for targeting molecular vulnerabilities of chemoresistant cancer cells whilst sparing non-cancer cells. A large panel of chemical library consisting of synthetic and natural compounds will be screened using human cell culture models. We aim to identify the most potent multimodal anticancer therapy with the least toxicity to prevent or reverse chemoresistance in HNSCC patients.
Key References
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