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  Key Publications  

Akıncılar SC, Khattar E, Boon PL, Unal B, Fullwood MJ, Tergaonkar V
Long-Range Chromatin Interactions Drive Mutant TERT Promoter Activation. 
Cancer Discovery. 2016 Nov;6(11):1276-1291.

Khattar E, Kumar P, Liu CY, Akıncılar SC, Raju A, Lakshmanan M, Maury JJ, Qiang Y, Li S, Tan EY, Hui KM, Shi M, Loh YH, Tergaonkar V.
Telomerase reverse transcriptase promotes cancer cell proliferation by augmenting tRNA expression. 
Journal of Clinical Investigation
. 2016 Oct 3;126(10):4045-4060. doi: 10.1172/JCI86042.

Li Y, Zhou QL, Sun W, Chandrasekharan P, Cheng HS, Ying Z, Lakshmanan M, Raju A, Tenen DG, Cheng SY, Chuang KH, Li J, Prabhakar S, Li M, Tergaonkar V.
Non-canonical NF-κB signalling and ETS1/2 cooperatively drive C250T mutant TERT promoter activation. 
Nature Cell Biology (article).
2015 Oct;17(10):1327-38

Cheryl M Koh, Ekta Khattar, Shi Chi Leow, Chia Yi Liu, Julius Muller, Wei Xia Ang, Yinghui Li, Guido Franzoso, Shang Li, Ernesto Guccione and Vinay Tergaonkar. (2015).
Telomerase regulates Myc dependent Oncogenesis independent of its reverse transcriptase activity.
Journal of Clinical Investigation. In Press.

Shin, E.M,. Lee, M., Goh , J., Ong, H., Ong, CW., Mendoz, E., Sun, W., Kong, X., Tan, T., Salto-Tellez, M., Putti, TC., Zhu, T., Thiery, J.P., Miyamoto, S., Kumar, A.P.,  Tergaonkar, V. (2014).
DP103 defines the metastatic potential of human breast cancers. 
Journal of Clinical Investigation.

Ghosh A, Saginc G, Leow SC, Khattar E, Shin EM, Yan TD, Wong M, Zhang Z, Li G, Sung WK, Zhou J, Chng WJ, Li S, Liu E, Tergaonkar V. (2012)
Telomerase directly regulates NF-κB-dependent transcription.
Nature Cell Biology (article) 2012 Dec;14(12):1270-81. doi: 10.1038/ncb2621. Epub 2012 Nov 18.

Zhao-Hui Wu, Ee Tsin Wong, Yuling Shi, Zhijian Chen, Shigeki Miyamoto and Vinay Tergaonkar. (2010).
ATM-dependent ELKS ubiquitination coordinates IKK activation in response to genotoxic stress.
Molecular Cell.
40(1): 75-86.

Hsiangling Teo, Sourav Ghosh , Hendrik Luesch , Ee Tsin Wong, Arkasubhra Ghosh, Najib Malik, Anthony Orth, Paul de Jesus, Anthony S Perry, Jeffrey D. Oliver, Nhan L. Tran, Lisa J. Speiser, Enrique Saez,  Peter Schultz, Sumit Chanda, Inder M Verma and Vinay Tergaonkar. (2010).
Telomere independent Rap1 is an IKK-adaptor and regulates NFkB- dependent gene expression.
Nature Cell Biology (article) 12(8): 758-67.

Chew J, Biswas S, Shreeram S, Humaidi M, Wong ET, Dhillion MK, Teo H, Hazra A, Fang CC, López-Collazo E, Bulavin DV, Tergaonkar V. (2009).
WIP1 phosphatase is a negative regulator of NF-kappaB signalling.
Nature Cell Biology.
11(5), 659-66.

Xia Y, Padre RC, De Mendoza TH, Bottero V, Tergaonkar VB*, Verma IM. (2009).
Phosphorylation of p53 by IkappaB kinase 2 promotes its degradation by beta-TrCP.
Proc Natl Acad Sci U S A. 106(8), 2629-34. * Corresponding Author

Vince JE, Wong WW, Khan N, Feltham R, Chau D, Ahmed AU, Benetatos CA, Chunduru SK, Condon SM, McKinlay M, Brink R, Leverkus M, Tergaonkar V, Schneider P, Callus BA, Koentgen F, Vaux DL, Silke J. (2007).
IAP antagonists target cIAP1 to induce TNFalpha-dependent apoptosis.
Cell. 131(4), 682-93.

Biswas SK, Bist P, Dhillon MK, Kajiji T, Del Fresno C, Yamamoto M, Lopez-Collazo E, Akira S, Tergaonkar V. (2007).
Role for MyD88-independent, TRIF pathway in lipid A/TLR4-induced endotoxin tolerance.
Journal of Immunology. 179(6), 4083-92. IF:6

Tergaonkar V*, Perkins ND. (2007).
p53 and NF-kappaB crosstalk: IKKalpha tips the balance.
Molecular Cell.
26(2), 158-9. *Corresponding author. IF:14

Basak S, Kim H, Kearns JD, Tergaonkar V, O'Dea E, Werner SL, Benedict CA, Ware CF, Ghosh G, Verma IM, Hoffmann A. (2007).
A fourth IkappaB protein within the NF-kappaB signaling module.
128(2), 369-81.

Ghosh S, Tergaonkar V*, Rothlin CV, Correa RG, Bottero V, Bist P, Verma IM, Hunter T. (2006).
Essential role of tuberous sclerosis genes TSC1 and TSC2 in NF-kappaB activation and cell survival.
Cancer Cell. 10(3), 215-26. *Co-first author

Tergaonkar, V., Correa, R.G., Ikawa, M. and Verma, I.M. (2005).
Distinct roles of IkappaB proteins in regulating constitutive NF-kappaB activity.
Nature Cell Biology. 7, 921-923.

Tergaonkar, V., Pando, M., Vafa, O., Wahl, G. and Verma I.M. (2002).
p53 stabilization is decreased upon NFkB activation: a role for NFkB in acquisition of resistance to chemotherapy.
Cancer Cell. 1, 493-503.


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Vinay Tergaonkar obtained his Ph.D in 2001. During his graduate studies he was awarded an international cancer society (UICC) fellowship for collaborative research at Tufts University, Boston, USA. He has been a fellow (2001-2004) and a special fellow (2004-present) of the Leukemia and Lymphoma Society of America and conducted his postdoctoral studies at the Salk Institute for Biological Studies, La Jolla, California. He joined IMCB in late 2005 as Principal Investigator and became a Senior Principal Investigator in 2010 and Research Director in 2015. He is also a Professor at the school of Medicine, National University of Singapore.

He also holds adjunct appointments at 1) Cancer Science Institute, Singapore, 2) Singapore Eye Research Institute and a visiting position at CCB/UniSA, Australia. He has been invited to speak at various international venues and meetings such as the Barossa and Hunter valley meetings in Australia, Genes and Cancer meeting in UK, The Argentine Pharmacological society meeting in Buenos Aires, Aichi and Japanese Cancer Society meetings in Japan and the Keystone Symposia. He serves on Editorial Boards of 1) Molecular and Cellular Biology (American Society for Microbiology), 2) Biochemical Journal (Portland Press) 3) Critical Reviews in Oncology/Hematology (Elsevier Press), 4) BMC Research Notes (Biomed Central) and 5) Telomeres and Telomerase. Work from his laboratories has led to international recognition, including the British council development award (2014) and the Premier's fellowship from Government of South Australia (2015).

    Inflammation, Cancer epigenetics and Metabolism

Inflammation involving the innate and adaptive immune systems is a normal response to infection. However, it is now known that when allowed to continue unchecked, chronic inflammation is a key underlying cause for the development of autoimmune disorders, neurodegenerative diseases, metabolic syndromes such as diabetes and cancer. Our lab studies a transcription factor called NFkB which is a master regulator of inflammation. Indeed deregulated activity of NFkB precedes and is causally linked to chronic inflammation and the development of several human ailments including metabolic syndromes and cancers. However, given that NFkB signaling is also essential for many housekeeping cellular and developmental events in normal human beings, simply blocking NFkB B to curb inflammation is not an option. Hence deciphering the regulation of NFkB signaling is crucial to understanding the mechanism and role of uncontrolled/unwanted NFkB activity seen in human ailments and in developing better and safer anti-inflammatory drug. We are focusing and our efforts to identify targets that will help develop drugs which will block NFkB /inflammation more selectively and not generically and hence may have less side effects.

a) Mechanisms that initiate and maintain chronic inflammation in cancer

Chronic Inflammation such as that triggered by infectious agents is a key driver of human cancers. Two sets of Nobel prizes were awarded in last 7 years (a) to discovery of Helicobacter as cause of gastric cancers (2005) and (b) to the discovery of Human Papilloma Virus as a causative agent for cervical cancer (2008). However, even in cancers where these infectious agents are not present, inflammation is now known as a key driver. That is why people on asprin (an anti-inflammatory drug) have significantly lower risk of some cancers and on the other hand, obese individual (who have chronic inflammation) without infectious agents have more cancers of certain kind. But what activates and sustains chronic inflammation in cancers is not understood at all. Another hallmark of all human cancers is that cancer cells divide endlessly and for this they need an enzyme called telomerase (discovery of which received Nobel prize in 2009). But many pieces of evidence suggest that telomerase enzyme has other roles apart from making cells divide endlessly. We find time that telomerase enzyme, is the key missing link that in addition to its role in cell division also kick starts and maintains chronic inflammation in cancers. Our findings have immense therapeutic implications and we are developing drugs blocking this enzyme and find that in experiental settings such thearpies are showing promising results in blocking cancer inflammation and cancer cell division.

b) New epigenetic controls of inflammation

Deciphering the regulation of critical regulators of inflammation such as NFkB is crucial to understanding the mechanism and role of constitutive NFkB activity seen in human ailments. Given that over 200 physiological stimuli activate NFkB, which in turn regulates an equally large number of genes, understanding how specificity is generated in such a pleiotropic pathway is also a major challenge. Using large-scale functional genomics and proteomic approaches, our group has identified several novel modifiers of NFkB activity. Using genetic and epigenetic approaches, we are keen to decipher the mechanisms by which these novel regulators modulate NFkB and hence chronic inflammation in human aimments.

c) Mechanisms that regulate chronic inflammation in metabolic syndrome

Type 2 diabetes (T2D) and one of its major risk factors, obesity are pandemic problem. Inherent genetic predispositions in combination with inappropriate diet and sedentary lifestyle contribute to the pathogenesis of these disorders. A better understanding of inflammatory signaling is critical for development of therapeutic strategies towards T2DM and obesity. As part of a directed screen to identify molecules that respond to dietary and inflammatory cues in adipose tissue during development of obesity and insulin resistance, we have identified several signaling molecules. Of particular mention is a protein called NUCKS (Nuclear Ubiquitous Casein and cyclin-dependent Kinase Substrate), expression of which is inversely correlated with body mass index in humans and body fat in mice. Ablation of NUCKS results in weight gain, increased body fat accumulation, glucose intolerance and insulin resistance. NUCKS is a key chromatin modifier and transcriptional regulator of a number of signaling genes. We are characterizing the roles of proteins like NUCKS in metabolic syndromes.

Prospective Graduate Students:

SINGA fellowships:

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Prospective Interns:

The Singapore International Pre-Graduate Award (SIPGA) supports short-term research attachments for international students at A*STAR. It provides a unique opportunity for top overseas students to experience the vibrant scientific environment in A*STAR Research Institutes and Consortia. Students will be able to work with distinguished and world- renowned researchers in A*STAR labs. This award will normally be for students in the later years of a Bachelor or Master level program. Students considering PhD studies in A*STAR are encouraged to apply
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