Manoor Prakash Hande, Ph.D., Associate Professor
Principal Investigator

 

 

 

 

 


Swaminathan Sethu
Research Fellow

One of my interests is to target aberrant regulators of cellular process and function in combination with telomerase inhibition in the management of cancer. I hope this approach will certainly increase the efficacy of the treatment regimen and also decrease the morbidity associated with regular management strategies. I am also looking at the effects of low doses of different types of radiations on normal human cells. Since, there is an increase in the frequency of exposure to low levels of ionizing radiation by the general population. This study is highly relevant to assess and predict the potential long and short term health risks in humans involved in exposure to such radiations.



Prarthana Srikanth
Research Assistant

Ataxia Telangiectasia patients are highly susceptible to oxidative stress, cancer and radiation. My research primarily concentrates on studying the extent of sensitivity of these Ataxia Telangiectasia Mutated knock out cells to different genotoxic agents. This study could have implications in identifying high risk groups in the populations with mutations in the ATM gene for their susceptibility to cancer. In addition, I study the effects of ionizing radiation and heavy ion radiation. The study will help in identifying biomarkers for determining risk levels in individuals, in the event of unwarranted exposures.





Khaw Aik Kia
Laboratory Technologist, Graduate Student

Brain tumours, unlike some tumour types, can cause fatality or impair normal functions in benign state. Treatment for brain tumours still have complications and non specific targeting of tumour cells is one of them. Phytochemicals has been reported to have minimal side effect as compared to synthetic drugs. I am particularly interested in studying the functional and molecular responses of brain cancer cells upon treatment with phytochemicals. This will help us understand the mechanism of action and pathways that are triggered by these phytochemicals.




Low Kah Mun, Grace
Research Assistant, Graduate Student

My hypothesis is that a dysfunctional nucleotide excision repair (NER) increases tolerance to oxidative stress while increasing the susceptibility to DNA damage, posing as a potential additional cancer risk factor to individuals deficient in the pathway. Thus I am currently investigating the mechanisms (if any) of how the NER is involved in oxidative stress protection. My other research interest lies is in the potential environmental and physiological hazards of environmental toxicants.

 



Dimphy Zeegers
Research Assistant

Cancer therapy usually involves agents that kill cancer cells more efficiently than normal tissue cells. Most cancer cells proliferate more rapidly than their normal counterparts so most cancer drugs target the cell cycle. Plant-derived compounds have been under investigation for their anticancer therapeutic and chemoprevention properties. The focus of my current research is to combine treatment with a natural plant product with inhibition of DNA repair pathway, to impair the DNA damage response resulting in a more selective killing of cancer cells.



Lakshmidevi Balakrishnan
Graduate Student

Oxidative damage in cells has been proposed to play a key role in the development of age-dependent diseases such as cancer, arteriosclerosis, arthritis, neurodegenerative disorders and other conditions. The base excision repair (BER) pathway is one of the primary mechanisms for the repair of oxidative DNA lesions. My current research interests revolve around the DNA damage sensor, Poly (ADP-Ribose) Polymerase 1 (PARP1), an active member of the base excision repair pathway. PARP1 has been established to have a synergistic role together with other repair proteins in telomere function and chromosomal stability. Hence, my work aims to gain a better understanding of the role of PARP1 and its interacting partners under conditions of DNA damage.


Resham Lal Gurung
Graduate Student

Telomerase expression is detected in majority of human tumours whereas it is suppressed in human somatic cells. Therefore, telomerase inhibition has a great potential in anti-tumour therapy. Our Lab has shown that some DNA repair proteins play a role in telomere length maintenance. My research focuses on understanding the mechanism of effects of Natural plant products on telomerase and growth inhibition in tumour cells. Another area of my research interest is to use a combinatorial approach for better selectivity in inducing cytotoxic and genotoxic effects in tumour cells.

 




Gopalakrishnan Kalpana

Graduate Student

My research focuses on one of the major DNA repair pathways, the nucleotide excision repair (NER). The role of NER in the repair of oxidative DNA damage is poorly characterized. I am currently studying this process using Xeroderma Pigmentosum (XP) as a model. XP, a rare autosomal recessive DNA repair disorder, arises from defects in XP genes in NER – one of which is Xeroderma Pigmentosum Type-B (XPB). By subjecting cells derived from XP patients to hydrogen peroxide-induced oxidative stress, we are elucidating the involvement of XPB and therefore, NER in oxidative stress response. Additionally, since XPB is referred to as a tumour suppressor, we hope to gain better insight into oncogenetic mechanisms associated with NER.



Yong Wei Yan, Jacklyn
Graduate Student

While the majority of cancer cells maintain their telomeres through the activation of telomerase, a subset of cancer cells do so by the activation of an alternative pathway of telomere lengthening termed ALT. Cancer therapy targeting the telomerase enzyme will have no effect on these telomerase-negative ALT cells, hence the need to elucidate this lesser known pathway in hope of finding new therapeutic targets. ALT cancer cells have distinct phenotypes from telomerase-positive cancer cells with the presence of heterogeneous telomere length and ALT-associated PML nuclear bodies. I am interested in studying the ALT pathway, particularly in the role of APBs in relation to the telomere maintenance mechanism via the ALT pathway.


Vinoth Kumar Jayaseelan
Graduate Student

Established mammalian cell lines are commonly used to analyze the cytotoxic and genotoxic potential of environmental factors, drugs, biomaterials as well as chemical, physical and biological agents in vitro. However, these cells vary in their susceptibility and response to the factors mentioned when compared to normal human primary cells. Therefore, much attention is given to find viable alternatives for such testing with physiological relevance and accuracy. Embryonic stem cells have been validated as a reliable source for in vitro developmental toxicology studies. Hence, my work investigates the potential for the application of hESCs and its derived progenies as plausible cellular models for in vitro genotoxicity testing.


Asharani P V Nair
Graduate Student

My research interest revolves around the synthesis, characterization and toxicity studies of metal nanoparticles which have medical applications. We are making an effort to identify critical parameters affecting uptake and interaction of these nanomaterials with biosystems. Uptake kinetics, intracellular distribution, toxicological endpoints and gene expression profiles are being explored in detail to study the mechanism of toxicity of these nanomaterials.

 

 

Inthrani D/O Raja Indran
Graduate Student

The star of my work is the human telomerase reverse transcriptase (hTERT) which is the catalytic subunit of the telomerase holoenzyme. It is required for telomerase maintenance and is re-activated in 70 to 90 percent of human cancers. hTERT has been widely used for cellular immortalization. However recent advances in the telomerase field suggest new functions for hTERT in conferring increased resistance against apoptosis inducing agents and DNA damaging drugs and especially oxidative stress. In an effort to unravel the biological activity of this remarkable protein, we are investigating the cross talk between hTERT and cellular redox status during the process of carcinogenesis. We hope this will help us further our understanding on how hTERT confers its non conventional roles and elicits a protective effect in cancer cells.




Tanny Lim Shi Ni
Honours Student

Telomerase has been suggested to be an almost universal marker for human cancer; hence an attractive target for cancer therapeutics would involve telomerase inhibition. My final year project surrounds the topic of how combinational therapies, especially natural plant products, will lead to telomere attrition with a rapid decline in cancer cell proliferation.




Keith Teo Yong Sheng
Honours Student

Ubiquitous environmental agents may cause increased cancer risk to individuals exposed to them. To assess the effects of these agents, genotoxicity tests in vitro can be conducted to elucidate the damage they may cause. Subsequently, complementary cell assays can be done to find out the mechanisms by which these agents exert their genotoxic effects. My final year project encompasses testing an environmental agent for its genotoxic effects and attempting other assays to unravel the mechanisms that govern its actions. The findings may be the key to explain its carcinogenicity, which contribute to increased risk of certain cancers in humans.




Gayathri A/P Rathamani
Honours Student

Many proteins functions as DNA repair proteins. The repair proteins might also be involved in other pathways which protect the genome intergrity. My hypothesis is that a particular protein may play a role as DNA repair protein and it may also be involved in other areas such as transcription factor and as an anti-oxidant. Thus my project is to functionally analyze the function of this protein.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Last modified on 27 March, 2009