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News Article | May 4, 2017
Site: www.cemag.us

Scientists from the National University of Singapore (NUS) have developed a novel nanodiamond-based contrast agent — a chemical "dye" used to enhance the visibility of internal body structures in magnetic resonance imaging (MRI) — that improves visualization of liver cancer tumors. Better and more sensitive imaging contributes towards detecting liver cancer and is crucial for planning for treatment. MRI is a medical imaging technique commonly used for cancer diagnosis and to track the progress of patients after treatment. Currently, there are two modes of MRI imaging, T1-weighted and T2-weighted imaging, and patients are often given contrast agents to improve imaging quality. However, each imaging mode requires a specific class of contrast agent which cannot be used together. This poses a greater challenge in the diagnosis of liver cancer, where T2-weighted imaging is still not considered reliable, and both T1- and T2-weighted imaging can be confounded by tumor vascularity. A research team led by Assistant Professor Edward Chow, Principal Investigator from the Cancer Science Institute of Singapore at NUS and Department of Pharmacology at NUS Yong Loo Lin of Medicine, has developed a dual-mode contrast agent which enables clearer and more accurate images of tumors to be obtained in both T1- and T2-weighted MRI scans, and with lower dosages of contrast agent. The novel dual-mode contrast agent, which was developed using nanodiamonds in combination with a manganese base, provides greater imaging contrast than existing clinical agents which are used to improve quality of MRIs. The team also found that liver tumors that are unable to be visualized without contrast agents become readily visible even at low dosages of the novel compound. Contrast agents work by altering the magnetic properties of nearby water molecules, which enhances the quality of MR images. Nanodiamonds, which are carbon-based particles of two to eight nanometers in diameter, have unique chemical properties that allow them to attract water molecules. This enables them to promote proton exchange between water molecules and paramagnetic ions (i.e. contrast agents) that accumulate in tissues. As a result, T1 and T2 relaxation is enhanced, giving better quality images. This is unlike existing nanotechnology-based approaches, where nanomaterials are used to improve delivery of paramagnetic ions to specific tumor sites. “Our experiments suggest that our dual-mode contrast agent holds great promise in improving imaging for liver cancer. We are hopeful that this advancement in nanomedicine will lead to safer and more accurate diagnosis of liver cancer. Moving forward, we plan to conduct further pre-clinical safety studies for our contrast agents, with the end goal being clinical implementation. We are also looking into using our contrast agents to improve imaging for glioma and ovarian cancer,” says Chow. The study was conducted in collaboration with the NUS Comparative Medicine Imaging Facility and the Agency for Science, Technology and Research’s Singapore Bioimaging Consortium. The findings of the study were published in the scientific journal Nanomedicine: Nanotechnology, Biology and Medicine in April 2017.


News Article | April 19, 2017
Site: www.eurekalert.org

A team of scientists from Singapore has discovered new ways in which cancers can escape the body's immune system. Focusing on gastric cancer (GC), the third leading cause of cancer death worldwide, the team's findings may also prove applicable to other major cancers with potential implications for how cancers might be better treated with immunotherapy, one of the most promising classes of anti-cancer drugs today. Promoters are regions in the genome that regulate the expression of genes, similar to the switch of a light bulb. Using an ultra-sensitive technique called NanoChIP-seq, the team surveyed the promoter landscape for GC to better understand the epigenetic mechanisms contributing to GC development. The team found that in GCs, gene promoters are dysregulated in a way that alters a tumour's antigenic profile to evade the body's immune system. The study, published in the leading journal Cancer Discovery, involved scientists and clinicians from Duke-NUS Medical School, Genome Institute of Singapore, Cancer Science Institute of Singapore (CSI Singapore) at the National University of Singapore (NUS), and National Cancer Centre Singapore (NCCS). "Using the NanoChIP-seq platform invented in Singapore, we created comprehensive epigenetic profiles for both GC and normal tissues," explained team leader Professor Patrick Tan. "Epigenetics is a process by which a cell's DNA is chemically modified by the environment, to change gene expression. By comparing the epigenetic profiles of gastric tumours to normal tissues from the same patient, we were able to identify those promoters specifically altered in GC tissues." Professor Tan is a Faculty Member of Duke-NUS Medical School, Deputy Executive Director of the Biomedical Research Council at the Agency for Science, Technology and Research (A*STAR), and also Senior Principal Investigator at CSI Singapore and Principal Investigator at NCCS. Just like how a light can be controlled by multiple switches to influence its intensity and colour, the team identified hundreds of genes controlled by multiple promoters, causing alternate versions of that gene to be produced. The team demonstrated that some of these gene variants are capable of stimulating cancer growth. Strikingly, the team also found that many of these alternate gene variants produced in gastric tumours were also less likely to stimulate the immune system compared with their normal counterparts. "Our data, combining computational, experimental assays, and analyses of human gastric cancers, indicates that the use of these less immunogenic variants may enhance the ability of a tumour to bypass the host's immune system. This process is referred to as tumour immunoediting," added Ms Aditi Qamra, graduate student at the Genome Institute of Singapore and first author of this study. She is also a graduate student with the Department of Physiology at the NUS Yong Loo Lin School of Medicine. The findings provide important insights into mechanisms used in cancer development and may have implications for cancer immunotherapy. While striking clinical responses have been seen in some patients treated with immunotherapy, these drugs are expensive, associated with side effects, and not all patients respond to the treatment. The team's results suggest that studying the promoter profiles of tumours may possibly identify those patients who would be responsive to immunotherapy. Moreover, the team also identified cellular pathways required by the tumour cell to maintain expression of the less immunogenic gene variants. The team is now exploring if targeting these pathways, combined with immunotherapy, can increase the proportion of patients that might respond to such drugs.


News Article | May 26, 2017
Site: www.futurity.org

A new nanodiamond-based contrast agent—a chemical “dye” that enhances the visibility of internal body structures in magnetic resonance imaging (MRI)—could improve visualization of liver cancer tumors. MRI is a medical imaging technique commonly used for cancer diagnosis and to track the progress of patients after treatment. Currently, there are two modes of MRI imaging, T1-weighted and T2-weighted imaging, and patients are often given contrast agents to improve imaging quality. Each imaging mode, however, requires a specific class of contrast agent which cannot be used together. This poses a greater challenge in the diagnosis of liver cancer, where T2-weighted imaging is still not considered reliable, and tumor vascularity can confound both T1- and T2-weighted imaging. A research team led by Edward Chow, from the Cancer Science Institute of Singapore at National University of Singapore and the department of pharmacology at NUS Yong Loo Lin of Medicine, has developed a dual-mode contrast agent that enables clearer and more accurate images of tumors from both T1- and T2-weighted MRI scans, and with lower dosages of contrast agent. The dual-mode contrast agent, which the researchers developed with nanodiamonds in combination with a manganese base, provides greater imaging contrast than existing options. The team also found that liver tumors that can’t be visualized without contrast agents become readily visible even at low dosages of the new compound. Contrast agents work by altering the magnetic properties of nearby water molecules, which enhances the quality of MR images. Nanodiamonds, which are carbon-based particles of two to eight nanometers in diameter, have unique chemical properties that allow them to attract water molecules. This enables them to promote proton exchange between water molecules and paramagnetic ions (i.e. contrast agents) that accumulate in tissues. “Our experiments suggest that our dual-mode contrast agent holds great promise in improving imaging for liver cancer,” says Chow. “We are hopeful that this advancement in nanomedicine will lead to safer and more accurate diagnosis of liver cancer. Moving forward, we plan to conduct further preclinical safety studies for our contrast agents, with the end goal being clinical implementation. We are also looking into using our contrast agents to improve imaging for glioma and ovarian cancer,” Chow adds. The study was a collaboration with the NUS Comparative Medicine Imaging Facility and the Agency for Science, Technology, and Research’s Singapore Bioimaging Consortium. The findings of the study appear in the journal Nanomedicine: Nanotechnology, Biology, and Medicine.


Lau W.M.,Cancer Science Institute of Singapore | Teng E.,Cancer Science Institute of Singapore | Chong H.S.,Cancer Science Institute of Singapore | Lopez K.A.P.,Cancer Science Institute of Singapore | And 6 more authors.
Cancer Research | Year: 2014

The surface marker CD44 has been identified as one of several markers associated with cancer stem cells (CSC) in solid tumors, but its ubiquitous expression in many cell types, including hematopoietic cells, has hindered its use in targeting CSCs. In this study, 28 paired primary tumor and adjacent nontumor gastric tissue samples were analyzed for cell surface protein expression. Cells that expressed pan-CD44 were found to occur at significantly higher frequency in gastric tumor tissues. We identified CD44v8-10 as the predominant CD44 variant expressed in gastric cancer cells and verified its role as a gastric CSC marker by limiting dilution and serial transplantation assays. Parallel experiments using CD133 failed to enrich for gastric CSCs. Analyses of another 26 primary samples showed significant CD44v8-10 upregulation in gastric tumor sites. Exogenous expression of CD44v8-10 but not CD44 standard (CD44s) increased the frequency of tumor initiation in immunocompromised mice. Reciprocal silencing of total CD44 resulted in reduced tumor-initiating potential of gastric cancer cells that could be rescued by CD44v8-10 but not CD44s expression. Our findings provide important functional evidence that CD44v8-10 marks human gastric CSCs and contributes to tumor initiation, possibly through enhancing oxidative stress defense. In addition, we showed that CD44v8-10 expression is low in normal tissues. Because CD44 also marks CSCs of numerous human cancers, many of which may also overexpress CD44v8-10, CD44v8-10 may provide an avenue to target CSCs in other human cancers. © 2014 AACR.


Kono K.,National University of Singapore | Kono K.,Cancer Science Institute of Singapore | Mimura K.,National University of Singapore
OncoImmunology | Year: 2013

Although it has been shown in murine models that chemoradiotherapy may induce immunogenic tumor cell death, which could trigger T-cell immunity upon the released of high-mobility group box 1 protein (HMGB1), whether this also occurs in clinical settings remains unclear. Here, we discuss tumor-antigen specific T-cell responses in esophageal cancer patients receiving chemoradiotherapy. Our findings indicate that chemoradiation induces tumor antigen-specific T-cell responses and that the release of HMGB1 is related to clinical outcome. © 2013 Landes Bioscience.


News Article | November 23, 2016
Site: www.eurekalert.org

A team of researchers from the Cancer Science Institute of Singapore (CSI Singapore) at the National University of Singapore (NUS) has found that controlling the levels of the TIP60 protein, which is a tumour suppressor, could potentially prevent the spread of breast cancer cells. Specifically, the research team that is led by Assistant Professor Sudhakar Jha from CSI Singapore discovered that TIP60 interacts with two other proteins called DNMT1 and SNAIL2, to inhibit the spread of cancer cells. This is the first study which reports the novel function of TIP60 in regulating DMNT1-SNAIL2 axis, and subsequently inhibiting metastasis, which is the spread of cancer cells to other parts of the body. "In this study, we found that the absence of TIP60 raises the levels of DNMT1, resulting in the activation of SNAIL-2 function. When this molecular program is turned on, epithelial cells - which protect or enclose organs - acquire migratory and invasive properties. This leads to the spreading of cancer cells. Understanding this mechanism holds the important key to suppressing the migration of cancer cells," explained Mr Zhang Yanzhou, a final year PhD student from CSI Singapore's Graduate Programme in Cancer Biology, and first author of the study. This is an important discovery for breast cancer patients with poor Overall Survival (OS) and Disease-Free Survival (DFS) prognoses, as it was previously found that TIP60 levels in these patients are low, thus reducing their defence against cancer cell metastasis. The team's discovery may have important implications for other cancers as patients with colon and cervical cancers have also been found to have irregular TIP60 levels. Hence, the direction of this study may open doors to potential treatment of different types of cancers in the future. "This study provides important evidence that TIP60 levels could possibly serve as prognostic marker of breast cancer progression, and the stabilisation of TIP60 could be a promising strategy to treat cancers. We are currently developing inhibitors which can increase TIP60 levels and in turn, prevent the spread of cancer. Moving forward, we are also looking into collaborating with clinician scientists from the National University Health System to initiate clinical trials using DNMT1 inhibitors to treat breast cancer patients and decrease metastasis by targeting cells that have lower levels of TIP60 as these cells are more likely to be invasive," said Asst Prof Jha. The findings of the study were published in the Journal of Molecular Cell Biology in September 2016.


News Article | November 1, 2016
Site: www.eurekalert.org

A team of scientists from the National University of Singapore (NUS) has established novel insights into the relationship between breast cancer tumour intracellular redox environment and the cancer cells' ability to become invasive. The study by Dr Alan Prem Kumar from the Cancer Science Institute of Singapore (CSI Singapore) at NUS and NUS Yong Loo Lin School of Medicine, together with Professor Shazib Pervaiz and Associate Professor Marie-Veronique Clement from NUS Yong Loo Lin School of Medicine, found that high levels of Manganese Superoxide Dismutase (MnSOD), a key enzyme involved in regulating the cellular redox milieu, has a role to play in causing breast cancer cells to turn aggressive, especially in triple negative breast cancer subtype tumours. These aggressive cells are able to invade other sites in the body, resulting in secondary tumours. "Our group's work over the years has highlighted the critical role of cancer cells' oxidative metabolism in drug resistance and cell survival. This study underscores the importance that MnSOD plays in the biology of breast cancer," said Assoc Prof Clement. The new findings build on the group's previous discovery of the presence of a significantly higher MnSOD levels in triple negative breast cancer patients. "MnSOD expression is decreased during the initial stages of cancer development. However, as the cancer advances, MnSOD expression increases and such high MnSOD levels are typically observed in triple negative breast cancer patients. In fact, we have shown that less aggressive tumours, when artificially made to increase MnSOD protein levels, adopt an aggressive behaviour. Our study shows that the amount of MnSOD levels in the tumour cell determines the predominant reactive oxygen species that will tell the tumour cells whether to stay put or to transform into an invasive form that is capable of moving to distal parts of the body," explained Dr Loo Ser Yue, a former graduate student from NUS Yong Loo Lin School of Medicine and the first author of the study. Triple negative breast cancer is a subtype of estrogen-independent breast cancer. Among female patients diagnosed with various subtypes of breast cancer in Singapore and worldwide, about 13 per cent of them are triple negative. While considerable progress has been made in the diagnosis and treatment of estrogen-dependent breast cancer, triple negative breast cancer is associated with poor diagnosis due to a lack of targeted therapeutic options. By studying the underlying cause of this subtype of breast cancer, the NUS research team hopes to design and develop effective therapeutic strategies to combat this disease. "Our study provides a novel mechanism for exploiting cancer's Achilles heel with potential implications for the design of target-specific therapies against aggressive breast cancer," said Professor Pervaiz. As part of their earlier study, the NUS team had shown a novel strategy of targeting this enhanced MnSOD expression and therefore its activity using other FDA-approved drugs to make the aggressive tumours more sensitive to conventional anti-cancer drugs. They also showed that this strategy would re-sensitise patients who develop resistance to conventional breast cancer drugs such as Docetaxel or Doxorubicin. The novel findings were published in the leading journal Antioxidants & Redox Signaling in August 2016. Their earlier findings were also published in the same journal in May 2014. Compared to normal cells, cancer cells experience higher oxidative stress, which is the imbalance between the production of free radicals and the body's antioxidant defences. MnSOD, which is a major antioxidant protein, is especially essential for cancer cells to cope with their high oxidative stress. However, the NUS research team found that too much of the MnSOD protein - as a result of the advancement of the cancer - activates a molecular program to convert a localised tumour to become aggressive and spread to neighbouring organs. The team's findings also suggest MnSOD as a potential target for treatment of aggressive cancers, beyond breast cancer. Breast cancer is the most frequently diagnosed cancer in Singaporean women, making up about 30 per cent of all female cancers. The increase in breast cancer incidence rate in Singaporean women is also amongst the highest globally. Different subtypes of breast cancer are inherently genetically diverse and different treatment strategies need to be devised against each subtype. Due to the lack of well-defined molecular targets in triple negative breast cancer patients, current treatment options rely heavily on chemotherapy, which is highly non-specific and has adverse side effects. "By suppressing MnSOD expression or its activity in triple negative breast cancer patients, we are able to make the tumour cells less aggressive and more sensitive to chemotherapy," said Dr Kumar. Moving forward, the NUS team is looking into selective killing of cancer cells by designing small molecules targeting MnSOD, to diminish the invasive properties of such tumours.


News Article | November 1, 2016
Site: www.sciencedaily.com

A team of scientists from the National University of Singapore (NUS) has established novel insights into the relationship between breast cancer tumour intracellular redox environment and the cancer cells' ability to become invasive. The study by Dr Alan Prem Kumar from the Cancer Science Institute of Singapore (CSI Singapore) at NUS and NUS Yong Loo Lin School of Medicine, together with Professor Shazib Pervaiz and Associate Professor Marie-Veronique Clement from NUS Yong Loo Lin School of Medicine, found that high levels of Manganese Superoxide Dismutase (MnSOD), a key enzyme involved in regulating the cellular redox milieu, has a role to play in causing breast cancer cells to turn aggressive, especially in triple negative breast cancer subtype tumours. These aggressive cells are able to invade other sites in the body, resulting in secondary tumours. "Our group's work over the years has highlighted the critical role of cancer cells' oxidative metabolism in drug resistance and cell survival. This study underscores the importance that MnSOD plays in the biology of breast cancer," said Assoc Prof Clement. The new findings build on the group's previous discovery of the presence of a significantly higher MnSOD levels in triple negative breast cancer patients. "MnSOD expression is decreased during the initial stages of cancer development. However, as the cancer advances, MnSOD expression increases and such high MnSOD levels are typically observed in triple negative breast cancer patients. In fact, we have shown that less aggressive tumours, when artificially made to increase MnSOD protein levels, adopt an aggressive behaviour. Our study shows that the amount of MnSOD levels in the tumour cell determines the predominant reactive oxygen species that will tell the tumour cells whether to stay put or to transform into an invasive form that is capable of moving to distal parts of the body," explained Dr Loo Ser Yue, a former graduate student from NUS Yong Loo Lin School of Medicine and the first author of the study. Triple negative breast cancer is a subtype of estrogen-independent breast cancer. Among female patients diagnosed with various subtypes of breast cancer in Singapore and worldwide, about 13 per cent of them are triple negative. While considerable progress has been made in the diagnosis and treatment of estrogen-dependent breast cancer, triple negative breast cancer is associated with poor diagnosis due to a lack of targeted therapeutic options. By studying the underlying cause of this subtype of breast cancer, the NUS research team hopes to design and develop effective therapeutic strategies to combat this disease. "Our study provides a novel mechanism for exploiting cancer's Achilles heel with potential implications for the design of target-specific therapies against aggressive breast cancer," said Professor Pervaiz. As part of their earlier study, the NUS team had shown a novel strategy of targeting this enhanced MnSOD expression and therefore its activity using other FDA-approved drugs to make the aggressive tumours more sensitive to conventional anti-cancer drugs. They also showed that this strategy would re-sensitise patients who develop resistance to conventional breast cancer drugs such as Docetaxel or Doxorubicin. The novel findings were published in the leading journal Antioxidants & Redox Signaling in August 2016. Their earlier findings were also published in the same journal in May 2014. Compared to normal cells, cancer cells experience higher oxidative stress, which is the imbalance between the production of free radicals and the body's antioxidant defences. MnSOD, which is a major antioxidant protein, is especially essential for cancer cells to cope with their high oxidative stress. However, the NUS research team found that too much of the MnSOD protein -- as a result of the advancement of the cancer -- activates a molecular program to convert a localised tumour to become aggressive and spread to neighbouring organs. The team's findings also suggest MnSOD as a potential target for treatment of aggressive cancers, beyond breast cancer. Breast cancer is the most frequently diagnosed cancer in Singaporean women, making up about 30 per cent of all female cancers. The increase in breast cancer incidence rate in Singaporean women is also amongst the highest globally. Different subtypes of breast cancer are inherently genetically diverse and different treatment strategies need to be devised against each subtype. Due to the lack of well-defined molecular targets in triple negative breast cancer patients, current treatment options rely heavily on chemotherapy, which is highly non-specific and has adverse side effects. "By suppressing MnSOD expression or its activity in triple negative breast cancer patients, we are able to make the tumour cells less aggressive and more sensitive to chemotherapy," said Dr Kumar. Moving forward, the NUS team is looking into selective killing of cancer cells by designing small molecules targeting MnSOD, to diminish the invasive properties of such tumours.


A recent discovery by researchers from the Cancer Science Institute of Singapore (CSI Singapore) at the National University of Singapore (NUS) may lead to a new treatment strategy for an aggressive ovarian cancer subtype. Ovarian cancer is the most deadly gynecological cancer and it is the seventh most common cancer in women worldwide. Most women with ovarian cancer are diagnosed at the advanced stage, which is more difficult to treat. In a study led by Dr Ruby Huang, Principal Investigator at CSI Singapore, researchers identified a molecule called AXL which is found to trigger the spread of an aggressive form of ovarian cancer called the Mes subtype. This is one of two aggressive subtypes of ovarian cancer -- the other subtype is called Stem-A -- that was identified by Dr Huang's group in an earlier study. These two subtypes of ovarian cancers have a higher ability to undergo Epithelial-Mesenchymal Transition (EMT). EMT is the process by which epithelial cells transform into mesenchymal cells, which have been associated with aggressive metastatic cancer. By carrying out experiments on Mes subtype ovarian cancer cells, Dr Huang and her team found that AXL, when activated, was able to interact with other proteins in the cell to form a cellular pathway that contributes to the aggressive spread of ovarian cancer cells. Results from this study were published in the October issue of the journal Science Signaling. Currently, there is no specific treatment for the Mes ovarian cancer subtype, and the findings from this study suggest that blocking AXL could be an effective treatment option for these patients. "Though earlier studies have suggested the role of AXL in contributing to the spreading of ovarian cancer cells, no study has investigated the AXL function in ovarian cancer with different molecular backgrounds. This study builds upon our previous efforts in understanding the biology among different ovarian cancer subtypes, and the current finding represents an advancement into novel roles of AXL in ovarian cancer and brings another layer of sophistication in ovarian cancer treatment," said Dr Huang. The research team from CSI Singapore is collaborating with several pharmaceutical companies to develop anti-AXL drugs, in order to bring the discovery from bench to bedside for ovarian cancer treatment. Dr David Tan, who holds dual appointments with CSI Singapore and National University Cancer Institute, will be leading the clinical development of the anti-AXL treatment. This study was carried out in collaboration with clinicians from the National University Hospital as well as scientists from Imperial College London, and supported by the National Research Foundation Singapore, Singapore Ministry of Education, and National Medical Research Council. The first author of the paper, Dr Jane Antony, had recently graduated from the joint PhD programme between NUS Graduate School for Integrative Sciences and Engineering as well as Imperial College London.


Home > Press > Unmasking new drivers of stomach cancer: Study advances understanding of stomach cancer progression and could lead to new therapeutic targets and improved clinical outcomes Abstract: Scientists have uncovered a new class of master control elements in stomach cancer called “super-enhancers”, which control critical cancer genes and proteins required for stomach tumours to survive and grow. The team’s generation of this unprecedented and comprehensive catalogue of stomach cancer super-enhancers is an important milestone for the community. Currently, stomach cancer is the fifth most common cancer worldwide and the third leading cause of global cancer death[1]. Most gastric cancers are diagnosed late, and the disease is often resistant to current clinical treatments. By studying super-enhancers in stomach tumours, the team was able to shed light on how these elements impact the risk of stomach cancer development and progression of the disease. For example, stomach cancer patients whose tumours exhibited high numbers of super-enhancers exhibited a significantly poorer survival rate. Selective activation of these super-enhancers could explain why certain groups of people are at risk of developing the disease. These tissue-specific super-enhancers also represent a previously untapped reservoir of cancer vulnerability, acting to bridge oncogenic signalling to tissue-specific features of malignancy. Thus, studying the mechanisms driving the development of super-enhancers in stomach cancer may lead to novel therapies. Specifically, the team also identified two DNA-binding proteins as drivers for the formation of tumour-specific super-enhancers. These may serve as potential drug targets for stomach cancer. The researchers were able to make this finding using a highly sensitive, “made-in-Singapore” technology, called Nano-ChIPseq. Developed at A*STAR’s Genome Institute of Singapore (GIS), Nano-ChIPseq enables the study of epigenomic changes in clinical samples obtained directly from stomach cancer patients, rather than laboratory cultured cell lines. Unlike DNA which is stable and unchanging, epigenomic instructions are strongly influenced by factors such as food, infectious agents, and chemicals, suggesting that they can be modified by environmental risk factors. The team is now working to commercialise the technology and develop data technologies, which will enable scientists to revolutionise cancer therapeutics. “Future work in our lab will investigate how such super-enhancers can be disrupted by drugs, which will open up new avenues for cancer therapy,” said the study’s corresponding author Prof Patrick Tan, Deputy Executive Director of A*STAR’s Biomedical Research Council and an associate faculty member at the GIS. “We hope that our findings will encourage the scientific community to embrace our technology as a means to rapidly uncover master control elements that are highly relevant to diseases and clinical outcomes. This effort may eventually change the way stomach and other cancers are managed, which will enhance the clinical outcomes of cancer patients.” Published in scientific journal Nature Communications, this study was led by GIS, in collaboration with Duke-NUS Medical School, Cancer Science Institute of Singapore at the National University of Singapore (NUS), Singapore General Hospital (SGH), Weatherall Institute of Molecular Medicine at Oxford University, and the Singapore Gastric Cancer Consortium (SGCC). Commercialisation of the Nano-ChIPseq platform is currently supported through gap funding awarded by ETPL Pte Ltd, the commercialisation arm of A*STAR. "I felt something awesome will be coming when I heard about the new method, Nano-ChIPseq. The study suggests that extensive alterations in gene regulation, and not genes themselves, explain deep mysteries of gastric cancer, which are known to exhibit small numbers of mutations and deep involvement of bacterial infection, an environmental factor. Naturally, development of novel therapeutic strategies must take account of these findings," said Dr Toshikazu Ushijima, Chief of Division of Epigenomics at the National Cancer Center Research Institute in Japan, and a member of the SGCC Scientific Advisory Board. GIS Executive Director Prof Ng Huck Hui added, “This is a remarkable technological breakthrough for the community. As we constantly work to find better treatments for cancer, it is also important that we find more efficient ways to study how epigenomic changes can drive the formation of cancerous cells from healthy cells. A greater understanding about molecular changes in diseases can potentially lead to early therapeutic intervention and improved care for the patients. 1Cancer Therapeutics and Stratified Oncology, Genome Institute of Singapore, 60 Biopolis Street, Genome #02-01, Singapore 138672, Singapore. 2Cancer and Stem Cell Biology Program, Duke-NUS Graduate Medical School, 8 College Road, Singapore 169857, Singapore. 3NUS Graduate School for Integrative Sciences and Engineering, National University of Singapore, 5 Lower Kent Ridge Road, Singapore 119074, Singapore. 4Cancer Science Institute of Singapore, National University of Singapore, 14 Medical Drive, #12-01, Singapore 117599, Singapore. 5Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, 2 Medical Drive #04-01, Singapore 117597, Singapore. 6Department of Human Genetics, Genome Institute of Singapore, 60 Biopolis Street, Genome #02-01, Singapore 138672, Singapore. 7Medical Research Council (MRC) Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, Oxford University, Oxford OX3 9DS, UK. 8Department of Upper Gastrointestinal & Bariatric Surgery, Singapore General Hospital, Singapore 169608, Singapore. 9Division of Surgical Oncology, National Cancer Centre Singapore, 11 Hospital Drive, Singapore 169610, Singapore. 10Department of General Surgery, Singapore General Hospital, Singapore 169608, Singapore. 11Department of Medical Oncology, Yonsei University College of Medicine, Seoul 120-752, South Korea. 12SingHealth/Duke-NUS Institute of Precision Medicine, National Heart Centre Singapore, Singapore 168752, Singapore. 13Laboratory of Cancer Epigenome, Department of Medical Sciences, National Cancer Centre, 11 Hospital Drive, Singapore 169610, Singapore. 14School of Biological Sciences, Nanyang Technological University, Singapore 637551, Singapore. 15Cellular and Molecular Research, National Cancer Centre, 11 Hospital Drive, Singapore 169610, Singapore. *These authors contributed equally to this work. About Genome Institute of Singapore, A*STAR The Genome Institute of Singapore (GIS) is an institute of the Agency for Science, Technology and Research (A*STAR). It has a global vision that seeks to use genomic sciences to achieve extraordinary improvements in human health and public prosperity. Established in 2000 as a centre for genomic discovery, the GIS will pursue the integration of technology, genetics and biology towards academic, economic and societal impact. The key research areas at the GIS include Human Genetics, Infectious Diseases, Cancer Therapeutics and Stratified Oncology, Stem Cell and Regenerative Biology, Cancer Stem Cell Biology, Computational and Systems Biology, and Translational Research. The genomics infrastructure at the GIS is utilised to train new scientific talent, to function as a bridge for academic and industrial research, and to explore scientific questions of high impact. For more information about GIS, please visit www.gis.a-star.edu.sg About the Agency for Science, Technology and Research (A*STAR) ​ The Agency for Science, Technology and Research (A*STAR) is Singapore's lead public sector agency that spearheads economic oriented research to advance scientific discovery and develop innovative technology. Through open innovation, we collaborate with our partners in both the public and private sectors to benefit society. As a Science and Technology Organisation, A*STAR bridges the gap between academia and industry. Our research creates economic growth and jobs for Singapore, and enhances lives by contributing to societal benefits such as improving outcomes in healthcare, urban living, and sustainability. We play a key role in nurturing and developing a diversity of talent and leaders in our Agency and Research Institutes, the wider research community and industry. A*STAR oversees 18 biomedical sciences and physical sciences and engineering research entities primarily located in Biopolis and Fusionopolis. For more information on A*STAR, please visit www.a-star.edu.sgFor more information about GIS, please visit www.gis.a-star.edu.sg For more information, please click If you have a comment, please us. Issuers of news releases, not 7th Wave, Inc. or Nanotechnology Now, are solely responsible for the accuracy of the content.

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