Richie Chuan Teck Soong
Email Address
mdcrcts@nus.edu.sg
Organizational Units
YONG LOO LIN SCH OF MEDICINE
faculty
PATHOLOGY
dept
MEDICINE
dept
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Publication Search Results
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Publication Molecular characterization of dedifferentiated mucoepidermoid carcinoma of the trachea using laser microdissection-based TP53 mutation analysis: Correspondence(2009-10) Subramaniam, M.M.; Ng, S.B.; Seah, S.B.; Anuar, D.; Soong, R.; Lee, V.K.; CANCER SCIENCE INSTITUTE OF SINGAPOREPublication Tissue microarrays characterise the clinical significance of a VEGF-A protein expression signature in gastrointestinal stromal tumours(2007) Salto-Tellez, M.; Nga, M.E.; Lee, C.K.; Wee, A.; Soong, R.; Han, H.C.; Anuar, D.; Ng, S.S.; Ho, M.; Wong, A.S.-C.; Chan, Y.H.; NATIONAL UNIVERSITY MEDICAL INSTITUTES; PATHOLOGYPublication Technical reproducibility of single-nucleotide and size-based DNA biomarker assessment using DNA extracted from formalin-fixed, paraffin-embedded tissues(Elsevier, 2015) Zhang Shenli; Tan Bee Huat Iain; Nur Sabrina Bte Sapari; Grabsch H.I.; Okines A.; Smyth E.C.; Aoyama T.; Hewitt L.C.; Inam I.; Bottomley D.; Nankivell M.; Stenning S.P.; Cunningham D.; Wotherspoon A.; Tsuburaya A.; Yoshikawa T.; Soong Chuan Teck Richie; Tan Boon Ooi Patrick; DUKE-NUS GRADUATE MEDICAL SCHOOL S'POREPublication RUNX3 downregulation in human lung adenocarcinoma is independent of p53, EGFR or KRAS status(2012-10) Omar, M.F.M.; Ito, K.; Nga, M.E.; Soo, R.; Peh, B.K.; Ismail, T.M.; Thakkar, B.; Soong, R.; Ito, Y.; Salto-Tellez, M.; CANCER SCIENCE INSTITUTE OF SINGAPORERUNX3 aberrations play a pivotal role in the oncogenesis of breast, gastric, colon, skin and lung tissues. The aim of this study was to characterize further the expression of RUNX3 in lung cancers. To achieve this, a lung cancer tissue microarray (TMA), frozen lung cancer tissues and lung cell lines were examined for RUNX3 expression by immunohistochemistry, while the TMAwas also examined for EGFR and p53 expression. RUNX3 promoter methylation status, and EGFR and KRAS mutation status were also investigated. Inactivation of RUNX3 was observed in 70% of the adenocarcinoma samples, and this was associated with promoter hypermethylation but not biased to EGFR/KRAS mutations. Our results suggest a central role of RUNX3 downregulation in pulmonary adenocarcinoma, which may not be dependent of other established cancer-causing pathways and may have important diagnostic and screening implications. © Arányi Lajos Foundation 2012.Publication MicroRNA-130b regulates the tumour suppressor RUNX3 in gastric cancer(2010) Lai, K.W.; Koh, K.X.; Loh, M.; Tada, K.; Subramaniam, M.M.; Lim, X.Y.; Vaithilingam, A.; Salto-Tellez, M.; Ito, Y.; Soong, R.; Iacopetta, B.; MEDICINE; NATIONAL UNIVERSITY MEDICAL INSTITUTES; CANCER SCIENCE INSTITUTE OF SINGAPORE; PATHOLOGYAim: Accumulating evidence indicates that RUNX3 is an important tumour suppressor that is inactivated in many cancer types. This study aimed to assess the role of microRNA (miRNA) in the regulation of RUNX3. Methods: Four bioinformatic algorithms were used to predict miRNA binding to RUNX3. The correlation between candidate miRNAs and RUNX3 expression in cell lines was determined by real-time reverse transcriptase quantitative PCR (RT-qPCR) and Western blot. Candidate miRNAs were tested for functional effects through transfection of miRNA precursors and inhibitors, and monitoring cell viability, apoptosis and Bim expression. miRNA and RUNX3 expression, RUNX3 methylation and RUNX3 protein levels were assessed in gastric tissue by RT-qPCR, Methylight analysis and immunohistochemistry, respectively. Results: Bioinformatics, gene and protein expression analysis in eight gastric cell lines identified miR-130b as the top candidate miRNA for RUNX3 binding. Overexpression of miR-130b increased cell viability, reduced cell death and decreased expression of Bim in TGF-β mediated apoptosis, subsequent to the downregulation of RUNX3 protein expression. In 15 gastric tumours, miR-130b expression was significantly higher compared to matched normal tissue, and was inversely associated with RUNX3 hypermethylation. Conclusion: Attenuation of RUNX3 protein levels by miRNA may reduce the growth suppressive potential of RUNX3 and contribute to tumourigenesis. Crown Copyright © 2010.Publication Clinical and therapeutic relevance of PIM1 kinase in gastric cancer(2012-04) Yan, B.; Yau, E.X.; Samanta, S.; Ong, C.W.; Yong, K.J.; Ng, L.K.; Bhattacharya, B.; Lim, K.H.; Soong, R.; Yeoh, K.G.; Deng, N.; Tan, P.; Lam, Y.; Salto-Tellez, M.; DUKE-NUS GRADUATE MEDICAL SCHOOL S'PORE; CANCER SCIENCE INSTITUTE OF SINGAPORE; CHEMISTRYBackground Gastric cancer is a leading cause of cancerrelated mortality, and chemotherapeutic options are currently limited. PIM1 kinase, an oncogene that promotes tumorigenesis in several cancer types, might represent a novel therapeutic target in gastric cancer. Methods We studied the expression and genomic status of PIM1 in human primary gastric normal and tumor tissue samples by immunohistochemistry and array-based comparative genomic hybridization (aCGH). To ascertain whether PIM1 expression predicted susceptibility to PIM1 kinase-specific inhibition, the cytotoxic effect of a previously reported PIM1-specific small molecular inhibitor (K00135) was investigated in two gastric cancer cell lines with high (IM95) and undetectable (NUGC-4) PIM1 expression levels. Results PIM1 expression was exclusively nuclear in normal gastric epithelial cells, while aberrant expression/localization (decreased nuclear and/or increased cytoplasmic expression) was observed in 75.6% (68/90) of the human gastric cancer tissue samples, with a significant inverse correlation between nuclear and cytoplasmic expression levels. Clinicopathological analyses revealed that decreased nuclear PIM1 expression correlated with poorer survival and greater depth of tumor invasion, while increased cytoplasmic PIM1 expression correlated inversely with the presence of lymphovascular invasion. Highlevel PIM1 amplification was identified in 10.5% of gastric cancers by aCGH. K00135 impaired the survival of IM95, while it had no significant effect on NUGC-4 survival. Conclusion Our findings demonstrate the clinical and therapeutic relevance of PIM1 in gastric cancers, and suggest that PIM1 represents a potential therapeutic target. © The International Gastric Cancer Association and The Japanese Gastric Cancer Association 2011.Publication Phenotyping of UGT1A1 Activity Using Raltegravir Predicts Pharmacokinetics and Toxicity of Irinotecan in FOLFIRI(Public Library of Science (PLoS), 2016) Lee L.S.-U.; Seng K.-Y.; Wang L.-Z.; Yong W.-P.; Hee K.-H.; Soh T.I.; Wong A.; Cheong P.F.; Soong R.; Sapari N.S.; Soo R.; Fan L.; Lee S.-C.; Goh B.C.; MEDICINE; PATHOLOGYPublication Whole exome sequencing of multi-regional biopsies from metastatic lesions to evaluate actionable truncal mutations using a single-pass percutaneous technique(MDPI AG, 2020) Heong V.; Tay D.; Goh S.E.; Wee B.; Tan T.Z.; Soo R.; Pang B.; Lim D.; Gopinathan A.; Ow S.; Chee C.E.; Goh B.C.; Lee S.C.; Yong W.P.; Wong A.; Omar M.F.M.; Soong R.; Tan D.S.P.; PHARMACOLOGY; DIAGNOSTIC RADIOLOGY; MEDICINE; NATIONAL UNIVERSITY MEDICAL INSTITUTES; CANCER SCIENCE INSTITUTE OF SINGAPORE; PATHOLOGYWe investigate the feasibility of obtaining multiple spatially-separated biopsies from a single lesion to explore intratumor heterogeneity and identify actionable truncal mutations using whole exome sequencing (WES). A single-pass radiologically-guided percutaneous technique was used to obtain four spatially-separated biopsies from a single metastatic lesion. WES was performed to identify putative truncal variants (PTVs), defined as a non-synonymous somatic (NSS) variant present in all four spatially separated biopsies. Actionable truncal mutations—filtered using the FoundationOne panel—were defined as clinically relevant PTVs. Mutational landscapes of each biopsy and their association with patient outcomes were assessed. WES on 50 biopsied samples from 13 patients across six cancer types were analyzed. Actionable truncal mutations were identified in 9/13 patients; 31.1 ± 5.12 more unique NSS variants were detected with every additional multi-region tumor biopsy (MRTB) analyzed. The number of PTVs dropped by 16.1 ± 17.9 with every additional MRTB, with the decrease most pronounced (36.8 ± 19.7) when two MRTB were analyzed compared to one. MRTB most reliably predicted PTV compared to in silico analysis of allele frequencies and cancer cell fraction based on one biopsy sample. Three patients treated with actionable truncal mutation-directed therapy derived clinical benefit. Multi-regional sampling for genomics analysis is feasible and informative to help prioritize precision-therapy strategies. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.Publication Elevated expression of Runx2 as a key parameter in the etiology of osteosarcoma(2009) Nathan, S.S.; Pereira, B.P.; Pho, R.W.H.; Van, Wijnen A.J.; Zhou, Y.-F.; Gupta, A.; Soong, R.; Salto-Tellez, M.; Dombrowski, C.; Cool, S.M.; Stein, G.S.; ORTHOPAEDIC SURGERY; NATIONAL UNIVERSITY MEDICAL INSTITUTES; CANCER SCIENCE INSTITUTE OF SINGAPORE; PATHOLOGYPublication Determinants of variability of five programmed death ligand-1 immunohistochemistry assays in non-small cell lung cancer samples(2018) Soo, R.A; Lim, J.S.Y; Asuncion, B.R; Fazreen, Z; Herrera, M.C; Omar, M.F.M; Phuong, N.H.D; Seet, J.E; Amanuel, B; Iacopetta, B; Byrne, D; Hendry, S; Fox, S; Soong, R; CANCER SCIENCE INSTITUTE OF SINGAPORE; PATHOLOGYProgrammed death ligand-1 (PD-L1) expression as determined by immunohistochemistry (IHC) is potentially predictive of clinical outcome. The aim of this study was to assess the concordance of reported PD-L1 IHC assays and investigate factors influencing variability. Consecutive sections from 20 non-small cell lung cancers (NSCLCs) comprising resection, core biopsy, cytology and pleural fluid samples underwent IHC with 5 different antibody/autostainer combinations: 22C3/Link48, 28-8/BOND-MAX, E1L3N/BOND-MAX, SP142/BenchMark and SP263/BenchMark. PDL1 RNA levels were assessed using RNAscope. The frequency of positive cases using scoring thresholds from clinical trials was 72%, 33%, 61%, 56%, and 33% for the 5 IHC protocols respectively, and 33% for RNAscope. Pairwise agreement on the classification of cases as positive or negative for PD-L1 expression ranged from 61%- 94%. On a continuous scale, the lowest correlation was between 28-8/BOND-MAX and SP142/BenchMark (R2=0.25) and highest was between 22C3/Link48 and E1L3N/ BOND-MAX (R2=0.71). When cases were ordered according to tumor cell (TC)%, a similar ranking of cases across IHC protocols could be observed, albeit with different quanta and limits of detection. Single-slide OPAL 7-color fluorescence IHC analysis revealed a high degree of co-localization of staining from the 5 PD-L1 antibodies. Using SP142 antibody in a BOND-MAX protocol led to increased TC% quanta, while retaining a similar ranking of samples according to TC%. The results of this study highlight tumor PD-L1 status can vary significantly according to IHC protocol. Protocoldependent staining intensities and nominated thresholds for positivity contribute to this variability, while the antibody used appears to be less of a factor. © Soo et al.