Search

Your search keyword '"Ooi, L-Y"' showing total 12 results
Start Over Author "Ooi, L-Y"
12 results on '"Ooi, L-Y"'

4. Additional file 3 of Oral vitamin D supplementation induces transcriptomic changes in rectal mucosa that are linked to anti-tumour effects

Author

Vaughan-Shaw, P. G., Grimes, G., Blackmur, J. P., Timofeeva, M., Walker, M., Ooi, L. Y., Svinti, Victoria, Donnelly, Kevin, Din, F. V. N., Farrington, S. M., and Dunlop, M. G.

Abstract

Additional file 3: Table S1. Full list of diagnoses in recruited participants. Table S2. Top 50 ranked genes in PHASE 1. Table S3. Top 50 ranked GO terms enriched in PHASE 1. Table S4. Candidate genes positively associated with 25-OHD level in the GO term ‘regulation of cell migration’ and published evidence of tumour suppressor/ biomarker activity. Table S5. Candidate genes positively associated with 25-OHD level in the GO term ‘regulation of programmed cell death’ and published evidence of tumour suppressor/ biomarker activity. Table S6. Association between relevant genetic variants and 25OHD fold-change after supplementation. Table S7. Direction and magnitude of effect in candidate genes with expression change after supplementation. Table S8. Top ranked Enriched GO terms after vitamin D supplementation. Table S9. Enrichment of candidate GO terms after supplementation in RNAseq data. Table S10. Characteristics of participants with rectal mucosa response to supplementation. Table S11. AUC values for blood biomarkers of rectal and blood response in the SCOVIDS and BEST-D studies. Figure S1. Gene-set enrichment plot for enrichment of candidate genes associated with 25-OHD level in those undergoing vitamin D supplementation. Figure S2. GO terms enriched in PHASE 1 and PHASE 2. Figure S3. Receiver-operator curve for putative blood biomarkers and rectal mucosal response to supplementation.

Published
2021
Full Text
View/download PDF

6. Low plasma Vitamin D is associated with adverse colorectal cancer survival after surgical resection, independent of systemic inflammatory response

Author

Vaughan-Shaw, P G, Zgaga, L, Ooi, L Y, Theodoratou, E, Timofeeva, M, Svinti, V., Walker, Marion, O'Sullivan, F, Ewing, A, Johnston, S, Din, F V N, Campbell, H, Farrington, S M, and Dunlop, M G

Subjects
Male, Vitamin D/analogs & derivatives, Genotype, vitamin D, colorectal cancer, Polymorphism, Single Nucleotide, Receptors, Calcitriol/genetics, surgery, Humans, Genetic Predisposition to Disease, Colorectal Neoplasms/blood, Aged, Vitamin D receptor gene, colon, cancer prevention, C-Reactive Protein/metabolism, Middle Aged, Prognosis, Systemic Inflammatory Response Syndrome/blood, Survival Analysis, 25-hydroxyvitamin D, Biomarkers, Tumor/blood, Case-Control Studies, colorectal surgery, Female, CRP, Follow-Up Studies
Abstract

Objective: We assessed the effect of surgical resection of colorectal cancer (CRC) on perioperative plasma vitamin D (25OHD) and C-reactive protein (CRP) level. We investigated the relationship between circulating vitamin D level and CRC survival.Design: We sequentially sampled 92 patients undergoing CRC resection, and measured plasma 25OHD and CRP. For survival analyses, we assayed 25OHD and CRP in two temporally distinct CRC patient cohorts (n=2006, n=2100) and investigated the association between survival outcome, circulating vitamin D and systemic inflammatory response.Results: Serial sampling revealed a postoperative fall (mean 17.3 nmol/L; p=3.6e-9) in plasma 25OHD (nadir days 1–2). CRP peaked 3–5 days postoperatively (143.1 mg/L; p=1.4e-12), yet the postoperative fall in 25OHD was independent of CRP. In cohort analyses, 25OHD was lower in the 12 months following operation (mean=48.8 nmol/L) than preoperatively (54.8 nmol/L; p=1.2e-5) recovering after 24 months (52.2 nmol/L; p=0.002). Survival analysis in American Joint Committee on Cancer stages I–III demonstrated associations between 25OHD tertile and CRC mortality (HR=0.69; 95% CI 0.46 to 0.91) and all-cause mortality (HR=0.68; 95% CI 0.50 to 0.85), and was independent of CRP. We observed interaction effects between plasma 25OHD and rs11568820 genotype (functional VDR polymorphism) with a strong protective effect of higher 25OHD only in patients with GG genotype (HR=0.51; 95% CI 0.21 to 0.81). We developed an online tool for predicted survival (https://apps.igmm.ed.ac.uk/mortalityCalculator/) that incorporates 25OHD with clinically useful predictive performance (area under the curve 0.77).Conclusions: CRC surgery induces a fall in circulating 25OHD. Plasma 25OHD level is a prognostic biomarker with low 25OHD associated with poorer survival, particularly in those with rs11568820 GG genotype. A randomised trial of vitamin D supplementation after CRC surgery has compelling rationale.

Published
2020
Full Text
View/download PDF

7. Low plasma vitamin D is associated with adverse colorectal cancer survival after surgical resection, independent of systemic inflammatory response

Author

Vaughan-Shaw, P G, primary, Zgaga, L, additional, Ooi, L Y, additional, Theodoratou, E, additional, Timofeeva, M, additional, Svinti, V, additional, Walker, M, additional, O’Sullivan, F, additional, Ewing, A, additional, Johnston, S, additional, Din, F V N, additional, Campbell, H, additional, Farrington, S M, additional, and Dunlop, M G, additional

Published
2019
Full Text
View/download PDF

8. Low plasma vitamin D is associated with adverse colorectal cancer survival after surgical resection, independent of systemic inflammatory response.

Author

Vaughan-Shaw, P. G., Zgaga, L., Ooi, L. Y., Theodoratou, E., Timofeeva, M., Svinti, V., Walker, M., O'Sullivan, F., Ewing, A., Johnston, S., Din, F. V. N., Campbell, H., Farrington, S. M., and Dunlop, M. G.

Subjects
VITAMIN D, SURGICAL excision, COLORECTAL cancer, VITAMIN therapy, HEALTH services administration
Published
2020
Full Text
View/download PDF

9. Recurrent Coding Sequence Variation Explains only A Small Fraction of the Genetic Architecture of Colorectal Cancer

Author

Timofeeva, M.N. (Maria N.), Kinnersley, B. (Ben), Farrington, S.M. (Susan M.), Whiffin, N. (Nicola), Palles, C. (Claire), Svinti, V. (Victoria), Lloyd, A. (Amy), Gorman, M. (Maggie), Ooi, L.-Y. (Li-Yin), Hosking, F. (Fay), Barclay, E. (Ella), Zgaga, L. (Lina), Dobbins, S.E. (Sara E.), Martin, L. (Lynn), Theodoratou, E. (Evropi), Broderick, P. (Peter), Tenesa, A. (Albert), Smillie, C. (Claire), Grimes, G. (Graeme), Hayward, C. (Caroline), Campbell, A. (Archie), Porteous, D. (David), Deary, I.J. (Ian), Harris, S.E. (Sarah), Northwood, J.B. (John Blackman), Barrett, J.H. (Jennifer H.), Smith, G. (Gillian), Wolf, R. (Roland), Forman, D. (David), Morreau, H. (Hans), Ruano, D. (Dina), Tops, C. (Carli), Wijnen, J.T. (Juul), Schrumpf, M. (Melanie), Boot, A. (Arnoud), Vasen, H. (Hans), Hes, F.J. (Frederik), Wezel, T. (Tom) van, Franke, A. (Andre), Lieb, W. (Wolgang), Schafmayer, C. (Clemens), Hampe, J. (Jochen), Buch, T. (Thorsten), Propping, P. (Peter), Hemminki, K. (Kari), Försti, A. (Asta), Westers, H. (Helga), Hofstra, R.M.W. (Robert), Pinheiro, M. (Manuela), Pinto, C. (Carla), Teixeira, P.J., Ruiz-Ponte, C. (Clara), Fernández-Rozadilla, C. (Ceres), Carracedo, A. (Angel), Castells, A., Castellví-Bel, S., Campbell, H. (Harry), Bishop, D.T. (David Timothy), Tomlinson, I. (Ian), Dunlop, M.G. (Malcolm), Houlston, R. (Richard), Timofeeva, M.N. (Maria N.), Kinnersley, B. (Ben), Farrington, S.M. (Susan M.), Whiffin, N. (Nicola), Palles, C. (Claire), Svinti, V. (Victoria), Lloyd, A. (Amy), Gorman, M. (Maggie), Ooi, L.-Y. (Li-Yin), Hosking, F. (Fay), Barclay, E. (Ella), Zgaga, L. (Lina), Dobbins, S.E. (Sara E.), Martin, L. (Lynn), Theodoratou, E. (Evropi), Broderick, P. (Peter), Tenesa, A. (Albert), Smillie, C. (Claire), Grimes, G. (Graeme), Hayward, C. (Caroline), Campbell, A. (Archie), Porteous, D. (David), Deary, I.J. (Ian), Harris, S.E. (Sarah), Northwood, J.B. (John Blackman), Barrett, J.H. (Jennifer H.), Smith, G. (Gillian), Wolf, R. (Roland), Forman, D. (David), Morreau, H. (Hans), Ruano, D. (Dina), Tops, C. (Carli), Wijnen, J.T. (Juul), Schrumpf, M. (Melanie), Boot, A. (Arnoud), Vasen, H. (Hans), Hes, F.J. (Frederik), Wezel, T. (Tom) van, Franke, A. (Andre), Lieb, W. (Wolgang), Schafmayer, C. (Clemens), Hampe, J. (Jochen), Buch, T. (Thorsten), Propping, P. (Peter), Hemminki, K. (Kari), Försti, A. (Asta), Westers, H. (Helga), Hofstra, R.M.W. (Robert), Pinheiro, M. (Manuela), Pinto, C. (Carla), Teixeira, P.J., Ruiz-Ponte, C. (Clara), Fernández-Rozadilla, C. (Ceres), Carracedo, A. (Angel), Castells, A., Castellví-Bel, S., Campbell, H. (Harry), Bishop, D.T. (David Timothy), Tomlinson, I. (Ian), Dunlop, M.G. (Malcolm), and Houlston, R. (Richard)

Abstract

Whilst common genetic variation in many non-coding genomic regulatory regions are known to impart risk of colorectal cancer (CRC), much of the heritability of CRC remains unexplained. To examine the role of recurrent coding sequence variation in CRC aetiology, we genotyped 12,638 CRCs cases and 29,045 controls from six European populations. Single-variant analysis identified a coding variant (rs3184504) in SH2B3 (12q24) associated with CRC risk (OR = 1.08, P = 3.9 × 10-7), and novel damaging coding variants in 3 genes previously tagged by GWAS efforts; rs16888728 (8q24) in UTP23 (OR = 1.15, P = 1.4 × 10-7); rs6580742 and rs12303082 (12q13) in FAM186A (OR = 1.11, P = 1.2 × 10-7

Published
2015
Full Text
View/download PDF

10. Common variation near CDKN1A, POLD3 and SHROOM2 influences colorectal cancer risk

Author

Dunlop, MG, Dobbins, SE, Farrington, SM, Jones, AM, Palles, C, Whiffin, N, Tenesa, A, Spain, S, Broderick, P, Ooi, L-Y, Domingo, E, Smillie, C, Henrion, M, Frampton, M, Martin, L, Grimes, G, Gorman, M, Semple, C, Ma, YP, Barclay, E, Prendergast, J, Cazier, J-B, Olver, B, Penegar, S, Lubbe, S, Chander, I, Carvajal-Carmona, LG, Ballereau, S, Lloyd, A, Vijayakrishnan, J, Zgaga, L, Rudan, I, Theodoratou, E, Starr, JM, Deary, I, Kirac, I, Kovacevic, D, Aaltonen, LA, Renkonen-Sinisalo, L, Mecklin, J-P, Matsuda, K, Nakamura, Y, Okada, Y, Gallinger, S, Duggan, DJ, Conti, D, Newcomb, P, Hopper, J, Jenkins, MA, Schumacher, F, Casey, G, Easton, D, Shah, M, Pharoah, P, Lindblom, A, Liu, T, Smith, CG, West, H, Cheadle, JP, Midgley, R, Kerr, DJ, Campbell, H, Tomlinson, IP, Houlston, RS, Dunlop, MG, Dobbins, SE, Farrington, SM, Jones, AM, Palles, C, Whiffin, N, Tenesa, A, Spain, S, Broderick, P, Ooi, L-Y, Domingo, E, Smillie, C, Henrion, M, Frampton, M, Martin, L, Grimes, G, Gorman, M, Semple, C, Ma, YP, Barclay, E, Prendergast, J, Cazier, J-B, Olver, B, Penegar, S, Lubbe, S, Chander, I, Carvajal-Carmona, LG, Ballereau, S, Lloyd, A, Vijayakrishnan, J, Zgaga, L, Rudan, I, Theodoratou, E, Starr, JM, Deary, I, Kirac, I, Kovacevic, D, Aaltonen, LA, Renkonen-Sinisalo, L, Mecklin, J-P, Matsuda, K, Nakamura, Y, Okada, Y, Gallinger, S, Duggan, DJ, Conti, D, Newcomb, P, Hopper, J, Jenkins, MA, Schumacher, F, Casey, G, Easton, D, Shah, M, Pharoah, P, Lindblom, A, Liu, T, Smith, CG, West, H, Cheadle, JP, Midgley, R, Kerr, DJ, Campbell, H, Tomlinson, IP, and Houlston, RS

Abstract

We performed a meta-analysis of five genome-wide association studies to identify common variants influencing colorectal cancer (CRC) risk comprising 8,682 cases and 9,649 controls. Replication analysis was performed in case-control sets totaling 21,096 cases and 19,555 controls. We identified three new CRC risk loci at 6p21 (rs1321311, near CDKN1A; P = 1.14 × 10(-10)), 11q13.4 (rs3824999, intronic to POLD3; P = 3.65 × 10(-10)) and Xp22.2 (rs5934683, near SHROOM2; P = 7.30 × 10(-10)) This brings the number of independent loci associated with CRC risk to 20 and provides further insight into the genetic architecture of inherited susceptibility to CRC.

Published
2012

12. Parapharyngeal metastasis in hepatocellular carcinoma-a rare entity.

Author

Chee J, Lee GH, Ooi LY, Seet JE, Loh T, and Ng LS

Subjects
Humans, Living Donors, Male, Middle Aged, Radiotherapy, Adjuvant, Carcinoma, Hepatocellular diagnostic imaging, Carcinoma, Hepatocellular therapy, Liver Neoplasms diagnostic imaging, Liver Transplantation
Abstract

Hepatocellular carcinoma (HCC) is the most common primary malignancy of the liver. It most commonly metastasizes haematogenously to the lungs and bones, less commonly via lymphatics to lymph nodes. However, metastasis to the parapharyngeal space has yet to be reported. This is the first clinical report of the treatment of parapharyngeal metastasis from HCC. The case of a 46-year-old man who was found to have a parapharyngeal soft tissue mass during routine follow-up 12 years post deceased-donor liver transplantation for hepatitis B-related HCC is reported here. This was investigated and diagnosed to be metastatic HCC. He underwent excision of the parapharyngeal metastasis, followed by adjuvant radiotherapy. Parapharyngeal metastasis is a rare occurrence in HCC. It is important to be cognizant of the possibility of disease spread to this location in order to ensure early detection and treatment. Surgical excision with adjuvant radiotherapy should be considered to achieve disease control., (Copyright © 2021 International Association of Oral and Maxillofacial Surgeons. Published by Elsevier Inc. All rights reserved.)

Published
2021
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results