Davidson, M., Aronson, L.I., Howard-Reeves, J., Bryant, H., Cutts, R.J., Hulkki-Wilson, S., Kouvelakis, K., Kalaitzaki, E., Watkins, D., Starling, N., et al.
(2019). Clonal diversity of MYC amplification evaluated by fluorescent in situ hybridisation and digital droplet polymerase chain reaction in oesophagogastric cancer: Results from a prospective clinical trial screening programme. European journal of cancer,
Balyasnikova, S., Vuong, T., Wale, A., Chong, I., Rutten, H. & Brown, G.
(2018). Session 3: Boosting primary and recurrent rectal cancer: how far can we push the radiotherapy envelope?. Colorectal disease,
Patel, A., Chang, G., Wale, A., Chong, I., Rutten, H., Nicholls, J., Hawkins, M., Steele, R.J., Marks, J. & Brown, G., et al.
(2018). Session 3: Intra-operative radiotherapy - creating new surgical boundaries. Colorectal disease,
Kühnl, A., Cunningham, D., Hutka, M., Peckitt, C., Rozati, H., Morano, F., Chong, I., Gillbanks, A., Wotherspoon, A., Harris, M., et al.
(2018). Rapid access clinic for unexplained lymphadenopathy and suspected malignancy: prospective analysis of 1000 patients. Bmc hematology,
Holme, H., Gulati, A., Brough, R., Fleuren, E.D., Bajrami, I., Campbell, J., Chong, I.Y., Costa-Cabral, S., Elliott, R., Fenton, T., et al.
(2018). Chemosensitivity profiling of osteosarcoma tumour cell lines identifies a model of BRCAness. Scientific reports,
Petty, R.D., Dahle-Smith, A., Stevenson, D.A., Osborne, A., Massie, D., Clark, C., Murray, G.I., Dutton, S.J., Roberts, C., Chong, I.Y., et al.
(2017). Gefitinib and EGFR Gene Copy Number Aberrations in Esophageal Cancer. J clin oncol,
Purpose The Cancer Esophagus Gefitinib trial demonstrated improved progression-free survival with the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor gefitinib relative to placebo in patients with advanced esophageal cancer who had disease progression after chemotherapy. Rapid and durable responses were observed in a minority of patients. We hypothesized that genetic aberration of the EGFR pathway would identify patients benefitting from gefitinib. Methods A prespecified, blinded molecular analysis of Cancer Esophagus Gefitinib trial tumors was conducted to compare efficacy of gefitinib with that of placebo according to EGFR copy number gain (CNG) and EGFR, KRAS, BRAF, and PIK3CA mutation status. EGFR CNG was determined by fluorescent in situ hybridization (FISH) using prespecified criteria and EGFR FISH-positive status was defined as high polysomy or amplification. Results Biomarker data were available for 340 patients. In EGFR FISH-positive tumors (20.2%), overall survival was improved with gefitinib compared with placebo (hazard ratio [HR] for death, 0.59; 95% CI, 0.35 to 1.00; P = .05). In EGFR FISH-negative tumors, there was no difference in overall survival with gefitinib compared with placebo (HR for death, 0.90; 95% CI, 0.69 to 1.18; P = .46). Patients with EGFR amplification (7.2%) gained greatest benefit from gefitinib (HR for death, 0.21; 95% CI, 0.07 to 0.64; P = .006). There was no difference in overall survival for gefitinib versus placebo for patients with EGFR, KRAS, BRAF, and PIK3CA mutations, or for any mutation versus none. Conclusion EGFR CNG assessed by FISH appears to identify a subgroup of patients with esophageal cancer who may benefit from gefitinib as a second-line treatment. Results of this study suggest that anti-EGFR therapies should be investigated in prospective clinical trials in different settings in EGFR FISH-positive and, in particular, EGFR-amplified esophageal cancer..
Battersby, N.J., Dattani, M., Rao, S., Cunningham, D., Tait, D., Adams, R., Moran, B.J., Khakoo, S., Tekkis, P., Rasheed, S., et al.
(2017). A rectal cancer feasibility study with an embedded phase III trial design assessing magnetic resonance tumour regression grade (mrTRG) as a novel biomarker to stratify management by good and poor response to chemoradiotherapy (TRIGGER): study protocol for a randomised controlled trial. Trials,
Campbell, J., Ryan, C.J., Brough, R., Bajrami, I., Pemberton, H.N., Chong, I.Y., Costa-Cabral, S., Frankum, J., Gulati, A., Holme, H., et al.
(2016). Large-Scale Profiling of Kinase Dependencies in Cancer Cell Lines. Cell reports,
Wetterskog, D., Shiu, K.-., Chong, I., Meijer, T., Mackay, A., Lambros, M., Cunningham, D., Reis-Filho, J.S., Lord, C.J. & Ashworth, A., et al.
(2014). Identification of novel determinants of resistance to lapatinib in ERBB2-amplified cancers. Oncogene,
Hoskin, P.J., Rojas, A.M., Peiris, S.N., Mullassery, V. & Chong, I.Y.
(2014). Pre-treatment Haemoglobin and Peripheral Blood Lymphocyte Count as Independent Predictors of Outcome in Carcinoma of Cervix. Clinical oncology,
Chong, I.Y., Cunningham, D., Barber, L.J., Campbell, J., Chen, L., Kozarewa, I., Fenwick, K., Assiotis, I., Guettler, S., Garcia-Murillas, I., et al.
(2013). The genomic landscape of oesophagogastric junctional adenocarcinoma. The journal of pathology,
Chong, I., Hawkins, M., Hansen, V., Thomas, K., McNair, H., O’Neill, B., Aitken, A. & Tait, D.
(2011). Quantification of Organ Motion During Chemoradiotherapy of Rectal Cancer Using Cone-Beam Computed Tomography. International journal of radiation oncology*biology*physics,
Wetterskog, D., Shiu, K.-., Chong, I., Meijer, T., Natrajan, R., Lord, C.J., Ashworth, A. & Reis-Filho, J.S.
(2011). Abstract 4987: Identification of novel genes and pathways involved in resistance to HER2-targeting agents in breast cancer. Cellular and molecular biology,
Chong, I., Wetterskog, D., Shiu, K.-., Meijer, T., Natrajan, R., Maryou, L., Reis-Filho, J., Lord, L.J., David, C. & Ashworth, A., et al.
(2011). Abstract 3039: Identification of a novel biomarker of resistance to lapatinib common to both breast and oesophagogastric cancer. Cellular and molecular biology,
Cunningham, D. & Chong, I.
(2010). Optimal treatment of metastatic pancreatic cancer. Gut,
Chong, I.Y., Brown, G., Heald, R.J., Thomas, K., Chau, I., Wotherspoon, A. & Tait, D.M.
(2010). A multicenter phase II clinical study evaluating the deferral of rectal surgery following a continued response to preoperative chemoradiotherapy (CRT). Journal of clinical oncology,
Chong, I.Y., Okines, A.F., Tait, D.M., Hawkins, M., Cunningham, D., Saffery, C., Thomas, K. & Chau, I.
(2010). A multicenter randomized phase II study of UFT/leucovorin and radiotherapy (RT) with or without cetuximab following induction gemcitabine plus capecitabine (GEM-CAP) in locally advanced pancreatic cancer (LAPC). Journal of clinical oncology,
Chong, I. & Hoskin, P.J.
(2008). Vaginal vault brachytherapy as sole postoperative treatment for low-risk endometrial cancer. Brachytherapy,
Mapping genetic vulnerabilities reveals BTK as a novel therapeutic target in oesophageal cancer. Gut,
Bajrami, I., Marlow, R., van de Ven, M., Brough, R., Pemberton, H., Frankum, J., Song, F., Raquif, R., Konde, A., Krastev, D., et al.
E-cadherin/ROS1 inhibitor synthetic lethality in breast cancer. Cancer discovery,
Lim, K., Halim, A., Lu, T.-., Ashworth, A. & Chong, I.
Klotho: A Major Shareholder in Vascular Aging Enterprises. International journal of molecular sciences,
Accelerated vascular aging is a condition that occurs as a complication of several highly prevalent inflammatory conditions such as chronic kidney disease, cancer, HIV infection and diabetes. Age-associated vascular alterations underlie a continuum of expression toward clinically overt cardiovascular disease. This has contributed to the striking epidemiologic transition whereby such noncommunicable diseases have taken center stage as modern-day global epidemics and public health problems. The identification of α-Klotho, a remarkable protein that confers powerful anti-aging properties has stimulated significant interest. In fact, emerging data have provided fundamental rationale for Klotho-based therapeutic intervention for vascular diseases and multiple other potential indications. However, the application of such discoveries in Klotho research remains fragmented due to significant gaps in our molecular understanding of Klotho biology, as well as hurdles in clinical research and experimental barriers that must first be overcome. These advances will be critical to establish the scientific platform from which future Klotho-based interventional trials and therapeutic enterprises can be successfully launched..