Royal Surrey County Hospital

About: Royal Surrey County Hospital is a healthcare organization based out in Guildford, United Kingdom. It is known for research contribution in the topics: Cancer & Population. The organization has 2222 authors who have published 3064 publications receiving 86753 citations.

A survey of patient doses from digital mammography systems in the UK in 2007 to 2009

Abstract: Patient dose data from across the UK were collated, and the information relating to full-field digital mammography systems were analysed, and compared with overall results for film-screen systems For CR systems, the average mean glandular doses was 2.19 ± 0.07 mGy which was similar to the average for film screen systems 2.15 ± 0.01 mGy The average patient dose for DR systems was 1.46 ± 0.02 mGy approximately 32% lower than for film screen systems When different DR systems were compared, the Sectra MDM L30 and the Siemens Novation and Inspiration had the lowest average mean glandular dose, at 0.95 ± 0.02 mGy, 1.16 ± 0.05 mGy and 1.21 ± 0.07 mGy, respectively It was shown that for DR systems the MGD to the standard breast was broadly correlated with the average MGD for oblique views of 50-60mm thick breasts, while the correlation for CR systems was much lower.

The cyclin-dependent kinase inhibitor p57(Kip2) is epigenetically regulated in carboplatin resistance and results in collateral sensitivity to the CDK inhibitor seliciclib in ovarian cancer.

Abstract: Carboplatin remains a first-line agent in the management of epithelial ovarian cancer (EOC). Unfortunately, platinum-resistant disease ultimately occurs in most patients. Using a novel EOC cell line with acquired resistance to carboplatin: PEO1CarbR, genome-wide micro-array profiling identified the cyclin-dependent kinase inhibitor p57(Kip2) as specifically downregulated in carboplatin resistance. Presently, we describe confirmation of these preliminary data with a variety of approaches.

Acquired resistance to anti-EGFR mAb ICR62 in cancer cells is accompanied by an increased EGFR expression, HER-2/HER-3 signalling and sensitivity to pan HER blockers.

Abstract: The human epidermal growth factor receptor (EGFR) is an important target for cancer treatment. Currently, only the EGFR antibodies cetuximab and panitumumab are approved for the treatment of patients with colorectal cancer. However, a major clinical challenge is a short-term response owing to development of acquired resistance during the course of the treatment. In this study, we investigated the molecular mechanisms underlying development of acquired resistance in DiFi colorectal cancer cells to the anti-EGFR mAb ICR62 (termed DiFi62) and to the small molecule tyrosine kinase inhibitor (TKI) gefitinib (termed DiFiG) using a range of techniques. Compared with the findings from parental DiFi and DiFiG cells, development of acquired resistance to anti-EGFR mAb ICR62 in DiFi62 cells was accompanied by an increase in cell surface EGFR and increased phosphorylation of HER-2 and HER-3. Interestingly, DiFi62 cells also acquired resistance to treatment with anti-EGFR mAbs cetuximab and ICR61, which bind to other distinct epitopes on the extracellular domain of EGFR, but these cells remained equally sensitive as the parental cells to treatment with pan-HER inhibitors such as afatinib. Our results provide a novel mechanistic insight into the development of acquired resistance to EGFR antibody-based therapy in colorectal cancer cells and justify further investigations on the therapeutic benefits of pan-HER family inhibitors in the treatment of colorectal cancer patients once acquired resistance to EGFR antibody-based therapy is developed.