18 research outputs found

    Demographic and psychological predictors of community pharmacists’ cancer-related conversations with patients: a cross-sectional analysis and survey study

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    BACKGROUND: There is increasing interest in the role of community pharmacy in the early diagnosis and prevention of cancer. This study set out to examine how often community pharmacists (CPs) encourage patients to spot or respond to potential signs and symptoms of cancer, and how often they help people to make an informed decision about taking part in bowel cancer screening. METHODS: Data from 400 UK CPs, who completed the 2018 Cancer Research UK Healthcare Professional Tracker survey, were analysed. The primary outcomes were: ‘how often CPs encourage patients to spot or respond to potential signs and symptoms of cancer’ and ‘how often CPs encourage eligible people to make an informed decision to participate in bowel cancer screening’. Associations between behaviours and demographic and psychological variables (Capability, Opportunity and Motivation) were assessed using multivariate logistic regression. RESULTS: Most (n = 331, 82.8%) CPs reported occasionally, frequently or always encouraging patients to spot or respond to potential signs and symptoms of cancer, while only half (n = 203, 50.8%) reported occasionally, frequently or always helping people make an informed decision to participate in bowel cancer screening. Female sex (aOR: 3.20, 95%CI: 1.51, 6.81; p < 0.01) and increased Opportunity (aOR: 1.72, 95%CIs: 1.12, 2.64; p < 0.05) and Motivation (aOR: 1.76, 95%CIs: 1.37, 2.27; p < 0.001) were associated with encouraging patients to spot or respond to potential signs and symptoms of cancer; all three psychological variables were associated with helping people to make an informed decision to participate in bowel cancer screening (Capability: aOR: 1.39, 95%CIs: 1.26, 1.52, p < 0.001; Opportunity: aOR: 1.44, 95%CIs: 1.11, 1.87; p < 0.01; Motivation: aOR: 1.45, 95%CIs: 1.05, 2.00; p < 0.05). CONCLUSIONS: Most CPs encourage patients to spot or respond to potential cancer symptoms, while only half help them make an informed decision to participate in bowel cancer screening. A multifaceted approach, targeting multiple COM-B components, is required to change these behaviours

    A Regulatory Role for NBS1 in Strand-Specific Mutagenesis during Somatic Hypermutation

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    Activation-induced cytidine deaminase (AID) is believed to initiate somatic hypermutation (SHM) by deamination of deoxycytidines to deoxyuridines within the immunoglobulin variable regions genes. The deaminated bases can subsequently be replicated over, processed by base excision repair or mismatch repair, leading to introduction of different types of point mutations (G/C transitions, G/C transversions and A/T mutations). It is evident that the base excision repair pathway is largely dependent on uracil-DNA glycosylase (UNG) through its uracil excision activity. It is not known, however, which endonuclease acts in the step immediately downstream of UNG, i.e. that cleaves at the abasic sites generated by the latter. Two candidates have been proposed, an apurinic/apyrimidinic endonuclease (APE) and the Mre11-Rad50-NBS1 complex. The latter is intriguing as this might explain how the mutagenic pathway is primed during SHM. We have investigated the latter possibility by studying the in vivo SHM pattern in B cells from ataxia-telangiectasia-like disorder (Mre11 deficient) and Nijmegen breakage syndrome (NBS1 deficient) patients. Our results show that, although the pattern of mutations in the variable heavy chain (VH) genes was altered in NBS1 deficient patients, with a significantly increased number of G (but not C) transversions occurring in the SHM and/or AID targeting hotspots, the general pattern of mutations in the VH genes in Mre11 deficient patients was only slightly altered, with an increased frequency of A to C transversions. The Mre11-Rad50-NBS1 complex is thus unlikely to be the major nuclease involved in cleavage of the abasic sites during SHM, whereas NBS1 might have a specific role in regulating the strand-biased repair during phase Ib mutagenesis
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