4 research outputs found

    One hundred years of external approach medialisation thyroplasty

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    It has been 100 years since Erwin Payr first developed an operation to improve the effects of a paralysed vocal fold, and operations based on this technique are still in use today. This technique, medialisation thyroplasty, aims to improve the symptoms caused by vocal fold palsy by realigning the lateralised vocal fold into the midline. Whilst the effects of vocal fold palsy were recognised in antiquity, it was only with the development of indirect laryngoscopy in the late nineteenth century that the vocal fold paralysis could be identified as an aetiology for poor phonation and dysphagia. Payr, in 1915, was the first to perform a recognisable form of medialisation thyroplasty, which was further developed in the early twentieth century, but medialisation thyroplasty did not begin to be widely used until the development of the modern technique by Isshiki et al., in 1974. Since then, medialisation thyroplasty has continued to be developed and is currently the most widely used technique for correcting the effects of vocal fold palsy. However, a wide array of therapeutic options is now available for vocal fold palsy and it is impossible to say whether or not medialisation thyroplasty will still be used in another 100 years

    Targeting FGFR inhibition in cholangiocarcinoma

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    Cholangiocarcinomas (CCAs) are rare but aggressive tumours of the bile ducts, which are often diagnosed at an advanced stage and have poor outcomes on systemic therapy. Somatic alterations with therapeutic implications have been identified in almost half of CCAs, in particular in intrahepatic CCA (iCCA), the subtype arising from bile ducts within the liver. Among patients with CCA, fibroblast growth factor receptor 2 (FGFR2) fusions or rearrangements occur almost exclusively in iCCA, where they are estimated to be found in up to 10–15% of patients. Clinical trials for selective FGFR kinase inhibitors have shown consistent activity of these agents in previously treated patients with iCCA harbouring FGFR alterations. Current FGFR kinase inhibitors show differences in their structure, mechanisms of target engagement, and specificities for FGFR1, 2, 3 and 4 and other related kinases. These agents offer the potential to improve outcomes in FGFR-driven CCA, and the impact of variations in the molecular profiles of the FGFR inhibitors on efficacy, safety, acquired resistance mechanisms, and patients’ health-related quality of life remains to be fully characterized. The most common adverse event associated with FGFR inhibitors is hyperphosphatemia, an on-target off-tumour effect of FGFR1 inhibition, and strategies to manage this include dose adjustment, chelators, and the use of a low phosphate diet. As FGFR inhibitors and other targeted agents enter the clinic for use in FGFR-driven CCA, molecular testing for actionable mutations and monitoring for the emergence of acquired resistance will be essential

    COVID-19 in cancer patients on systemic anti-cancer therapies: outcomes from the CAPITOL (COVID-19 Cancer PatIenT Outcomes in North London) cohort study

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    Background: Patients with cancer are hypothesised to be at increased risk of contracting COVID-19, leading to changes in treatment pathways in those treated with systemic anti-cancer treatments (SACT). This study investigated the outcomes of patients receiving SACT to assess whether they were at greater risk of contracting COVID-19 or having more severe outcomes. / Methods: Data was collected from all patients receiving SACT in two cancer centres as part of CAPITOL (COVID-19 Cancer PatIenT Outcomes in North London). The primary outcome was the effect of clinical characteristics on the incidence and severity of COVID-19 infection in patients on SACT. We used univariable and multivariable models to analyse outcomes, adjusting for age, gender and comorbidities. / Results: A total of 2871 patients receiving SACT from 2 March to 31 May 2020 were analysed; 68 (2.4%) were diagnosed with COVID-19. Cancer patients receiving SACT were more likely to die if they contracted COVID-19 than those who did not [adjusted (adj.) odds ratio (OR) 9.84; 95% confidence interval (CI) 5.73–16.9]. Receiving chemotherapy increased the risk of developing COVID-19 (adj. OR 2.99; 95% CI = 1.72–5.21), with high dose chemotherapy significantly increasing risk (adj. OR 2.36, 95% CI 1.35–6.48), as did the presence of comorbidities (adj. OR 2.29; 95% CI 1.19–4.38), and having a respiratory or intrathoracic neoplasm (adj. OR 2.12; 95% CI 1.04–4.36). Receiving targeted treatment had a protective effect (adj. OR 0.53; 95% CI 0.30–0.95). Treatment intent (curative versus palliative), hormonal- or immunotherapy and solid versus haematological cancers had no significant effect on risk. / Conclusion: Patients on SACT are more likely to die if they contract COVID-19. Those on chemotherapy, particularly high dose chemotherapy, are more likely to contract COVID-19, while targeted treatment appears to be protective
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