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Introduction Radiation-induced xerostomia can result in increased caries incidence, necessitating more dental extractions and a resultant increased risk of debilitating osteoradionecrosis (ORN). Patients undergoing head and neck radiotherapy are routinely treated with a topical preventative regime consisting of fluoride and CPP-ACP (Tooth Mousse). There is limited evidence specifically relating to fluoride prevention regimes in head and neck cancer patients. Other novel remineralising aids using calcium and phosphate have been proposed for use in head and neck cancer patients, but again, there is limited evidence.Aims To retrospectively analyse head and neck cancer patients treated with radiotherapy and placed on a fluoride/CPP-ACP prevention regime at a single institution. To assess the incidence of caries, extractions and ORN.Materials and methods Case records for 95 patients were retrospectively assessed. This involved review of paper and computerised clinical notes, correspondence letters and radiographs.Results The mean number of carious teeth was 6.63 (SD 6.81) and the mean number of extractions was 4.88 (SD 5.84). The teeth most frequently affected by caries and extractions were the mandibular incisors, and 28.4% of patients developed ORN (81.5% of cases occurring in the mandible).Conclusion Development of caries and extraction was a very common event. There is a need for further research into the efficacy of topical prevention regimes.First trimester miscarriage is common, occurring in approximately 6.4-12.0% of pregnancies. Women who experience first trimester miscarriage will often have no other significant health conditions and the healthcare professional they most frequently visit could be their dentist or dental care professional. For this reason, it is important that the dental team is aware of the management of first trimester miscarriage in order to allow for a better understanding of the patient's experience and situation. The choice of language used by healthcare professionals with patients who are grieving is also important to ensure effective and open communication.This article aims to provide the dental team with knowledge of first trimester miscarriage, how the effects of this can be relevant within the dental setting, and how to communicate effectively and appropriately with patients who have experienced this traumatic event.A key tenet of protection from infection for dentists is to know who is not infectious. The evidence base regarding protection from respiratory pathogens in dentistry is poor. Those with a positive SARS-CoV-2 IgG antibody are non-infectious (>99% certainty) and can be safely treated with good universal precautions, even for aerosol generating procedures. Viral infectivity with SARS-CoV-2 lasts eight days, unlike viral polymerase chain reaction (PCR) swab tests which can persist for as long as seven weeks. SARS-CoV-2 IgG antibody becomes detectable from 11 days after infection. Bay 11-7085 SARS-CoV-2 IgG antibodies are usually neutralising against the virus and their direct antiviral activity was partially demonstrated in 33,000 patients with COVID-19 treated with convalescent plasma in the USA. So, a positive SARS-CoV-2 IgG antibody is a much more accurate determination of infectiousness than a repeat PCR which is only 70% sensitive. It remains to be seen whether SARS-Cov-2 vaccine responses include protective IgG titres and, once vaccines become widespread, can be used to assist decision-making on appropriate personal protective equipment (PPE) in dentistry.Ether-à-go-go-1 (EAG1), one of the potassium channels, is involved in various physiological processes and plays an important role in the tumorigenesis of many kinds of cancer. EAG1 is highly expressed in hepatocarcinoma cells and is closely related to clinical prognosis, but the molecular mechanism remains elusive. In this study, we verified that EAG1 promotes the proliferation of hepatocellular carcinoma (HCC) both in vitro and in vivo. It promotes cell cycle progression by inhibiting the ubiquitination of SKP2. In addition, EAG1 promotes the migration and invasion of HCC by promoting cell pseudopod formation. Furthermore, in a high-pressure plasmid-injected mouse liver orthotopic carcinoma model, astemizole, an EAG family blocker, can significantly inhibit the formation of liver cancer. Meanwhile, liver-specific EAG1 knockout mice show resistance to hepatocarcinogenesis. This research demonstrated that EAG1 plays an important role in the progression of HCC, and could be a potential therapeutic target for HCC.Little is known about the mutational landscape of advanced hepatocellular carcinoma (HCC), and predictive biomarkers of response to systemic therapies are lacking. We aimed to describe the mutational landscape of advanced HCC and to identify predictors of primary resistance to systemic therapies using circulating tumor DNA (ctDNA). We prospectively enrolled 121 patients between October 2015 and January 2019. We performed targeted ultra-deep sequencing of 25 genes and Digital Droplet PCR of TERT promoter, including sequential samples throughout treatment. Primary endpoint was progression-free survival (PFS) stratified by mutation profiles in ctDNA. Secondary endpoints were overall survival and objective response rate. The most frequent mutations in ctDNA of advanced HCC were TERT promoter (51%), TP53 (32%), CTNNB1 (17%), PTEN (8%), AXIN1, ARID2, KMT2D, and TSC2 (each 6%). TP53 and CTNNB1 mutations were mutually exclusive. Patients with mutations in the PI3K/MTOR pathway had significantly shorter PFS than those without these mutations after tyrosine kinase inhibitors (2.1 vs 3.7 months, p  less then  0.001), but not after immune checkpoint inhibition (CPI). WNT pathway mutations were not associated with PFS, overall survival, or objective response after CPI. Serial profiling of ctDNA in a subset correlated with treatment response. Mutation profiling of ctDNA in advanced HCC shows similar mutation frequencies for known HCC drivers compared to early stages and identifies predictive biomarkers of response to systemic therapies.The control of cell fate is critical to homeostasis and cancer. Cell cycle cdk inhibitor p21CIP1 has a central and paradoxical role in the regulatory crossroads leading to senescence, apoptosis, or differentiation. p21 is an essential target of tumor suppressor p53, but it also is regulated independently. In squamous self-renewal epithelia continuously exposed to mutagenesis, p21 controls cell fate by mechanisms still intriguing. We previously identified a novel epidermoid DNA damage-differentiation response. We here show that p21 intervenes in the mitosis block that is required for the squamous differentiation response to cell cycle deregulation and replication stress. The inactivation of endogenous p21 in human primary keratinocytes alleviated the differentiation response to oncogenic loss of p53 or overexpression of the DNA replication major regulator Cyclin E. The bypass of p21-induced mitotic block involving upregulation of Cyclin B allowed DNA damaged cells to escape differentiation and continue to proliferate.

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