Hit and Run oncogeneses in Head and Neck Cancers requires greater investigation

alexandrossfakianakis shared this article with you from Inoreader Hit and Run oncogeneses in Head and Neck Cancers requires greater investigation via Journal of Medical Virology Abstract Head and neck cancers are unique in so far that 2 major oncogenic viruses, EBV and HPV infect adjacent anatomy and cause nasopharyngeal and oropharyngeal cancers respectively. Dominant recognised carcinogens are alcohol and tobacco but some head and neck cancers have been found to have mixed carcinogens (including betel leaf, areca nuts, slaked lime, viruses, etc) involved in their oncogenesis and conversely, groups of patients with unknown or less dominant carcinogens involved in their development. These cancers may have had viral involvement in the past but then lost most of their viral nucleic acids (be they DNA and/or RNA) below a detection threshold, thus rendering them virus-negative. Some of these virus-negative tumours appear to have mutagenic signatures associated with virus-positive cancers i.e. from the APOBEC defence mechanism which is known to mutate viral nucleic acids as well as cause collateral damage to host DNA, with subsequent development of strongly viral prejudiced mutational signatures. These mechanisms are likely to be less efficient at oncogenesis than traditional direct EBV and HPV oncogenes driving mutagenesis, thus accounting for the smaller frequencies of these cancers found. More profound investigations of these unusual tumours are warranted to dissect out these mechanistic pathways. This article is protected by copyright. All rights reserved. View on Web

Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Subgingival host‐microbiome metatranscriptomic changes following scaling and root planning in Grade II/III Periodontitis

alexandrossfakianakis shared this article with you from Inoreader Subgingival host‐microbiome metatranscriptomic changes following scaling and root planning in Grade II/III Periodontitis via Journal of Clinical Periodontology Abstract Aims To assess the effects of scaling and root planning (SRP) on the dynamics of gene expression by the host and the microbiome in subgingival plaque samples. Methods Fourteen periodontitis patients were closely monitored in the absence of periodontal treatment for 12 months. During this period, comprehensive periodontal examination and subgingival biofilm sample collection were performed bi-monthly. After 12 months, clinical attachment level (CAL) data was compiled and analyzed using linear mixed models (LMM) fitted to longitudinal CAL measurements for each tooth site. LMM classified sites as stable (S), progressing (P), or fluctuating (F). After 12 month visit, subjects received SRP and at 15 months they received comprehensive examination and supportive periodontal therapy (SPT). Those procedures were repeated at the 18 month visit, when patients were also sampled. Each patient contributed with one S, one P and one F site collected at 12 and 18 month visits. Samples were analyzed using Dual RNA-Sequencing to capture host and bacterial transcriptomes simultaneously. Results Microbiome and host response behavior were specific to the site's progression classification (i.e., S, P or F). Microbial profiles of pre and post-treatment samples exhibited specific microbiome changes, with progressing sites showing the most significant changes. Among them, P. gingivalis was reduced after treatment, while F. nucleatum showed an increase in proportion. Transcriptome analysis of the host response showed that IL-17, TNF signaling pathways, and neutrophil extracellular trap (NETs) formation were the primary immune response activities impacted by periodontal treatment. Conclusion Scaling and root planing resulted in a significant "rewiring" of host and microbial activities in the progressing sites, while in stable and fluctuating sites, the restructuring of the microbiome was minor. This article is protected by copyright. All rights reserved. View on Web

Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Influence of genetic polymorphisms on mechanical pain sensitivity and endogenous pain modulation of trigeminal and spinal areas

alexandrossfakianakis shared this article with you from Inoreader Influence of genetic polymorphisms on mechanical pain sensitivity and endogenous pain modulation of trigeminal and spinal areas via Journal of Oral Rehabilitation Abstract Background Previous evidence indicates significant association between genetic polymorphisms and phenotypes related to pain sensitivity in patients with temporomandibular disorders (TMD). Despite the important advances in cataloging diverse factors such as sleep disorders, anxiety and depression, the interrelated mechanisms of painful TMD etiopathogenesis still need investigation. Objectives This case-control study aimed to evaluate the influence of genetic polymorphisms (rs6296, rs6295, rs1799971, rs4680, rs4633, rs4818) and psychosocial factors on the mechanical pain sensitivity and endogenous pain modulation in women with painful TMD and asymptomatic controls. Methods We evaluated six independent variables: anxiety levels, depression, stress, sleep quality, pain catastrophizing and genetic polymorphisms, and four dependent variables: mechanical pain threshold (MPT), pressure pain threshold (PPT), wind-up ratio (WUR) and conditioned pain modulation (CPM) collected at masseter (trigeminal) and hand (spinal) areas in a sample of 95 painful TMD patients and 85 controls. A regression model was used to test the possible effect of the independent variables on dependent variables. Results The regression model was significant for MPT (F11,168 = 9.772; R2=0.390). Painful TMD diagnoses and sleep quality were associated with trigeminal MPT (B coefficient = -0.499; and B coefficient = -0.211, respectively). WUR was associated with rs6295 and rs6746030 for, respectively, the spinal and trigeminal area. Conclusion Genetic polymorphisms had a slight contribution to endogenous pain modulation as indicated by the significant association with WUR but did not contribute to mechanical pain sensitivity. On the other hand, the presence of painful TMD and the sleep quality contributed significantly to mechanical pain sensitivity. View on Web

Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.