Objective and designTo investigate the healing mechanism of Delonix regia galactomannan (GM-DR) in a mice model of excisional cutaneous wound. Materials and subjectsFemale Swiss mice were used in all treatments.Treatment GM-DR (% 0.01-1) was topically applied to the wounds during 14 days. MethodsThe wound healing effect of GM-DR was evaluated by the following parameters: wound closure, clinical signs (hyperemia, edema, exsudate, nociception), oxidative stress markers (malondialdehyde -MDA, reduced glutathione -GSH), histopathological and histomorphometric analysis (collagenesis, blood vessels, polymorphonuclear, mononuclear, broblast/myo broblast cells) and immunohistochemical (in ammatory growth factor mediators). ResultsGM-DR reduced wound area (7 -14 th day) and hypernociception (6 h -5 th day), leukocyte in ltration (2 -7 th day), expression and levels of IL-1β (2 th day), IL-6 (2 th day), MDA (44% -2 th day), and increased broblast/myo broblast, granulation tissue, collagen deposition, GSH (25 -50%, 2-5 th day), Transforming Growth Factor Beta (TGF-β) expression (7-10 th day) and Smooth Muscle Alpha Actin (a-SMA) (7-14 th day). ConclusionsGM-DR accelerates the mice healing process acting both in the in ammatory and proliferative phases.
Background Penile cancer is one of the most aggressive male tumors. Although it is preventable, the main etiologic causes are lifestyle behaviors and viral infection, such as human papillomavirus (HPV). Long-term epigenetic changes due to environmental factors change cell fate and promote carcinogenesis, being an important marker of prognosis. We evaluated epidemiological aspects of penile squamous cell carcinoma (SCC) and the prevalence of HPV infection using high-risk HPV (hrHPV) and p16INK4A expression of 224 participants. Global DNA methylation was evaluated through 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC). Results The incidence of HPV was 53.2% for hrHPV and 22.32% for p16INK4a. hrHPV was not related to systemic or lymph node metastasis and locoregional recurrence, nor influenced the survival rate. P16INK4a seems to be a protective factor for death, which does not affect metastasis or tumor recurrence. Lymph node and systemic metastases and locoregional recurrence increase the risk of death. An increased 5mC mark was observed in penile SCC regardless of HPV infection. However, there is a reduction of the 5hmC mark for p16INK4a + (P = 0.024). Increased 5mC/5hmC ratio (> 1) was observed in 94.2% of penile SCC, irrespective of HPV infection. Despite the increase in 5mC, it seems not to affect the survival rate (HR = 1.06; 95% CI 0.33–3.38). Conclusions P16INK4a seems to be a good prognosis marker for penile SCC and the increase in 5mC, an epigenetic mark of genomic stability, may support tumor progression leading to poor prognosis.
AimsDNA methylation has its distribution influenced by DNA demethylation processes with the catalytic conversion of 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC). Myelodysplastic syndrome (MDS) has been associated with epigenetic dysregulation of genes related to DNA repair system, chronic immune response and cell cycle.MethodsWe evaluated the tissue DNA methylation/hydroxymethylation in bone marrow trephine biopsies of 73 patients with MDS, trying to correlate with the mRNA expression of 21 genes (POLH, POLL, REV3L, POLN, POLQ, POLI, POLK, IRF-1, IRF-2, IRF-3, IRF-4, IRF-5, IRF6, IRF-7, IRF-8,IRF-9, MAD2, CDC20, AURKA, AURKB and TPX2).ResultsThe M-score (5mC) was significantly higher in patients with chromosomal abnormalities than patients with normal karyotype (95% CI –27.127779 to –2.368020; p=0.022). We observed a higher 5mC/5hmC ratio in patients classified as high-risk subtypes compared with low-risk subtypes (95% CI –72.922115 to –1.855662; p=0.040) as well as patients with hypercellular bone marrow compared with patients with normocellular/hypocellular bone marrow (95% CI –69.189259 to –0.511828; p=0.047) and with the presence of dyserythropoiesis (95% CI 17.077703 to 51.331388; p=0.001). DNA pols with translesion activity are significantly influenced by methylation. As 5mC immunoexpression increases, the expressions of POLH (r=−0.816; r2 =0.665; p=0.000), POLQ (r=−0.790; r2=0.624; p=0.001), PCNA (r=−0.635; r2=0.403; p=0.020), POLK (r=−0.633; r2=0.400; p=0.036 and REV1 (r=−0.578; r2=0.334; p=0.049) decrease.ConclusionsOur results confirm that there is an imbalance in the DNA methylation in MDS, influencing the development of chromosomal abnormalities which may be associated with the low expression of DNA polymerases with translesion synthesis polymerases activity.
Background Malignant neoplasms that affect children and adolescents are predominantly embryonic and generally affect blood system cells and supporting tissues. Aim This study aimed to summarize the scientific evidence about the prevalence of malignant lesions in the oral cavity of children and adolescents. Design In this systematic review and meta‐analysis (PROSPERO CRD42020158338), data were obtained from seven databases and the gray literature. Cross‐sectional observational studies on the prevalence of biopsied oral pediatric malignancies were included. The Newcastle‐Ottawa Scale assessed the quality of the included studies, and the GRADE approach evaluated the evidence certainty. The meta‐analysis prevalence was calculated using MedCalc® software, adopting a 95% confidence level (CI; random‐effect model). Results Forty‐two studies were included in the meta‐analysis. Of the 64,522 biopsies, the prevalence of malignant lesions was 1.93% (n = 1,100; 95% CI = 1.21%‐2.80%). Countries with a low socioeconomic profile showed the highest prevalence. The sample size did not influence the prevalence of oral malignancies, and unspecified lymphomas (12.08%; 95% CI = 5.73%‐20.37%) and rhabdomyosarcoma (10.53%; 95% CI = 7.28%‐14.30%) were the most common lesions. Conclusions Oral malignant lesions biopsied in children and adolescents had a prevalence of <3%, and lymphomas and sarcomas were the most prevalent lesions.
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