This manuscript provides an update to the literature on molecules with roles in tumor resistance therapy in head and neck squamous cell carcinoma (HNSCC). Although significant improvements have been made in the treatment for head and neck squamous cell carcinoma, physicians face yet another challenge—that of preserving oral functions, which involves the use of multidisciplinary therapies, such as multiple chemotherapies (CT) and radiotherapy (RT). Designing personalized therapeutic options requires the study of genes involved in drug resistance. This review provides an overview of the molecules that have been linked to resistance to chemotherapy in HNSCC, including the family of ATP-binding cassette transporters (ABCs), nucleotide excision repair/base excision repair (NER/BER) enzymatic complexes (which act on nonspecific DNA lesions generated by gamma and ultraviolet radiation by cross-linking and forming intra/interchain chemical adducts), cisplatin (a chemotherapeutic agent that causes DNA damage and induces apoptosis, which is a paradox because its effectiveness is based on the integrity of the genes involved in apoptotic signaling pathways), and cetuximab, including a discussion of the genes involved in the cell cycle and the proliferation of possible markers that confer resistance to cetuximab.
Objective: To identify adolescents’ self-perception of dental fluorosis from two areas with different socioeconomic levels. Methods: A cross-sectional, descriptive study was conducted with 15-year-old youths by applying a questionnaire designed and validated to assess self-perceptions of dental fluorosis in two areas with different socioeconomic statuses (SESs). Fluorosis was clinically evaluated by applying the Thylstrup and Fejerkov (TF) index on the upper front teeth. Results: A total of 308 adolescents were included in the study. The medium-SES population, which was exposed to 2.5 ppm of fluoride in water, and the low-SES population, which was exposed to 5.1 ppm, presented the following levels of dental fluorosis: TF 2–3 (50%), TF 4–5 (45.6%) and TF 6–7 (4.4%) for medium SES and TF 2–3 (12.3%), TF 4–5 (67.1%) and TF 67 (20.6%) for low SES. A significant association was found between self-perception and dental fluorosis in those with medium and low SESs (p < 0.05). The multiple regression model found differences between TF levels and self-perception, with a 6–7 TF level for concerns about color (OR = 1.6), smile (OR = 1.2) and appearance (OR = 3.36). Conclusions: Self-perceptions of dental fluorosis affect adolescents such that adolescents with a medium SES have more negative perceptions than those with a low SES. Such perceptions increase as the TF index increases.
The aim of this study was to evaluate the effects of alcohol-containing mouthwash on the induction of micronuclei and nuclear anomalies in exfoliated buccal cells, including binucleated cells, cells with nuclear buds, and karyolitic, karyorrhectic, condensed chromatin, and pyknotic cells. Buccal mucosa cells were collected from 107 healthy participants who were divided into three groups: control subjects who did not use mouthwash (n = 33), subjects who were exposed for 30 days and two times rinsing with 30 seconds each time to alcohol-containing mouthwash (n = 38; 26% ethanol concentration); and subjects exposed to a non-alcohol-containing mouthwash (n = 36). A slide was used to collect cells from the oral mucosa from the inner lining of both cheeks. Samples were spread directly onto two separate, precleaned and precoded slides. Smears were air-dried, fixed, stained, and analyzed by microscopy for micronuclei and nuclear anomalies. Frequency of micronuclei, nuclear buds, and karyolitic, karyorrhectic, and condensed chromatin cells increased significantly (P < 0.05) in the alcohol-containing mouthwash group after mouthwash exposition, compared with both the control and the non-alcohol-containing mouthwash groups. Our results suggest that subjects exposed to alcohol-containing mouthwash exhibited an increase in frequency of micronuclei and nuclear anomalies in oral mucosal cells, which is directly related to DNA damage.
Background Low protein expression of E-cadherin in oral squamous cell carcinoma (OSCC) has been associated with clinical and histopathological traits such as metastases, recurrence, low survival and poor tumor differentiation, and it is considered a high-risk marker of malignancy. However, it is still unknown whether low expression of E-cadherin is also present at the mRNA level in OSCC cases. Objective: The aim of this study was to compare E-cadherin mRNA expression in OSCC patients and controls and to correlate the expression with clinical and prospective characteristics. Material and Methods Forty patients and 40 controls were enrolled. E-cadherin mRNA expression was evaluated by quantitative real-time polymerase chain reaction using TaqMan probes. Results E-cadherin mRNA expression was significantly decreased in OSCC patients compared to that of controls ( p <0.001). Whereas no significant association between clinical parameters and E-cadherin expression levels was observed, we noted lower E-cadherin expression levels in patients with positive lymph node metastasis. Conclusions E-cadherin mRNA expression was markedly diminished in OSCC, in agreement with previous results that examined E-cadherin expression at the protein level. E-cadherin is downregulated in the early clinical stages of OSCC, and its mRNA levels do not change significantly in the advanced stages, suggesting that there is limited usefulness of this parameter for predicting disease progression. Key words: Oral cancer, E-Cadherin, gene expression.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.