Evaluating Alterations of the Oral Microbiome and Its Link to Oral Cancer among Betel Quid Chewers: Prospecting Reversal through Probiotic Intervention.

Areca nut and slaked lime, with or without tobacco wrapped in Piper betle leaf, prepared as betel quid, is extensively consumed as a masticatory product in many countries across the world. Betel Quid can promote the malignant transformation of oral lesions as well as trigger benign cellular and molecular changes. In the oral cavity, it causes changes at the compositional level in oral microbiota called dysbiosis. This dysbiosis may play an important role in Oral Cancer in betel quid chewers. The abnormal presence and increase of bacteria Fusobacterium nucleatum, Capnocytophaga gingivalis, Prevotella melaninogenica, Peptostreptococcus sp., Porphyromonas gingivalis, and Streptococcus mitis in saliva and/or other oral sites of the cancer patients has attracted frequent attention for its association with oral cancer development. In the present review, the authors have analysed the literature reports to revisit the oncogenic potential of betel quid and oral microbiome alterations, evaluating the potential of oral microbiota both as a driver and biomarker of oral cancer. The authors have also shared a perspective that the restoration of local microbiota can become a potentially therapeutic or prophylactic strategy for the delay or reversal of lip and oral cavity cancers, especially in high-risk population groups.

Identifying oral microbiome alterations in adult betel quid chewing population of Delhi, India.

The study targets to establish a factorial association of oral microbiome alterations (oral dysbiosis) with betel quid chewing habits through a comparison of the oral microbiome of Betel quid chewers and non-chewing individuals. Oral microbiome analysis of 22 adult individuals in the Delhi region of India through the 16S sequencing approach was carried out to observe the differences in taxonomic abundance and diversity. A significant difference in diversity and richness among Betel Quid Chewers (BQC) and Betel Quid Non-Chewers (BQNC) groups was observed. There were significant differences in alpha diversity among the BQC in comparison to BQNC. However, in the age group of 21-30 years old young BQC and BQNC there was no significant difference in alpha diversity. Similar result was obtained while comparing BQC and Smoker-alcoholic BQC. BQ smoker-chewers expressed significant variance in comparison to BQC, based on cluster pattern analysis. The OTU-based Venn Diagram Analysis revealed an altered microbiota, for BQ chewing group with 0-10 years exposure in comparison to those with 10 years and above. The change in the microbial niche in early chewers may be due to abrupt chemical component exposure affecting the oral cavity, and thereafter establishing a unique microenvironment in the long-term BQC. Linear discriminant analysis revealed, 55 significant features among BQC and Alcoholic-Smoker BQC; and 20 significant features among BQC and Smoker BQC respectively. The study shows the abundance of novel bacterial genera in the BQC oral cavity in addition to the commonly found ones. Since the oral microbiome plays a significant role in maintaining local homeostasis, investigating the link between its imbalance in such conditions that are known to have an association with oral diseases including cancers may lead to the identification of specific microbiome-based signatures for its early diagnosis.

Roscovitine inhibits activation of promoters in herpes simplex virus type 1 genomes independently of promoter-specific factors.

Flavopiridol, roscovitine, and other inhibitors of Cyclin-Dependent Kinases (CDK) inhibit the replication of a variety of viruses in vitro while proving nontoxic in human clinical trials of their effects against cancer. Consequently, these and other Pharmacological CDK inhibitors (PCIs) have been proposed as potential antivirals. Flavopiridol potently inhibits all tested CDKs and inhibits the transcription of most cellular and viral genes. In contrast, roscovitine and other purine PCIs inhibit with high potency only CDK1, CDK2, CDK5, and CDK7, and they specifically inhibit the expression of viral but not cellular genes. The levels at which purine PCIs inhibit gene expression are unknown, as are the factors which determine their specificity for expression of viral but not cellular genes. We show herein that roscovitine prevents the initiation of transcription of herpes simplex virus type 1 (HSV-1) genes but has no effect on transcription elongation. We further show that roscovitine does not inhibit the initiation or elongation of cellular transcription and that its inhibitory effects are specific for promoters in HSV-1 genomes. Therefore, we have identified a novel biological activity for PCIs, i.e., their ability to prevent the initiation of transcription. We have also identified genome location as one of the factors that determine whether the transcription of a given gene is inhibited by roscovitine. The activities of roscovitine on viral transcription resemble one of the antiherpesvirus activities of alpha interferon and could be used as a model for the development of novel antivirals. The genome-specific effects of roscovitine may also be important for its development against virus-induced cancers.