Epigenetic Reprogramming Therapy for Increasing Therapeutic Gain in Oral Cancer: Prevention of Radiation-induced Oral Mucositis and Inhibition of Chemical-induced Oral Carcinogenesis

Objective: To estimate the efficacy of traditional Chinese medicine (Chining decoction, CHIN) for radiation-induced oral mucositis in patients with head and neck cancer. Methods: From May 2014 to December 2015, 70 consecutive patients were randomly assigned to receive CHIN (treatment group) or recombinant human epidermal growth factor (rhEGF) spray (control group) at a 1:1 ratio. CHIN was administered to treatment group from the first day of radiotherapy until the completion of radiotherapy. Simultaneously, the rhEGF spray was administered to control group on the oral mucosa of irradiated area. The clinical benefit was determined by gradation of mucositis (Common Terminology Criteria for Adverse Events v4.0), oral pain, and xerostomia (visual analysis scale) for each week during radiotherapy. Body mass index was evaluated before and after radiotherapy. Results: Patients in the treatment group had prominent remission of oral pain and grade of mucositis on each observing point compared with those in control group ( P < .01). Xerostomia was decreased notably in treatment group compared with control group ( P < .01). Body mass index in the treatment group exhibited advantage over control group after radiotherapy, but there was no statistical significance (19.8 ± 3.26 vs 18.8 ± 2.5 kg/m2, P = .153, >.05). Conclusions: CHIN presented an obvious advantage in preventing radiation-induced oral mucositis compared with rhEGF spray.

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Role of Oral Microbiome Signatures in Diagnosis and Prognosis of Oral Cancer

Technology in Cancer Research & Treatment ◽

10.1177/1533033819867354 ◽

2019 ◽

Vol 18 ◽

pp. 153303381986735 ◽

Cited By ~ 13

Author(s):

Indranil Chattopadhyay ◽

Mukesh Verma ◽

Madhusmita Panda

Keyword(s):

Oral Cancer ◽

Epithelial Cells ◽

Oral Cavity ◽

Bacterial Species ◽

Treatment Strategies ◽

Genetic Alterations ◽

Oral Microbiome ◽

Oral Carcinogenesis ◽

Early Diagnostic

Despite advancement in cancer treatment, oral cancer has a poor prognosis and is often detected at late stage. To overcome these challenges, investigators should search for early diagnostic and prognostic biomarkers. More than 700 bacterial species reside in the oral cavity. The oral microbiome population varies by saliva and different habitats of oral cavity. Tobacco, alcohol, and betel nut, which are causative factors of oral cancer, may alter the oral microbiome composition. Both pathogenic and commensal strains of bacteria have significantly contributed to oral cancer. Numerous bacterial species in the oral cavity are involved in chronic inflammation that lead to development of oral carcinogenesis. Bacterial products and its metabolic by-products may induce permanent genetic alterations in epithelial cells of the host that drive proliferation and/or survival of epithelial cells. Porphyromonas gingivalis and Fusobacterium nucleatum induce production of inflammatory cytokines, cell proliferation, and inhibition of apoptosis, cellular invasion, and migration thorough host cell genomic alterations. Recent advancement in metagenomic technologies may be useful in identifying oral cancer–related microbiome, their genomes, virulence properties, and their interaction with host immunity. It is very important to address which bacterial species is responsible for driving oral carcinogenesis. Alteration in the oral commensal microbial communities have potential application as a diagnostic tool to predict oral squamous cell carcinoma. Clinicians should be aware that the protective properties of the resident microflora are beneficial to define treatment strategies. To develop highly precise and effective therapeutic approaches, identification of specific oral microbiomes may be required. In this review, we narrate the role of microbiome in the progression of oral cancer and its role as an early diagnostic and prognostic biomarker for oral cancer.

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A correlative study of copper, iron, zinc and haematological parameters in oral cancer patients

MedPulse International Journal of Biochemistry ◽

10.26611/10021923 ◽

2021 ◽

Vol 19 (2) ◽

pp. 22-25

Author(s):

Joel Sabu ◽

Keyword(s):

Trace Elements ◽

Oral Cancer ◽

Serum Level ◽

Cancer Patients ◽

Serum Levels ◽

Haematological Parameters ◽

Oral Carcinogenesis ◽

Group I ◽

Iron And Zinc ◽

Oral Cancer Patients

Background: Alteration in levels of copper, iron and zinc variate the enzymatic actions in our body and thereby play a major role in etiopathogenesis of oral carcinogenesis. Aim of the study: The present study was mainly aimed to estimate, compare and correlate the serum levels of copper, iron and zinc with haematological parameters in oral cancer patients in comparison to normal controls. Methods: The collected serum of cases and controls were analyzed by using standard spectrophotometric methods in spectrophotometer analyzer and the data obtained was analysed and represented as Mean ± SD, mean difference was analyzed by Student’s T-test and Chi- square test for significance and strength of association by Karl Pearson’s correlation using SPSSv23 software. Results: Mean serum level of iron was significantly lower and the levels of zinc and copper in patients with oral cancerous lesions were significantly higher than that of healthy individuals. Pearson’s r data analysis, revealed a significant negative correlation between iron with platelets, and MCHC (Mean Corpuscular Haemoglobin Concentration). A significant positive correlation was seen between iron with haemoglobin and lymphocytes; between copper with leucocytes. Conclusions: The serum levels of zinc and copper in group I were significantly higher when compared to controls. There was a significant lower serum level of iron in Group-I when compared to controls. A significant correlation was seen in between serum trace elements and haematological parameters in oral cancer. This suggests the involvement of trace elements in variations of haematological parameters in the pathogenesis of oral carcinogenesis.

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