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Background Newly, chemo‐preventive technique might be a hopeful advancement in developing countries for treating cancers with the aid of toxic less natural based constituents. Malignancy urges to augment effectual chemo‐preventive agents that are look forward to suppress the tumours which may be stimulated by chewing and smoking of tobacco and over alcohol consumption related with the high prevalence of human oral cancer (OC) patients. Methods In the present research, we examined to assess antioxidants, lipid peroxidation (LPO) and detoxification enzymes levels of anticancer activity of mangiferin on 0.5% 7.12‐dimethylbenz[a]anthracene (DMBA) provoked hamster cheek pouch carcinoma (HCPC). OC on hamster buccal pouch (HBP) was incited by DMBA treatment for thrice per week for over 14 weeks. Results 100% well defined OC establishment with body weight (bw), tumour burden (TB), antioxidant, LPO and liver marker enzymes and also histological changes were observed on DMBA‐challenged buccal pouch carcinoma (BPC) in hamsters. Orally treated mangiferin at an effective dosage of 50 mg/kg bw, to DMBA painted hamsters were significantly averted the body weight, succession of tumour, the biochemical as well as histopathological changes. Conclusion Findings of this work clearly suggest that the anti‐carcinoma effect of mangiferin possesses the modulator effects on potent antioxidant, anti‐LPO and detoxification agents to expel the metabolites of malignant cells, on DMBA‐provoked BPC in hamsters.

Systemic hyalinosis is a rare autosomal recessive inheritance disease characterized by accumulation of amorphous, unidentified hyaline material in skin and other organs, which leads to papulonodular skin lesions, gingival hypertrophy, flexion contractures of the joints, and large subcutaneous tumors. It is composed of 2 allelic syndromes, infantile systemic hyalinosis and juvenile hyaline fibromatosis. Here we describe a patient with juvenile hyaline fibromatosis confirmed by clinical and histopathologic findings, and genetic analysis, which revealed a novel homozygous splice site mutation IVS14+1G→T on exon 14 in anthrax toxin receptor 2 gene.

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