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Abstract Background Transformation and progression of lymphoma after treatment is well known; however, since the advent of chemotherapy and radiotherapy, progression in untreated lymphoma is seldom seen. We present a case which was misdiagnosed and treated as abdominal tuberculosis later presented with progression and involvement of oral cavity. Case presentation A 41-year-old male who presented with urinary symptoms and abdominal pain was diagnosed as abdominal tuberculosis and treated. Two years later, he presented with B symptoms and oral cavity lesion that was diagnosed as diffuse large B cell lymphoma. The patient was treated with R-CHOP chemotherapy with complete regression of the lesion. Conclusion Involvement of extranodal sites in predominantly nodal disease does occur; however, involvement of oral cavity is rare. Though primary extranodal lymphoma is reported to occur in oral cavity and oropharynx, natural progression in untreated disease is seldom documented.

Abstract Oral squamous cell cancer (OSCC) is a common malignancy attributed to use of chewing smokeless tobacco and smoking. Most of the targeted strategies are based on EGFR expression and mutation; however, none of them has shown significant improvement in survival and response rates. We carried out this study to evaluate mutational profile of tobacco associated oral carcinoma with special emphasis on EGFR and its downstream events. Patients and methods A total of 46 histologically proven cases were recruited between January 2017 and January 2019. Apart from detailed clinical and histological studies, the paraffin-embedded tissue was submitted for expression of 50 genes using Next Generation Sequencing using Ion Ampliseq Cancer Hotspot Panel v2. Results The mean age of patients was 47.8 ± 10.9 years. Majority had tumors on buccal mucosa (24) and tongue (13). Nineteen of these tumors were larger than 4 cm, and 5 had adjacent site involvement. Thirty one were node positive. TP53 mutations were commonest seen in 19 followed by CDKN2A in 11, HRAS in 8, PIK3CA in 3, SMARCB1 in 2, and KIT, EGFR, BRAF, STK11, ABL1, RB1 in one case each. Concomitant TP53 mutation was identified with other mutations like CDKN2A, HRAS, KIT, PIK3CA, STK11, SMARCB1, ABL1, and RB1 making tobacco-associated OSCC as a heterogeneous mutational tumor with multiple events. A patient with TP53 mutations has poor disease free survival (47.4 vs 63% p = 0.17); however, this was not statistically significant. Conclusion The study shows a heterogeneous mutational spectrum with multiple mutational events in OSCC. The low EGFR mutation rates and higher mutations in EGFR downstream pathways including that in TP53 and HRAS suggest that anti EGFR strategies may not succeed in these tumors and newer agents and therapeutic combinations need to be tried.