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Objective: To assess the feasibility of 18F-2-fluoro-2-deoxy-D-glucose positron emission tomography/computed tomography (FDG-PET/CT) scan limited to the original sites of lymphoma in 1st follow-up (F/U) post-chemotherapy to reduce patient’s radiation exposure and scan time. Patients and methods: FDG PET/CT scans of 100 lymphoma patients were reviewed and the sites of disease in pre-Chemotherapy and the 1st F/U post-chemotherapy scans were recorded. The supposed saved time from PET part of the scan and reduction in radiation dose from CT part if PET/CT scan limited to the original sites of lymphoma in 1st F/U post-chemotherapy scan is used, were calculated. Result: 45% of 1st F/U post-chemotherapy PET/CT scans showed no significant residual FDG-uptake indicating complete metabolic response. Significant residual FDG-uptake at known disease sites was seen in 55% of 1st F/U post-chemotherapy scans indicating residual disease. No lesions with significant FDG uptake in new sites were detected in the 1st F/U post-chemotherapy PET/CT indicating no unexpected sites of lymphoma. The supposed reduction in the mean scan time and radiation dose is 5.3 ± 1.47 minutes and 4.2 ± 1.2 mSv respectively if scan limited to the sites of known disease is used in 1st FU-P-CHT, without missing any significant findings. Conclusion: It is not mandatory to do WB 18F-FDG PET/CT scan in assessment of early response to chemotherapy in curable lymphoma and it may be sufficient to limit scans to the sites of known disease without missing any significant findings, resulting in significant reduction in total radiation dose and time saving.

The limited effectiveness of therapy for patients with advanced stage head and neck squamous cell carcinoma (HNSCC) or recurrent disease is a reflection of an incomplete understanding of the molecular basis of HNSCC pathogenesis. MUC4, a high molecular weight glycoprotein, is differentially overexpressed in many human cancers and implicated in cancer progression and resistance to several chemotherapies. However, its clinical relevance and the molecular mechanisms through which it mediates HNSCC progression are not well understood. This study revealed a significant upregulation of MUC4 in 78% (68/87) of HNSCC tissues compared with 10% positivity (1/10) in benign samples (P=0.006, odds ratio (95% confidence interval)=10.74 (2.0-57.56). MUC4 knockdown (KD) in SCC1 and SCC10B HNSCC cell lines resulted in significant inhibition of growth in vitro and in vivo, increased senescence as indicated by an increase in the number of flat, enlarged and senescence-associated β-galactosidase (SA-β-Gal)-positive cells. Decreased cellular proliferation was associated with G0/G1 cell cycle arrest and decrease expression of cell cycle regulatory proteins like cyclin E, cyclin D1 and decrease in BrdU incorporation. Mechanistic studies revealed upregulation of p16, pRb dephosphorylation and its interaction with histone deacetylase 1/2. This resulted in decreased histone acetylation (H3K9) at cyclin E promoter leading to its downregulation. Orthotopic implantation of MUC4 KD SCC1 cells into the floor of the mouth in nude mice resulted in the formation of significantly smaller tumors (170±18.30 mg) compared to those (375±17.29 mg) formed by control cells (P=0.00007). In conclusion, our findings showed that MUC4 overexpression has a critical role by regulating proliferation and cellular senescence of HNSCC cells. Downregulation of MUC4 may be a promising therapeutic approach for treating HNSCC patients.