Browsing by Author "Dipanjan Biswas"

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Altered expression of NKX3.1 has significant prognostic value in gallbladder cancer
(Elsevier Inc, 2019) Deepika Singh; Amisha Bharti; Dipanjan Biswas; Mallika Tewari; Mumtaz Ahmed Ansari; Sunita Singh; Gopeshwar Narayan
Introduction: NKX3.1, an androgen regulated prostate specific transcription factor, inhibits prostate tumorigenesis. However, its role in GBC is not understood. We aimed to investigate NKX3.1 expression profile to define its role in GBC. Methods: We analyzed the expression of NKX3.1 in 52 GBC and 52 paired adjacent control samples at mRNA level through Real time RT-PCR and validated at protein level through Western blotting. The transcript level data was correlated with clinico-pathological parameters. Promoter hypermethylation was analyzed through methylation specific PCR (MSP). Results: NKX3.1 shows down regulation in 55.8%, up regulation in 25% whereas no change in 19.2% of samples. Its mRNA expression is significantly down regulated in late stage tumors (p =0.0103), in tumors with nodal metastasis (p =0 .0036) and in high grade tumors (p =0 .0173). Interestingly, NKX3.1 is significantly higher in male patients than female patients (p =0 .0057). Kaplan-Meyier analysis reveals prolonged median survival of patients with higher level of NKX3.1 expression compared with patients having low or no change in expression. Conclusion: Our findings suggest that loss or lower expression of NKX3.1 may be a critical in determining the phenotype of GBC. Its expression profile may serve as positive prognostic marker for GBC. © 2019 Elsevier Inc.
Clinical Significance of Overexpression of Oct4 in Advanced Stage Gallbladder Carcinoma
(Springer, 2023) Deepika Singh; Dipanjan Biswas; Mallika Tewari; Amrita Ghosh Kar; Mumtaz Ahmad Ansari; Sunita Singh; Gopeshwar Narayan
Background: Oct4 has critical role in maintaining pluripotency, proliferative potential, and self-renewal capacity in embryonic stem and germ cells. Although Oct4 has been shown to be upregulated in many cancers, its clinical significance in gallbladder carcinoma is poorly understood. Methods: We studied the expression profile of Oct4 in 61 GBC and 30 chronic cholecystitis (as control) using real time RT-PCR, western blotting, and immunohistochemistry. The expression data was correlated with clinico-pathological parameters. The diagnostic utility was assessed through ROC curve, and prognostic value was analyzed by Kaplan–Meier method. Results: Oct4 was significantly upregulated at mRNA as well as protein levels. The higher mRNA expression shows significant association with late stage, late T stage, and higher grade of tumor. A significant positive correlation was also observed with stage, T stage, and tumor grade. Sum score analysis of protein expression shows positive correlation with stage and the presence or absence of gallstone in tumor samples. The ROC curve analysis revealed the moderate diagnostic potential of Oct4. Kaplan–Meier analysis showed that patients having higher expression of Oct4 were having low mean survival compared with the patients with lower Oct4 expression. Conclusion: In conclusion, our data suggests that higher expression of Oct4 may serve as potential biological indicator for tumor aggressiveness and poor prognosis of GBC. © 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
Co-existence of Diffuse Serous Cystadenoma and Pancreatic Neuroendocrine Tumor
(Springer India, 2017) Mallika Tewari; Shashikant Patne; Richa Katiyar; Dipanjan Biswas; Hs Shukla
Diffuse serous cystic neoplasm (SCN) associated with pancreatic neuroendocrine tumor (PNET) is a rare finding reported previously in only three patients to the best of our knowledge. We herein present one such interesting report of a diffuse serous cystic adenoma (SCA) and co-existent PNET in a 25-year old lady who presented with abdominal pain for past 6 months. A triple-phase pancreatic protocol computed tomography (CT) scan revealed multiple cysts involving the entire pancreas. The cysts were thin walled, ranging from 2 to 8 cm in width, with no calcification or central scar that was confirmed at laparotomy. A frozen section revealed a neuroendocrine tumor and she underwent total pancreatectomy. Diffuse SCA with co-existent PNET infiltrating nerve bundles of the pancreatic parenchyma was made upon histopathology further verified by chromogranin-A immunostaining. The patient is insulin dependent and doing well at 2 years of follow-up. The origin of endocrine tumors from multipotent ductular stem cells has been suggested. © 2017, Association of Surgeons of India.
Frequent Downregulation and Promoter Hypermethylation of DLC1: Relationship with Clinical Outcome in Gallbladder Cancer
(Springer, 2022) Deepika Singh; Amisha Bharti; Dipanjan Biswas; Mallika Tewari; Amrita Ghosh Kar; Mumtaz Ahmed Ansari; Sunita Singh; Gopeshwar Narayan
Introduction: Down regulation of DLC1 is associated with poor prognosis in many cancers, however, its role in gallbladder cancer (GBC) is still unclear. In present study, we investigated the expression profile and promoter methylation status of DLC1. Methods: Expression profiles of DLC1 in 55 GBC and their paired adjacent control samples were analyzed through real time RT-PCR and immunohistochemistry. The mRNA data was correlated with clinico-pathological parameters. Promoter hypermethylation was analyzed through MSP. Results: DLC1 shows downregulation in 76.4%, upregulation in 10.9% whereas no change in 12.7% of GBC samples. Its underexpression shows significant correlation with tumor grade and nodal spread. IHC shows cytoplasmic expression of DLC1 in normal as well as tumor samples. IHC result was concordant to mRNA result. Samples having downregulated DLC1 expression show heterozygous methylation in 83.3% of samples and homozygous methylation in 9.5% of samples whereas 7% of samples have no methylation. Kaplan–Meier analysis shows patient with decreased mRNA of DLC1 have significant low mean survival compared to patients with higher mRNA expression of DLC1. Conclusion: Our findings suggested that dysregulated expression of DLC1 and its hypermethylation may be one of the events playing roles in tumorigenesis of GBC and may serve as a potential target for development of future GBC gene therapy. © 2021, Springer Science+Business Media, LLC, part of Springer Nature.
TRAIL receptors are differentially regulated and clinically significant in gallbladder cancer
(Elsevier B.V., 2020) Deepika Singh; Chandra Bhushan Prasad; Dipanjan Biswas; Mallika Tewari; Amrita Ghosh Kar; Mumtaz Ahmed Ansari; Sunita Singh; Gopeshwar Narayan
Deregulation of the receptors of TNF-related apoptosis inducing ligand (TRAIL) has been reported in various cancers. In an effort to define the role of these receptors we profiled their expression in gallbladder cancer (GBC) and explored their clinical significance. Expression of TRAIL receptors' mRNA in GBC was analysed through reverse transcriptase polymerase chain reaction (RT-PCR), and protein through western blotting, immunohistochemistry and enzyme-linked immunosorbent assay (ELISA). mRNA data show frequent higher expression of TRAIL receptors in GBC samples. Death receptors DR4 and DR5 showed significant negative correlation with tumour stage, T stage and tumour grade; DcR1 transcript showed positive correlation with tumour stage, N stage, M stage and tumour grade. Similarly, IHC showed frequent positive staining for DR4, DR5 and DcR1in GBC samples. Cytoplasmic and nuclear DR4 protein showed negative correlation with T stage and tumour grade, whereas cytoplasmic DcR1 protein showed positive correlation with tumour stage and N stage. Nuclear DcR1 showed positive correlation with N stage. ELISA results showed significantly higher expression of secretory DcR1 in GBC patients. Kaplan–Meier analysis demonstrated significantly decreased mean survival of patients with positive staining of cytoplasmic DcR1. High level of death receptors identified the patients with early gallbladder cancer, whereas high DcR1 expression served as a prognostic factor for poor outcome. © 2020 Royal College of Pathologists of Australasia