 Hello everyone, I am Dr. Shivani Chandra, post-graduate resident in the Department of Radio Diagnosis at Atul Bihari Vajpayee Institute of Medical Sciences and Dr. RML Hospital, New Delhi. I will be presenting my paper on the topic of role of multi-detector computer tomography in evaluation of pancreatic neoplasms. MDCT is touted as the main workhorse for the evaluation of pancreatic tumors. In quick and cost effective, it also allows for multi-phasic imaging, enabling excellent characterization of the mass lesion. It provides information about the extent, vascular infiltration and sites of metastasis, all of which are crucial determinants for receptability. In this review, we discussed the imaging findings of cystic as well as solid pancreatic tumors using MDCT. The aim of the study is to characterize pancreatic neoplasms using MDCT. This was a cross-sectional observation study conducted at Atul Bihari Vajpayee Institute of Medical Sciences and Dr. RML Hospital. The scans were performed on semen somatom definition flash 128th fly scanner in the Department of Radio Diagnosis. The phase is used to a non-contrast earlier arterial pancreatic and delayed portal venous using rapid contrast agent administration at 3 to 5 millilitres per second, oral administration of 500 to 700 millilitres of water approximately 30 minutes before imaging time was also done. A total of 40 patients were included, out of which 55% demonstrated solid pancreatic lesions and 45% had cystic pancreatic neoplasms. Out of the solid neoplasms, 77% were pancreatic adenocarcinomas, 9% were metastatic deposits, 9% were neuroendocrine tumors, and one case was pancreatic lymphoma. In the remaining cystic group of lesions, 44% comprised of IPMNs, 27% comprised of mucinous cyst adenomas, and another 27% were of serous cyst adenomas. According to the individual cases, this was the case of pancreatic adenocarcinoma, here we can see a heterogeneous hypodense mass in the pancreatic head with a trophy of the pancreatic tail and a dilated NPD. There is associated IHBRD. In INSET 1, we can see that there is obliteration of the spleen or portal confluence and in INSET 2, we see that there is infiltration into the D2 segment of the diurnal. This was the case of pancreatic neuroendocrine tumor, where we can see a hypervascular enhancing mass in the arterial phase in the pancreatic neck. This was also associated with multiple hypervascular enhancing lesions in the liver, as well as a paracavel lymph node metastatic deposit. This was the case of a pancreatic metastasis from a lung primary. Here we can see a heterogeneously enhancing mass lesion in the right lung, along with a hypovascular rounded metastatic deposit in the pancreatic body. This was the case of pancreatic lymphoma, where we can see multiple round, hypotenuating masses seen in the pancreatic body and tail. Bilateral kidneys show evidence of multiple hypo-enhancing masses with enlarged aotokaval and para-aotic lymph node masses. This was the case of pancreatic IPMN. In here, we can see a cystic attenuation lesion in the pancreatic insinid process, which is communicating with the main pancreatic duct. These findings are suggestive of a side branch IPMN. This was the case of pancreatic mucinocystadenoma, where we can see a unilocular cystic lesion in the pancreatic insinid process and the head region, and there is no communication with the NPD. This was the case of pancreatic searcystadenoma, where we can see a multi-lobulated microcystic lesion in the pancreatic head and there is no obvious communication to the main pancreatic duct. The age group mostly affected by pancreatic mass lesions in this study was 50 to 75 years, which is in accordance with the findings of Jamath et al. who reported that these were uncommon below the age of 40 years. Pancreatic neoplastic lesions were more common in males and out of the solid pancreatic neoplasms, the most common entity was a pancreatic adenocarcinoma, comprising 77% of the solid neoplasms. Out of the cystic pancreatic neoplasms, the most common entity was IPMN, which comprised of 44% of the cystic neoplasms. Coming to the MDCT imaging findings in each case, pancreatic adenomas present as poorly marginated hyper-enhancing masses mostly located in the head and insinid process. They show the double duct sign which is dilatation of the NPD as well as the CBD, signs of vascular encasement and spread to adjacent organs. Pancreatic neuroendocrine tumors are hypervascular. They present as homogeneous masses if they are small and heterogeneous and cystic masses if large. They are displaced rather than inlating vessels. Pancreatic lymphomas present as hyper-enhancing homogeneous tumors with associated peripancreatic lymph nodal enlargement and they encase rather than inlaid vessels. Pancreatic metastases have a variable appearance and they depend on the primary, commonly arising from renal cell carcinomas, melanomas, lung carcinomas and breast carcinoma. In the cystic pancreatic neoplasms, pancreatic IPMN presents as a cystic lesion which communicates with the NPD mostly located in the pancreatic head and they may be multifocal. Pancreatic mucinocystic neoplasms present as macrocystic masses with thick walls and peripheral mule calcifications typically showing no communication with the NPD mostly located in the pancreatic body and the tail. Pancreatic serocystic neoplasms present as microcystic lobulated masses and they have no communication with NPD. Sometimes they show a central scar with calcification which allows for a more specific diagnosis. Thus, NBCT plays a central role in the differential diagnosis of pancreatic neoplasms. It can characterize lesions as solid or cystic and determine the extent of vascularity. Further, it can determine the extent of the lesion and the most resides of metastasis and vascular involvement. Thus enabling radiologists to play pivotal roles in deciding the lines of management and in determining patient promises. These are my references. Thank you.