Pancreatic Tumors. Группа авторов
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Название: Pancreatic Tumors
Автор: Группа авторов
Издательство: Ingram
Жанр: Медицина
Серия: Monographs in Clinical Cytology
isbn: 9783318066043
isbn:
For the assessment of pancreatic cystic lesions, ancillary tests that aid in the diagnosis are CA19-9, CEA, and amylase levels in the cyst fluid, and some special stains. Special stains such as periodic acid-Schiff (PAS) and PAS with diastase (dPAS) detect the presence of glycogen. Glycogen is present in the clear cytoplasm of the cuboidal cells of serous cystadenoma and in the zymogen granules of the acinar cell lesions. PAS, mucicarmine (for neutral mucin), and Alcian blue (acid mucin) are used to detect the presence of intracellular and extracellular mucin. The cyst fluid CEA level is a very good test to diagnose if the cyst is mucinous, in which case the level usually exceeds 192 ng/mL [57]. Cyst fluid amylase levels help to diagnose pseudocyst where the levels are typically elevated into thousands. This test, however, does not distinguish IPMN from MCN as both can show slightly elevated levels.
Immunostaining for Smad4 is a good surrogate for SMAD4 genetic alterations and is useful in establishing a diagnosis of adenocarcinoma as it is retained in benign pancreatic ducts and is lost in more than half of PDACs [58]. Overexpression of mesothelin favors a diagnosis of adenocarcinoma. Trypsin and chymotrypsin positivity helps to diagnose ACC.
For PanNETs, immunostains synaptophysin, chromogranin, and the proliferation marker Ki-67 can be extremely helpful. Ki-67 is of importance in the histologic grading of PanNETs, but its utility in cytological preparations remains to be determined [59]. Strong nuclear staining for beta-catenin is diagnostic for SPNs in the pancreas.
Fig. 2. Flowchart depicting an algorithmic approach to pancreatic lesions for diagnostic purposes.
Cystic lesions of the pancreas exhibit a specific distinctive mutational profile for each subtype. SCNs have VHL mutations, CTNNB1 mutation is diagnostic of SPNs, MCNs have mutations involving the RNF43, KRAS, TP53, and SMAD4 genes, and IPMNs have mutations involving the genes KRAS, RNF43, GNAS, P53, and SMAD4 [60, 61].
Algorithmic Approach to Cytological Evaluation of Pancreatic Masses
Indications for pancreatic FNA are the presence of a solid or cystic mass. It is important to distinguish benign, indolent, or inflammatory processes which may be treated with observation, compared to neoplastic processes which require surgery or neoadjuvant or adjuvant chemotherapy. An algorithmic approach in the evaluation of pancreatic lesions includes clinical history, radiographic findings, cytological findings, and ancillary studies to yield the most clinically relevant interpretation of the aspirated material (Fig. 2).
Some of the pancreatic tumors show certain age and gender predilections as MCNs occur in middle-aged women and pancreatoblastoma is a childhood tumor. Imaging findings are very informative as to whether the mass is cystic or solid. This information determines the cytopathological algorithm. Different entities are considered on the radiographic information depending on whether the mass is solid, solid and cystic, entirely cystic, or cystic with connection to the pancreatic ductal system. If the lesion is solid, entities such as chronic pancreatitis, lobular atrophy, adenocarcinoma, pancreatic endocrine tumor, ACC, and metastases are some of the main differential diagnoses that are considered. Any solid tumor that undergoes cystic degeneration may present radiographically as a solid and cystic lesion. Tumors that present as solid and cystic lesions include PanNETs and SPNs. Purely cystic lesions include MCNs, serous cystadenoma, side branch IPMN, and pseudocysts. When a dilated main pancreatic duct is present or a connection of the cyst to the ductal system is demonstrated, a diagnosis of IPMN may be made. Gross evaluation of the material aspirated is very useful, especially in cystic lesions. Evaluation of the smears starts at a low-power examination where the cellularity, architecture, and background information are collected. At intermediate power, assessments made at low power are confirmed and architectural patterns can be further analyzed. At high power, nuclear and cytological features and mitotic figures are appreciated. Ancillary studies include immunohistochemistry, flow cytometry for suspected lymphoma, cyst fluid analysis for CEA, amylase, and occasionally for k-RAS mutations and loss of heterozygosity.
Disclosure Statement
The author has no conflicts of interest to disclose.
References
1Gill AJ, Klimstra DS, Lam AK, Washington MK: 10 Tumours of the pancreas; in WHO Classification of Tumours Editorial Board: Digestive System Tumours. WHO Classification of Tumours. 5th Edition. Lyon, IARC, 2019, pp 295–372.
2Rawla P, Sunkara T, Gaduputi V: Epidemiology of pancreatic cancer: global trends, etiology and risk factors. World J Oncol 2019;10:10–27.
3Bosetti C, Lucenteforte E, Silverman DT, Petersen G, Bracci PM, Ji BT, Negri E, Li D, Risch HA, Olson SH, Gallinger S, Miller AB, Bueno-de-Mesquita HB, Talamini R, Polesel J, Ghadirian P, Baghurst PA, Zatonski W, Fontham E, Bamlet WR, Holly EA, Bertuccio P, Gao YT, Hassan M, Yu H, Kurtz RC, Cotterchio M, Su J, Maisonneuve P, Duell EJ, Boffetta P, La Vecchia C: Cigarette smoking and pancreatic cancer: an analysis from the International Pancreatic Cancer Case-Control Consortium (Panc4). Ann Oncol 2012;23:1880–1888.
4Michaud DS: Obesity and pancreatic cancer. Recent results. Cancer Res 2016;208:95–105.
5McWilliams RR, Rabe KG, Olswold C, De Andrade M, Petersen GM: Risk of malignancy in first degree relatives of patients with pancreatic carcinoma. Cancer 2005;104:388–394.
6Hruban RH, Canto MI, Goggins M, Schulick R, Klein AP: Update on familial pancreatic cancer. Adv Surg 2010;44:293–311.
7Klein AP, Brune KA, Petersen GM, Goggins M, Tersmette AC, Offerhaus GJ, Griffin C, Cameron JL, Yeo CJ, Kern S, Hruban RH: Prospective risk of pancreatic cancer in familial pancreatic cancer kindreds. Cancer Res 2004;64:2634–2638.
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