A New Paradigm in Salivary Gland Tumor Cytopathology

Justin A Bishop^*
*Correspondence: Justin A Bishop, Department of Pathology, University of Texas Southwestern Medical Center at Dallas, 6201 Harry Hines Boulevard, Dallas, United States, Email:

Introduction

We are amidst an intriguing analytic upset in salivary organ pathology. It is presently grounded that a developing number of second rate to middle of the road level salivary organ neoplasms are characterized by certain hereditary modifications, eg, MAML2 combinations in mucoepidermoid carcinoma, ETV6 combinations for secretory carcinoma, and MYB/MYBL1 combinations for adenoid cystic carcinoma, among numerous others [1]. Awareness of these changes has refined salivary organ characterization by expanding the perceived morphologic spectra of these tumors, uncovering new variations, and, at times, characterizing altogether new entities [2,3]. More significant, as in regions like delicate tissue pathology, these atomic progressions have improved on the determination of specific tumors. On the off chance that a tumor is found to hold onto a MAML2 combination, for instance, it is a mucoepidermoid carcinoma, basically regardless. The value of these tumor-characterizing hereditary modifications is generally clear in cytopathology, where pathologists don't have the advantage of evaluating tumor engineering and intrusiveness. An adenoid cystic-like cribriform example can be seen in numerous considerate and dangerous tumors, yet, combined with proof of MYB combination, an authoritative finding of adenoid cystic carcinoma can be made preoperatively, permitting specialists to design their activity fittingly. Shockingly, atomic investigation has not yet reformed salivary organ cytopathology practice in a far reaching way. Modern atomic testing procedures like fluorescence in situ hybridization (FISH) and cutting edge sequencing are not broadly accessible external scholarly medical focuses. In addition, the low cellularity normal in fine-needle yearnings regularly delivers atomic examination ineffectual. An ideal arrangement would be the presentation of immunohistochemical proxies for the demonstrative hereditary tests, like NUT immunostain, which is a profoundly delicate and explicit test for the uncommon carcinomas that are characterized by NUTM1 fusions [4]. For generally scholarly and private pathology works on, acquiring another immunohistochemical stain is substantially more plausible than adding another FISH test; and, in certain conditions, the immunostain is more touchy than FISH.4 A couple of these immunostains have been presented in salivary organ cytopathology, with to a great extent baffling outcomes. MYB protein is reliably communicated in adenoid cystic carcinoma, however it is so regularly seen in indicative mimickers that the immunostain has basically no practical value [5]. Although PLAG1 and HMGA2 proteins are generally seen in pleomorphic adenomas, they are likewise communicated in different carcinomas ex-pleomorphic adenoma, so a positive immunostain can't recognize considerate and harmful tumors [6].

Since the new disclosure of NR4A3 combinations in by far most of acinic cell carcinomas, salivary organ pathologists have enthusiastically stood by to see whether NR4A3 immunohistochemistry would be a powerful analytic device. Early outcomes have been very encouraging. Haller et al exhibited that like MYB in adenoid cystic carcinoma, NR4A3 is reliably communicated in acinic cell carcinoma. Conversely, be that as it may, NR4A3 immunostaining gave off an impression of being significantly more explicit, just infrequently staining other salivary organ tumor types. In this issue of Cancer Cytopathology, Skaugen and partners present energizing discoveries that expand on this work. These creators show that NR4A3 immunostaining is profoundly valuable in cell blocks from fine-needle yearnings, beating DOG1 immunostaining as well as NR4A3 FISH. The determination of acinic cell carcinoma, albeit generally clear in tissue, is frequently extremely testing in fine-needle goals since this tumor intently takes after ordinary salivary acini. The most regularly utilized acinar markers DOG1 and SOX10 don't assist with this differential determination, however the creators exhibit that, since ordinary acini are negative, NR4A3 immunostaining settles this exemplary symptomatic situation easily. NR4A3 immunostaining is additionally viable in inadequate examples that don't pass quality affirmation for sub-atomic analysister. To put it plainly, this immunohistochemical marker seems to have turned the conclusion of acinic cell carcinoma in fine-needle desires from one of the more hard to perhaps the most clear in salivary organ cytopathology. All the more extensively, it is my expectation that the achievement of the NR4A3 immunostain will introduce another time of utilizing touchy and explicit immunostains as substitutes for sub-atomic investigation in salivary organ pathology, which would serve to improve and democratize the analysis of numerous tumor types.

References

1. Skálová Alena, Göran Stenman, Roderick HW Simpson, Henrik Hellquist and David Slouka et al. "The role of molecular testing in the differential diagnosis of salivary gland carcinomas." Am J Surg Pathol. 42(2018):e11-e27.
2. Skálová Alena, Tomas Vanecek, Radek Sima, Jan Laco and Ilan Weinreb et al. "Mammary analogue secretory carcinoma of salivary glands, containing the ETV6-NTRK3 fusion gene: a hitherto undescribed salivary gland tumor entity." Am J Surg Pathol. 34(2010): 599-608.
3. Bishop, Justin A., Ilan Weinreb, David Swanson, William H. Westra, Hina S. Qureshi, James Sciubba, Christina MacMillan, Lisa M. Rooper, and Brendan C. Dickson. "Microsecretory Adenocarcinoma." Am J Surg Pathol. 43(2019):1023-1032.                       
4. Haack Herbert, Laura A Johnson, Christopher J Fry, Katherine Crosby and Roberto D Polakiewicz et al. "Diagnosis of NUT midline carcinoma using a NUT-specific monoclonal antibody." Am J Surg Pathol. 33(2009):984.
5. Brill Louis B, William A Kanner, André Fehr, Ywonne Andrén and Christopher A Moskaluk et al. "Analysis of MYB expression and MYB-NFIB gene fusions in adenoid cystic carcinoma and other salivary neoplasms." Mod Pathol. 24(2011):1169-1176.
6. Katabi Nora, Bin Xu, Achim A Jungbluth, Lei Zhang and Sung Y Shao et al. "PLAG1 immunohistochemistry is a sensitive marker for pleomorphic adenoma: a comparative study with PLAG1 genetic abnormalities."Histopathology 72(2018):285-293.