Activation of the interleukin-6/Janus kinase/STAT3 pathway in pleomorphic adenoma of the parotid gland

AbstractThe presence of melanin pigment and melanocytic markers expression have been rarely reported in salivary gland tumors. Herein, two cases of carcinoma arising in pleomorphic adenoma of the parotid gland and showing diffuse expression of myoepithelial and melanocytic markers are described. The clinical-pathological clues useful in the differential diagnosis with melanoma are discussed. In addition, a review of the pertinent literature is also proposed, discussing the pathologic mechanisms potentially involved in this phenomenon.

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Interleukin-6 promotes primitive endoderm development in bovine blastocysts

BMC Developmental Biology ◽

10.1186/s12861-020-00235-z ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Lydia K. Wooldridge ◽

Alan D. Ealy

Keyword(s):

Interleukin 6 ◽

Inner Cell Mass ◽

Cell Mass ◽

Cell Types ◽

Janus Kinase ◽

Primitive Endoderm ◽

Cell Numbers ◽

Downstream Target ◽

Dependent Signal ◽

Endoderm Development

Abstract Background Interleukin-6 (IL6) was recently identified as an embryotrophic factor in bovine embryos, where it acts primarily to mediate inner cell mass (ICM) size. This work explored whether IL6 affects epiblast (EPI) and primitive endoderm (PE) development, the two embryonic lineages generated from the ICM after its formation. Nuclear markers for EPI (NANOG) and PE (GATA6) were used to differentiate the two cell types. Results Increases (P < 0.05) in total ICM cell numbers and PE cell numbers were detected in bovine blastocysts at day 8 and 9 post-fertilization after exposure to 100 ng/ml recombinant bovine IL6. Also, IL6 increased (P < 0.05) the number of undifferentiated ICM cells (cells containing both PE and EPI markers). The effects of IL6 on EPI cell numbers were inconsistent. Studies were also completed to explore the importance of Janus kinase 2 (JAK2)-dependent signaling in bovine PE cells. Definitive activation of STAT3, a downstream target for JAK2, was observed in PE cells. Also, pharmacological inhibition of JAK2 decreased (P < 0.05) PE cell numbers. Conclusions To conclude, IL6 manipulates ICM development after EPI/PE cell fates are established. The PE cells are the target for IL6, where a JAK-dependent signal is used to regulate PE numbers.

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Giant Cell Carcinosarcoma of the Parotid Gland With a PLAG 1 Translocation in Association With a Pleomorphic Adenoma With HMGA2 Translocation

American Journal of Clinical Pathology ◽

10.1093/ajcp/aqaa104 ◽

2020 ◽

Vol 154 (6) ◽

pp. 811-815

Author(s):

Levon Katsakhyan ◽

Virginia A LiVolsi ◽

Ara A Chalian ◽

Paul J Zhang

Keyword(s):

Salivary Gland ◽

In Situ Hybridization ◽

Parotid Gland ◽

Giant Cell ◽

Pleomorphic Adenoma ◽

De Novo ◽

Sarcomatous Component ◽

Gland Tumor ◽

Parotid Gland Tumor

Abstract Objectives Carcinosarcomas of the salivary gland are rare neoplasms and have been described arising de novo or in association with pleomorphic adenoma (PA). PLAG1 and HMGA2 translocations are known to occur in PAs and carcinomas ex PA but are mutually exclusive. Methods We report a case of a carcinosarcoma in the parotid gland of a 77-year-old man with unusual anaplastic sarcomatoid giant cell morphology. Results Microscopically, a small separate PA was found adjacent to the carcinosarcoma. By conventional notion, the PA and carcinosarcoma would be considered related, as carcinosarcomas are well known to arise from PAs (carcinosarcoma ex PA). However, fluorescence in situ hybridization (FISH) assay demonstrated PLAG1 translocation in the carcinosarcoma and HMGA2 translocation in the separate PA. Conclusions These findings support that the carcinosarcoma likely originated from another PA with a PLAG1 translocation or de novo but not from the coexisting PA harboring a different translocation. To our knowledge, the case is the first to demonstrate PLAG1 translocation by FISH in a sarcomatous component of any parotid gland tumor, which may help better classify these tumors. In addition, multiple PAs are commonly found in the salivary gland, and to our knowledge, our case is the first to demonstrate that the same parotid gland can host PAs and PA-related tumors with different translocations.

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