scholarly journals Sinonasal Secretory Carcinoma of Salivary Gland with High Grade Transformation: A Case Report of this Under-Recognized Diagnostic Entity with Prognostic and Therapeutic Implications

2017 ◽  
Vol 12 (2) ◽  
pp. 274-278 ◽  
Author(s):  
Bin Xu ◽  
Ruth Aryeequaye ◽  
Lu Wang ◽  
Nora Katabi
Keyword(s):  
Salivary Gland ◽  
Case Report ◽  
High Grade ◽  
Secretory Carcinoma ◽  
Therapeutic Implications ◽  
High Grade Transformation

scholarly journals Secretory Carcinoma of Salivary Gland with High-Grade Histology Arising in Hard Palate: A Case Report

Reports ◽  
2020 ◽  
Vol 3 (2) ◽  
pp. 6
Author(s):  
Kiyofumi Takabatake ◽  
Keisuke Nakano ◽  
Hotaka Kawai ◽  
Saori Yoshida ◽  
Haruka Omori ◽  
...  
Keyword(s):  
Salivary Gland ◽  
Hard Palate ◽  
Relevant Literature ◽  
Salivary Gland Tumor ◽  
World Health ◽  
Fusion Product ◽  
Low Grade ◽  
High Grade ◽  
Secretory Carcinoma ◽  
High Grade Transformation

Secretory carcinoma (SC) is a recently described salivary gland tumor reported in the fourth edition of World Health Organization classification of head and neck tumors. SC is characterized by strong S-100 protein, mammaglobin, and vimentin immunoexpression, and harbors a t(12;15)(p13;q25) translocation which leads to ETV6-NTRK3 fusion product. Histologically, SC displays a lobulated growth pattern and is often composed of microcystic, tubular, and solid structures with abundant eosinophilic homogenous or bubbly secretion. SC is generally recognized as low-grade malignancy with low-grade histopathologic features, and metastasis is relatively uncommon. In this case, we described a SC of hard palate that underwent high grade transformation and metastasis to the cervical lymph node in a 54-year-old patient. In addition, this case showed different histological findings between primary lesion and metastasis lesion. Therefore, the diagnosis was confirmed by the presence of ETV6 translocation. Here, we report a case that occurred SC with high-grade transformation in the palate, and a review of the relevant literature is also presented.

Salivary Gland Secretory Carcinoma With High-Grade Transformation, CDKN2A/B Loss, Distant Metastasis, and Lack of Sustained Response to Crizotinib

2017 ◽  
Vol 25 (7) ◽  
pp. 613-618 ◽  
Author(s):  
Nicole A. Cipriani ◽  
Elizabeth A. Blair ◽  
Joshua Finkle ◽  
Jennifer L. Kraninger ◽  
Christopher M. Straus ◽  
...  
Keyword(s):  
Salivary Gland ◽  
Molecular Genetic ◽  
Low Grade ◽  
High Grade ◽  
Secretory Carcinoma ◽  
Parotid Duct ◽  
Pleural Metastases ◽  
High Grade Transformation ◽  
Magnetic Resonance Imaging Mri ◽  
The Right

Background. Salivary gland secretory carcinoma is usually a low-grade neoplasm. However, high-grade transformation can occur and has important implications for clinical outcome. Methods. A patient presented with an enlarging buccal mass. Magnetic resonance imaging (MRI) showed a tumor with a biphasic appearance along the right parotid duct. Local excision and histopathologic examination confirmed the diagnosis of secretory carcinoma with high-grade transformation. ETV6-NTRK3 translocation and loss of CDKN2A/B were identified. Results. The patient subsequently presented with cough and dyspnea and was found to have pleural metastases. Carboplatin and paclitaxel exacerbated the symptoms. Crizotinib resulted in initial symptomatic and radiographic improvement; however, the patient soon succumbed to progressive intrathoracic disease. Conclusions. High-grade salivary gland secretory carcinoma can have a biphasic appearance on MRI. Diagnosis is confirmed by the histologic appearance and associated ETV6-NTRK3 fusion. Additional molecular genetic events leading to transformation are unknown; however, loss of CDKN2A/B may have contributed. Treatment with multimodal chemotherapy was of limited benefit.

scholarly journals Histological surprise, mammary analogue secretory carcinoma of parotid gland

2021 ◽  
Vol 8 (12) ◽  
pp. 3731
Author(s):  
Iram T. Pasha ◽  
Akhila K. ◽  
Ravikumar V. ◽  
Sandeep Kumar
Keyword(s):  
Salivary Gland ◽  
Case Report ◽  
Parotid Gland ◽  
Low Grade ◽  
Secretory Carcinoma ◽  
Carcinoma Of The Breast ◽  
Mammary Analogue Secretory Carcinoma ◽  
Male Preponderance ◽  
Slow Growing

A recent described entity, mammary analogue secretary carcinoma (MASC) in 2010 by Skalova et al whose morphological and immunohistochemical features are similar in secretory carcinoma of the breast and salivary gland. This is a low-grade carcinoma which presents as a firm, slow-growing, circumscribed lesion with male preponderance. We present a case report of MASC.

scholarly journals Oncogenic Orphan Nuclear Receptor NR4A3 Interacts and Cooperates with MYB in Acinic Cell Carcinoma

Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2433
Author(s):  
David Y. Lee ◽  
Kathryn J. Brayer ◽  
Yoshitsugu Mitani ◽  
Eric A. Burns ◽  
Pulivarthi H. Rao ◽  
...  
Keyword(s):  
Salivary Gland ◽  
Cell Carcinoma ◽  
Salivary Gland Tumor ◽  
Binding Domain ◽  
Acinic Cell Carcinoma ◽  
High Grade ◽  
Orphan Nuclear Receptor ◽  
Acinic Cell ◽  
High Grade Transformation ◽  
Domain Transformation

Acinic cell carcinoma (AcCC) is a morphologically distinctive salivary gland malignancy often associated with chromosome rearrangements leading to overexpression of the NR4A3 transcription factor. However, little is known about how NR4A3 contributes to AcCC biology. Detailed RNA-sequencing of 21 archived AcCC samples revealed fusion reads arising from recurrent t(4;9), t(9;12), t(8;9) or t(2;4) chromosomal translocations, which positioned highly active enhancers adjacent to the promoter of the NR4A3 gene or the closely related NR4A2 gene, resulting in their aberrant overexpression. Transcriptome analyses revealed several distinct subgroups of AcCC tumors, including a subgroup that overexpressed both NR4A3 and MSANTD3. A poor survival subset of the tumors with high-grade transformation expressed NR4A3 and POMC as well as MYB, an oncogene that is the major driver in a different type of salivary gland tumor, adenoid cystic carcinoma. The combination of NR4A3 and MYB showed cooperativity in regulating a distinct set of genes. In addition, the ligand binding domain of NR4A3 directly bound the Myb DNA binding domain. Transformation assays indicated that, while overexpressed NR4A3 was sufficient to generate transformed colonies, the combination of NR4A3 plus Myb was more potent, leading to anchorage-independent growth and increased cellular invasiveness. The results confirm that NR4A3 and NR4A2 are the main driver genes of AcCC and suggest that concurrent overexpression of NR4A3 and MYB defines a subset of AcCC patients with high-grade transformation that display exceptionally poor outcome.

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