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Head and Neck Pathology
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
Ram Moorthy, Adrian T. Warfield, Max Robinson
Acinic cell carcinoma accounts for 7–17.5% of all malignant salivary gland neoplasms. Approximately 80% arise from the parotid gland, with the remaining 20% arising mainly from the minor salivary glands or submandibular glands, and only 1% from the sublingual gland. There is a male preponderance and they usually present in the third decade of life.11, 12
Surgical and other investigations
Published in John Dudley Langdon, Mohan Francis Patel, Robert Andrew Ord, Peter Brennan, Operative Oral and Maxillofacial Surgery, 2017
As tumours are increasingly studied at the molecular level, the list of identified tumour-specific and defining translocations grows by the year. Study of salivary gland tumours at the genetic level is one example where in recent times; new information gained from these studies has led to addition of a new entity to the classification, namely mammary analogue secretory carcinoma. Rather than this being a newly occurring tumour, it is most likely that these have previously been designated as acinic cell carcinoma. Information gained from molecular investigation may in future be used to provide prognostic information or guide treatment.
Targeting human EGFR 2 (HER2) in salivary gland carcinoma
Published in Expert Review of Anticancer Therapy, 2023
Michael Wotman, Adel El-Naggar, Renata Ferrarotto
While some patients with metastatic SGC may forgo active treatment in favor of surveillance, such as those with indolent, asymptomatic adenoid cystic or acinic cell carcinoma, individuals with high-grade carcinomas often require immediate therapy, especially when tumors cause symptoms, compromise organ function, or demonstrate rapid growth [51]. Traditionally, there have been limited options in this setting as cytotoxic chemotherapy has suboptimal response rates, a short duration of response, and significant toxicity [52,53]. Anti-HER2 therapies may offer a better alternative to chemotherapy alone in HER2-positive tumors. Small phase II and larger basket trials have evaluated the effectiveness of different HER2-targeting agents in patients with unresectable locally advanced, recurrent, or metastatic HER2-positive SGC and will be reviewed below.
A Parotid Gland Mammary Analogue Secretory Carcinoma in a 4-Year-Old Boy: Case Report and Literature Review
Published in Fetal and Pediatric Pathology, 2023
Zhao Meng, Wu Si, Zhu Xiuli, Yueping Liu
The histologic features of the MASC reported herein are typical of those described in primary salivary gland tumors: Eosinophilic vacuolated cytoplasm within cystic, tubular, and/or papillary architecture indicative of true acinar differentiation, low-grade and pale nuclei, infrequent mitotic figures [17–20]. There is no prominent fibrosclerotic stroma and thick hyalinized fibrous septa. MASC and secretory carcinoma of the breast also have common immuno-histochemical findings such positivity for S100 and mammaglobin, usually with a diffuse and strong staining pattern [21], while being negative for ER/PR/Her2. STAT5 was also reported to be a useful marker in the differential diagnosis of MASC. Strauss et al. [22] indicated that the MASC expressed by STAT5 might be related to t(12;15)(p13;q25) chromosomal translocation. The expression of nuclear and cytoplasmic STAT5 immunoreactivity is not specific, as positivity for this marker is observed in acinic cell carcinoma (ACC) [1].
Genomics in non-adenoid cystic group of salivary gland cancers: one or more druggable entities?
Published in Expert Opinion on Investigational Drugs, 2019
Stefano Cavalieri, Francesca Platini, Cristiana Bergamini, Carlo Resteghini, Donata Galbiati, Paolo Bossi, Federica Perrone, Elena Tamborini, Pasquale Quattrone, Lisa Licitra, Laura Deborah Locati, Salvatore Alfieri
Tropomyosin receptor kinases (TRK) are a group of transmembrane receptors binding nerve growth factor (NGF). In 2010, Skalova et al. first described a subset of salivary gland cancers, formerly diagnosed as acinic cell carcinoma or cystadenocarcinoma, resembling secretory carcinoma of the breast and bearing t(12;15) (p13;q25) ETV6-NTRK3 translocation [42]. Thereafter, this particular tumor type was recognized as mammary analogue secretory carcinoma (MASC) becoming a specific pathologic entity in the landscape of non-ACC group included in the WHO classification for the first time in 2017. Besides, it is worth noticing that not all secretory carcinomas have NTRK3 as fusion partner, a subset has an ETV6-RET fusion which is shared only with a rare subtype of sinonasal carcinoma [43–45]. MASC is usually indolent, and patients are effectively cured by loco-regional treatments. Thus, systemic therapies are not indicated except for sporadic cases of metastatic disease. Specific drugs, as entrectinib [46] and larotrectinib [47], exert a pan-TRK blockade, including the product of ETV6-NTRK3 translocation. TRK inhibitors showed activity in cases of recurrent or metastatic mammary analogue secretory carcinoma [48]. An impressive activity of entrectinib within three phase I/II basket trials (ALKA, STARTRK-1, STARTRK-2) was recently reported across tumors harboring NTRK rearrangement [49]. Due to these promising results, all patients with advanced ETV6-NTRK3 translocated mammary analogue secretory carcinomas requiring systemic therapies deserve to be treated with TRK inhibitors.