Frankly Invasive Carcinoma Ex-intraductal Carcinoma: Expanding on an Emerging and Perplexing Concept in Salivary Gland Tumor Pathology

Author(s):  
Anne C. McLean-Holden ◽  
Lisa M. Rooper ◽  
Daniel J. Lubin ◽  
Kelly R. Magliocca ◽  
Varsha Manucha ◽  
...  
2017 ◽  
Vol 141 (3) ◽  
pp. 381-395 ◽  
Author(s):  
Christopher C. Griffith ◽  
Alessandra C. Schmitt ◽  
James L. Little ◽  
Kelly R. Magliocca

Accurate diagnosis of salivary gland tumors can be challenging because of the many diagnostic entities, the sometimes extensive morphologic overlap, and the rarity of most tumor types. Ancillary testing is beginning to ameliorate some of these challenges through access to newer immunohistochemical stains and fluorescence in situ hybridization probes, which can limit differential diagnostic considerations in some cases. These ancillary testing strategies are especially useful in small biopsy samples, including aspiration cytology. Molecular techniques are also expanding our understanding of salivary gland tumor pathology and are helping to identify potential targets that may improve treatment for some of these tumors. Here, we summarize the clinical use of new immunohistochemical markers in our practice and review the current understanding of chromosomal rearrangements in salivary gland tumor pathology, emphasizing the prospects for exploiting molecular alterations in salivary gland tumors for diagnosis and targeted therapy. We find that immunohistochemistry and fluorescence in situ hybridization are powerful tools toward the diagnosis of salivary gland tumors, especially when used in a systematic manner based on morphologic differential-diagnostic considerations. As new targeted therapies emerge, it will become increasingly vital to incorporate appropriate molecular testing into the pathologic evaluation of salivary gland cancers.


2015 ◽  
Vol 5 (1) ◽  
pp. 53-56
Author(s):  
Junya Nojima ◽  
Mitsuhiko Nakahira ◽  
Hiroshi Yamaguchi ◽  
Shoichiro Kokabu ◽  
Tetsuya Yoda ◽  
...  

2000 ◽  
Vol 14 (1) ◽  
pp. 81-83 ◽  
Author(s):  
M.L. Voz ◽  
W.J.M. Van de Ven ◽  
K. Kas

Pleomorphic adenoma, or mixed tumor of the salivary glands, is a benign tumor originating from the major and minor salivary glands. Eighty-five percent of these tumors are found in the parotid gland, 10% in the minor (sublingual) salivary glands, and 5% in the submandibular gland. It is the most common type of salivary gland tumor, accounting for almost 50% of all neoplasms in these organs. In fact, after the first observation of recurrent loss of chromosome 22 in meningioma, this was the second type of benign tumor for which non-random chromosomal changes were reported. The rate of malignant change with the potential to metastasize has been reported to be only 2 to 3%, and only a few cases of metastasizing pleomorphic salivary gland adenomas have been described to date. The fact that these tumors arise in organs located in an ontogenetic transitional zone, a region where endoderm and ectoderm meet, might be one of the reasons for the often-problematic histopathological classification. This type of benign tumor has been cytogenetically very well-characterized, with several hundreds of tumors karyotyped. In addition to the cytogenetic subgroup with an apparently normal diploid stemline (making up approximately 30% of the cases), three major cytogenetic subgroups can be distinguished. In addition to a subgroup showing non-recurrent clonal abnormalities, another subgroup is composed of tumors with various translocations involving 12ql5. By far the largest cytogenetic subgroup, however, consists of tumors with chromosome 8 abnormalities, mainly showing translocations involving region 8ql2. The most frequently encountered aberration in this group is a t(3;8)(p21;q12).


Cancers ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 45
Author(s):  
Candace A. Frerich ◽  
Hailey N. Sedam ◽  
Huining Kang ◽  
Yoshitsugu Mitani ◽  
Adel K. El-Naggar ◽  
...  

Adenoid cystic carcinoma (ACC) is an aggressive salivary gland tumor that frequently displays perineural invasion and is often associated with translocations or overexpression of the MYB oncogene. Detailed analyses of MYB transcripts from ACC patient samples revealed that ACC tumors utilize an alternative MYB promoter, which is rarely used in normal cells or other tumor types. The alternative promoter transcripts produce N-terminally truncated Myb proteins lacking a highly conserved and phosphorylated domain, which includes the pS11 epitope that is frequently used to detect Myb proteins. In RNA-seq assays, Myb isoforms lacking the N-terminal domain displayed unique transcriptional activities, regulating many genes differently than full-length Myb. Thus, a regulatory pathway unique to ACC activates the alternative MYB promoter, leading to the production of a truncated Myb protein with altered transcriptional activities. This could provide new therapeutic opportunities for ACC patients.


2021 ◽  
Vol 12 (2) ◽  
pp. 89-91
Author(s):  
Tharun Ganapathy Chitrambalam ◽  
Sidhu Sekhar ◽  
Preetham Anguraj ◽  
Koshy M Panicker

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