Adenoid cystic carcinoma of minor salivary glands. Analysis of 86 cases

Chomette, G; Auriol, M; Tranbaloc, P; Vaillant, Jean

doi:10.1007/bf00429355

Cited by 91 publications

(17 citation statements)

References 22 publications

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“…This tendency was particularly exemplified in pleomorphic adenomas. The calponin immunoreactivity in tumor cells negative for h-caldesmon and αSMA may reflect the occurrence of tonofilaments [10,12,18,19,23,43] and/or nerve proteins such as S-100 protein and glial fibrillary acidic protein [1,3,6,11,23,30,32,39,40,56,59]. Therefore, it is safe to conclude so far that the calponin immunoreactivity in the tumor cells both in the previous [48] and the present studies does not necessarily represent the exact distribution of MEC-related cells.…”

Section: Resultsmentioning

confidence: 99%

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Keratin 14 immunoreactive cells in pleomorphic adenomas and adenoid cystic carcinomas of salivary glands

et al. 2000

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Our recent study of developing myoepithelial cells (MECs) in rat salivary glands demonstrated that developing MECs begin to express alpha-smooth muscle actin (alphaSMA) first and, thereafter, keratin 14. Therefore, it is unlikely that duct basal cells expressing keratin 14 alone are immature or undifferentiated MECs. In this study we carried out immunohistochemistry of pleomorphic adenomas and adenoid cystic carcinomas including normal salivary glands using monoclonal antibodies to keratin 14, smooth muscle proteins and keratin 19. The smooth muscle proteins examined included alphaSMA, h-caldesmon and h1-calponin; h1-calponin was observed in keratinocytes and nerve fibers, indicating that the protein is not specific to smooth muscle, whereas alphaSMA and h-caldesmon turned out to be highly specific markers for smooth muscle cells in normal tissues. In normal glands, MECs were positive for both keratin 14 and smooth muscle proteins (alphaSMA and h-caldesmon). Non-MEC cells were essentially devoid of smooth muscle proteins. Non-MEC duct basal cells expressed keratin 14 with or without keratin 19, and luminal cells keratin 19 with or without keratin 14. This suggests that the keratin 14-positive, smooth muscle proteins-negative duct basal cells are luminal cell progenitors. Luminal cells in tubular structures of both tumors were positive for keratin 19 with or without keratin 14. Nonluminal peripheral cells of pleomorphic adenomas were mostly positive for keratin 14, and a small fraction of them expressed smooth muscle proteins. Conversely, peripheral cells of adenoid cystic carcinomas were mostly positive for smooth muscle proteins, and some of them expressed keratin 14. These results strongly suggest (1) that the luminal cell progenitors transform into major constituents of pleomorphic adenoma cells with keratin 14 but not smooth muscle proteins, and (2) that the peripheral cells of adenoid cystic carcinoma are derived from undifferentiated MECs. Solid structures of pleomorphic adenomas were formed by proliferation of the peripheral cells. MECs were observed only occasionally in the periphery. Solid and cribriform structures of adenoid cystic carcinomas were formed by proliferation of the luminal cells. MECs were observed in the periphery and around the pseudocyst.

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Section: Resultsmentioning

confidence: 99%

“…They usually surrounded the pseudocysts and/or localized to the periphery of both structures. Here again, MECs are thought to be engaged in the production of extracellular matrix [10,12,16,43,54], but their abundance suggests that they have a more prominent role in adenoid cystic carcinomas than do pleomorphic adenomas.…”

Section: Discussionmentioning

confidence: 99%

Keratin 14 immunoreactive cells in pleomorphic adenomas and adenoid cystic carcinomas of salivary glands

et al. 2000

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“…Adenoid cystic carcinoma (ACC), the second most common salivary gland malignancy, is characterized by a remarkable morphologic heterogeneity and protracted clinical course (1–3). Approximately 50% of ACC patients experience recurrence and metastasis in 5 to 10 years, to which no effective therapy is available (4–6).…”

Section: Introductionmentioning

confidence: 99%

Novel MYBL1 Gene Rearrangements with Recurrent MYBL1–NFIB Fusions in Salivary Adenoid Cystic Carcinomas Lacking t(6;9) Translocations

Mitani

Liu

Rao

et al. 2016

Clinical Cancer Research

177

165

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Purpose Adenoid cystic carcinoma (ACC) is an indolent salivary gland malignancy, characterized by t(6;9) translocations and MYB-NFIB gene fusions in approximately 50% of the tumors. The genetic alterations underlying t(6;9)-negative and t(6;9)-positive/MYB-NFIB-fusion negative ACC remain unknown. To uncover the genetic alterations in ACC lacking the canonical translocation and fusion transcript and identify new abnormalities in translocation positive tumors. Experimental Design We performed whole genome sequencing in 21 salivary ACCs and conducted targeted molecular analyses in a validation set (81 patients). Microarray gene expression data was also analyzed to explore the biological differences between fusion positive and negative tumors. Results We identified a novel MYBL1-NFIB gene fusion as a result of t(8;9) translocation and multiple rearrangements in the MYBL1 gene in 35% of the t(6;9)-negative ACCs. All MYBL1 alterations involved deletion of the C-terminal negative regulatory domain and were associated with high MYBL1 expression. Reciprocal MYB and MYBL1 expression was consistently found in ACCs. Additionally, 5’-NFIB fusions that did not involve MYB/MYBL1 genes were identified in a subset of t(6;9)-positive/fusion-negative tumors. We also delineated distinct gene expression profiles in ACCs associated with the length of the MYB or MYBL1 fusions, suggesting a biological importance of the C-terminal part of these fusions. Conclusion Our study defines new molecular subclasses of ACC characterized by MYBL1 rearrangements and 5’-NFIB gene fusions.

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“…Attempts to understand the development and progression of these tumors have been unrewarding due to the lack of neoplastic precursors, difficulty in cultivating them and the absence of an animal model [1,2]. Identifying unique and consistent chromosomal abnormalities in this entity is necessary for the characterization of genetic events associated with its evolution and the development of novel biological targets for therapy [3][4][5][6][7][8][9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Translocation t(6;14) as the Sole Chromosomal Abnormality in Adenoid Cystic Carcinoma of the Base of Tongue

Bell

Zhao

Rao

et al. 2007

Head and Neck Pathol

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We present an adenoid cystic carcinoma of the base of tongue in a 48-year-old male with a restricted chromosomal alteration by cytogenetic and spectral karyotypic analysis (SKY). SKY and G-banding analyses identified the t(6;14)(q25;q13) as the sole structural aberration in all metaphases analyzed. This finding supports a critical role for this event in the development of this tumor. The implications of chromosome 6q translocation in this case and in previously reported adenoid cystic carcinomas are highlighted and discussed.

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Adenoid cystic carcinoma of minor salivary glands. Analysis of 86 cases

Cited by 91 publications

References 22 publications

Keratin 14 immunoreactive cells in pleomorphic adenomas and adenoid cystic carcinomas of salivary glands

Keratin 14 immunoreactive cells in pleomorphic adenomas and adenoid cystic carcinomas of salivary glands

Novel MYBL1 Gene Rearrangements with Recurrent MYBL1–NFIB Fusions in Salivary Adenoid Cystic Carcinomas Lacking t(6;9) Translocations

Translocation t(6;14) as the Sole Chromosomal Abnormality in Adenoid Cystic Carcinoma of the Base of Tongue

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