Carcinoma ex-pleomorphic adenoma of the parotid gland consisting of high-grade salivary duct carcinoma and keratinizing squamous cell carcinoma

2015 ◽  
Vol 120 (3) ◽  
pp. e169-e173 ◽  
Author(s):  
Shino D. Magaki ◽  
Sunita Bhuta ◽  
Elliot Abemayor ◽  
Vishad Nabili ◽  
Ali R. Sepahdari ◽  
...  
2016 ◽  
Vol 66 (8) ◽  
pp. 460-465 ◽  
Author(s):  
Tomohiro Enokida ◽  
Satoshi Fujii ◽  
Hirofumi Kuno ◽  
Takashi Mukaigawa ◽  
Makoto Tahara ◽  
...  

2015 ◽  
Vol 16 (2) ◽  
pp. 118-121 ◽  
Author(s):  
SM Khodeza Nahar Begum ◽  
M Alamgir Chowdhury ◽  
Afroza Suraya Mojumder ◽  
Omid Khan

Pleomorphic adenoma, though essentially benign can undergo malignant transformation. This is the case report of a 72 year old male with a giant tumor of parotid gland measuring 20.0X18.0X16.5cm & weighing 7 kg. Pleomorphic adenoma can rarely transform into carcinoma ex pleomorphic adenoma over time as it enlarges; moreover, histologically, squamous cell carcinoma (SCC) is exceedingly rare. Patient developed the tumor for a period over 20 years & it caused withdrawal from social contact. The tumor gradually enlarged without any pain or other complication except for rapid growth & pain a year before. Postoperative facial function and local control of tumor was achieved. Despite Of having a cancer with significant extracapsular invasion, our patient did not present any metastatic focus. Besides morphological patterns, authors need to categorize invasive carcinoma ex pleomorphic adenoma according to its potentiality to metastasize. Various parameters which can predict malignant transformation in pleomorphic adenoma is also yet to be explored.J MEDICINE July 2015; 16 (2) : 118-121


Author(s):  
R.H. Khonsari ◽  
C. Bertoïa-Caufourier ◽  
G. Murcier ◽  
G. Hervé ◽  
A. Assouline ◽  
...  

2012 ◽  
Vol 136 (11) ◽  
pp. 1359-1365 ◽  
Author(s):  
Alfred Wellenhofer ◽  
Hermann Brustmann

Context.—Human telomerase reverse transcriptase (hTERT), an enzyme that enables cells to overcome replicative senescence and to divide indefinitely, is overexpressed in many cancers and their precursor lesions. Objective.—To test whether hTERT expression is related to neoplastic progression and resistance to apoptosis in vulvar epithelia. Design.—Immunoexpression of hTERT was evaluated in 101 formalin-fixed, paraffin-embedded archival vulvar epithelia consisting of normal squamous vulvar epithelia (n  =  25), lichen sclerosus (n  =  10), high-grade classic vulvar intraepithelial neoplasia (n  =  16), differentiated vulvar intraepithelial neoplasia (n  =  18), and vulvar invasive keratinizing squamous cell carcinoma (n  =  32) and related to survivin and p53 expression. Immunostaining for all factors was scored for moderate and strong intensities with regard to quantity to determine upregulation and overexpression (score 0, 0% immunoreactive cells; score 1+, <5% immunoreactive cells; score 2+, 5% to 50% immunoreactive cells; score 3+, >50% immunoreactive cells). Score 3+ was considered as overexpression. Results.—Nuclear hTERT immunoexpression was closely related to survivin reactivity, increased from normal vulvar squamous epithelia to lichen sclerosus and to high-grade classic vulvar intraepithelial neoplasia, differentiated vulvar intraepithelial neoplasia, and invasive keratinizing squamous cell carcinoma (P < .001), and followed the morphologic distribution of atypical squamous epithelial cells. Overexpression of hTERT was comparable to that seen for p53 in invasive keratinizing squamous cell carcinoma (P  =  .62); significant differences were calculated for differentiated vulvar intraepithelial neoplasia (P  =  .003) and high-grade classic vulvar intraepithelial neoplasia (P  =  .001). Conclusion.—Human telomerase reverse transcriptase is upregulated in vulvar intraepithelial neoplasia and invasive keratinizing squamous cell carcinoma compared with nonneoplastic squamous epithelia of the vulva as an apparently early and preinvasive event in the neoplastic transformation, with development of cellular longevity and resistance to apoptosis by survivin activation as associated features, independent of the etiology of vulvar intraepithelial neoplasia.


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