Transformation of pleomorphic adenoma to carcinoma ex pleomorphic adenoma of the parotid gland is independent of p53 mutations

Gedlicka, Claudia; Item, Chike B.; Wögerbauer, Markus; Martinek, Helga; Heiduschka, Gregor; Erovic, Boban M.; Grasl, Matthäus Ch.; Thurnher, Dietmar

doi:10.1002/jso.21444

Cited by 16 publications

(14 citation statements)

References 27 publications

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“…In one study [27], the protein was detected in 79 % of cases of Ca ex PA while TP53 mutation was only detected in 37 % and, in addition, some of the cases with protein overexpression did not reveal any mutation in TP53. Moreover, TP53 mutation was not detected in any of the 11 Ca ex PA studied by Gedlicka [40]. In view of this data we cannot firmly establish a role for a mutated TP53 in the malignant progression of the PA in our case.…”

Section: Discussioncontrasting

confidence: 54%

Carcinosarcoma ex Non-Recurrent Pleomorphic Adenoma Composed of TTF-1 Positive Large Cell Neuroendocrine Carcinoma and Myofibrosarcoma: Apropos a Rare Case

Petersson

Loh

2012

Head and Neck Pathol

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We present a carcinosarcoma ex non-recurrent pleomorphic adenoma composed of a large cell neuroendocrine carcinomatous component and a spindle cell sarcoma with myofibroblastic differentiation. The tumor contained a hyalinized transition zone where the classical PA appeared to acquire two different histopathological patterns of malignant transformation of the epithelial component. The carcinomatous component was strongly and diffusely positive for low-molecular weight cytokeratins (AE1-3), synaptophysin, thyroid transcription factor-1 and focally positive for chromogranin A. All these markers were negative in the sarcomatous component. The sarcomatous component displayed immunoreactivity for smooth muscle actin with a predominantly linear, subplasmalemmal pattern. No expression of CD31, S100 protein, h-caldesmon, desmin, CD34, p63, myogenin, Myo D1 and c-kit was detected. Strong immunohistochemical expression of p53 was documented in both the carcinomatous and sarcomatous components as well as in the atypical epithelial component in the transition zone associated with the hyalinized pleomorphic adenoma.

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Section: Discussioncontrasting

confidence: 54%

Carcinosarcoma ex Non-Recurrent Pleomorphic Adenoma Composed of TTF-1 Positive Large Cell Neuroendocrine Carcinoma and Myofibrosarcoma: Apropos a Rare Case

Petersson

Loh

2012

Head and Neck Pathol

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“…Similar results concerning p53 overexpression and mutation were also noted previously by Nordkvist et al [37]. These studies suggest a role for p53 in the malignant transformation of Ca ex PA. A recent study by Gedlicka et al [38], however, did not find any p53 mutations in the 11 cases of Ca ex PA studied. Thus, p53-independent progression of PA to Ca ex PA is possible.…”

Section: Tumour Suppressors and Cell Cycle Controlmentioning

confidence: 65%

Carcinoma ex Pleomorphic Adenoma: A Comprehensive Review of Clinical, Pathological and Molecular Data

Antony

Gopalan

Smith

et al. 2011

Head and Neck Pathol

214

243

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Carcinoma ex pleomorphic adenoma (Ca ex PA) is a carcinoma arising from a primary or recurrent benign pleomorphic adenoma. It often poses a diagnostic challenge to clinicians and pathologists. This study intends to review the literature and highlight the current clinical and molecular perspectives about this entity. The most common clinical presentation of CA ex PA is of a firm mass in the parotid gland. The proportion of adenoma and carcinoma components determines the macroscopic features of this neoplasm. The entity is difficult to diagnose pre-operatively. Pathologic assessment is the gold standard for making the diagnosis. Treatment for Ca ex PA often involves an ablative surgical procedure which may be followed by radiotherapy. Overall, patients with Ca ex PA have a poor prognosis. Accurate diagnosis and aggressive surgical management of patients presenting with Ca ex PA can increase their survival rates. Molecular studies have revealed that the development of Ca ex PA follows a multistep model of carcinogenesis, with the progressive loss of heterozygosity at chromosomal arms 8q, then 12q and finally 17p. There are specific candidate genes in these regions that are associated with particular stages in the progression of Ca ex PA. In addition, many genes which regulate tumour suppression, cell cycle control, growth factors and cell-cell adhesion play a role in the development and progression of Ca ex PA. It is hopeful that these molecular data can give clues for the diagnosis and management of the disease.

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“…It seems more likely that malignant degeneration may be triggered by a variety of mechanisms, rather than a single genetic event responsible for all tumors. The role of p53 mutation in malignant transformation of PA, however, has already been looked at, and refuted by mutational analysis of 11 cases [40].…”

Section: Discussionmentioning

confidence: 99%

PLAG1 Alteration in Carcinoma Ex Pleomorphic Adenoma: Immunohistochemical and Fluorescence In Situ Hybridization Studies of 22 Cases

Bahrami

Dalton

Bangalore

et al. 2012

Head and Neck Pathol

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Transformation of pleomorphic adenoma to carcinoma ex pleomorphic adenoma of the parotid gland is independent of p53 mutations

Abstract: We could not detect mutations of p53 neither in benign nor malignant parotid tumors and we therefore assume that p53 plays no role in the transformation from pleomorphic adenoma to carcinoma ex pleomorphic adenoma.

Cited by 16 publications

References 27 publications

Carcinosarcoma ex Non-Recurrent Pleomorphic Adenoma Composed of TTF-1 Positive Large Cell Neuroendocrine Carcinoma and Myofibrosarcoma: Apropos a Rare Case

Carcinosarcoma ex Non-Recurrent Pleomorphic Adenoma Composed of TTF-1 Positive Large Cell Neuroendocrine Carcinoma and Myofibrosarcoma: Apropos a Rare Case

Carcinoma ex Pleomorphic Adenoma: A Comprehensive Review of Clinical, Pathological and Molecular Data

PLAG1 Alteration in Carcinoma Ex Pleomorphic Adenoma: Immunohistochemical and Fluorescence In Situ Hybridization Studies of 22 Cases

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