Cribriform-Morular Variant of Papillary Thyroid Carcinoma Displaying Poorly Differentiated Features

Nakazawa, Tadao; Celestino, Ricardo; Machado, José Carlos; Cameselle-Teijeiro, José; Vinagre, João; Eloy, Catarina; Benserai, F.; Lameche, Samia; Soares, Paula; Sobrinho-Simões, Manuel

doi:10.1177/1066896912473355

Cited by 35 publications

(42 citation statements)

References 26 publications

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“…K-RAS mutation has been reported once in an 18-year-old woman with FAP and CMV-PTC by Giannelli and coworkers (Giannelli et al 2014). On the other hand, the other 7 cases tested in the literature were negative for RAS mutations (Rossi et al 2012, Nakazawa et al 2013, Kwon et al 2015, Brehar et al 2016, Oh et al 2016). It appears that RAS mutation is uncommon in CMV-PTC.…”

Section: Mapk and Pi3k/act Pathways And Tertmentioning

confidence: 99%

“…Multinational studies have demonstrated that BRAF mutation in papillary thyroid carcinoma is associated with increased mortality and cancer recurrent rate (Xing et al 2013(Xing et al , 2015. In the literature, BRAF mutation was tested in 18 cases of CMV-PTC (Rossi et al 2012, Nakazawa et al 2013, Giannelli et al 2014, Kwon et al 2015, Brehar et al 2016, Oh et al 2016, and the results showed that these cancers were negative for BRAF mutation. The absence of BRAF mutation in CMV-PTC may explain the relative indolent nature of this type of papillary thyroid carcinoma.…”

Section: Mapk and Pi3k/act Pathways And Tertmentioning

confidence: 99%

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Cribriform-morular variant of papillary thyroid carcinoma: a distinctive type of thyroid cancer

Lam¹,

Saremi²

2017

Endocrine-Related Cancer

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The aim of this systematic review is to study the features of cribriform-morular variant of papillary thyroid carcinoma (CMV-PTC) by analysing the 129 documented cases in the English literature. The disease occurred almost exclusively in women. The median age of presentation for CMV-PTC was 24 years. Slightly over half of the patients with CMV-PTC had familial adenomatous polyposis (FAP). CMV-PTC presented before the colonic manifestations in approximately half of the patients with FAP. Patients with FAP often have multifocal tumours in the thyroid. Microscopic examination of CMV-PTC revealed predominately cribriform and morular pattern of cancer cells with characteristic nuclear features of papillary thyroid carcinoma. Psammoma body is rare. On immunohistochemical studies, β-catenin is diffusely positive in CMV-PTC. The morular cells in CMV-PTC are strongly positive for CD10, bcl-2 and E-cadherin. Pre-operative diagnosis of CMV-PTC by fine-needle aspiration biopsy could be aided by cribriform architecture, epithelial morules and β-catenin immunostaining. Mutations of APC gene are found in the patients with CMV-PTC associated with FAP. In addition, mutations in CTNNB1, RET/PTC rearrangement and PI3K3CA mutations have been reported. BRAF mutation is negative in all CMV-PTC tested. Compared to conventional papillary thyroid carcinoma, CMV-PTC had a lower frequency of lymph node metastases at presentation (12%) and distant metastases (3%) as well as lower recurrence rates (8.5%) and patients' mortality rates (2%). To conclude, patients with CMV-PTC have distinctive clinical, pathological and molecular profiles when compared to conventional papillary thyroid carcinoma.

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Section: Mapk and Pi3k/act Pathways And Tertmentioning

confidence: 99%

Section: Mapk and Pi3k/act Pathways And Tertmentioning

confidence: 99%

Cribriform-morular variant of papillary thyroid carcinoma: a distinctive type of thyroid cancer

Lam¹,

Saremi²

2017

Endocrine-Related Cancer

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“…It appears possible that germline or acquired mutations in genes of the Wnt/b-catenin pathway, such as APC, may correlate with a morular phenotype in a variety of benign or malignant neoplasms arising in the thyroid gland or odontogenic tissues. Immunohistochemically, the morules demonstrate positivity for b-catenin, cyclin D1, bcl-2, PTEN and CD10 but are consistently negative for thyroglobulin, estrogen and progesterone receptors and CK19 [32,33,38]. We attempted to further characterize the CD10 immunoprofile of the whorl or morule-like structure seen in the KCOT, however this spherical formation was not present in the tissue section stained for CD10.…”

Section: Discussionmentioning

confidence: 99%

Orthokeratinized Odontogenic Cyst with an Associated Keratocystic Odontogenic Tumor Component and Ghost Cell Keratinization and Calcifications in a Patient with Gardner Syndrome

Argyris

Koutlas

2016

Head and Neck Pathol

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Gardner syndrome (GS) is caused by mutations in the APC and besides adenomatous colorectal polyps includes such manifestations as osteomas, epidermoid cysts (ECs) and occasionally multiple pilomatricomas. More than 50 % of ECs in patients with GS exhibit pilomatricoma-like ghost cell keratinization. The latter may be explained by the fact that the development of both GS and pilomatricoma is driven by activation of the Wnt/b-catenin signaling pathway. A 62-year-old, Caucasian male with history of GS presented with a unilocular, mixed radiopaque/radiolucent mandibular lesion causing divergence and external root resorption of involved teeth. Histopathologically, the lesion was composed of two cystic components, an orthokeratinized odontogenic cyst (OOC) and a smaller one with characteristics of keratocystic odontogenic tumor (KCOT) featuring, focally, ghost cells and an epithelial morule-like structure. Dystrophic calcifications essentially similar to those seen in pilomatricomas were observed in the fibrous connective tissue wall. The KCOT and OOC epithelia revealed strong and diffuse cytokeratin (AE1/AE3) and b-catenin immunoreactivity. CD10 positive immunostaining was seen in the keratin and superficial spinous cell layers in both OOC and KCOT. The intraepithelial and mural ghost cells showed a cytokeratin (?), b-catenin and CD10 (-) immunophenotype. The diagnosis of OOC with ghost cell calcifications in association with KCOT was rendered. The patient was lost to follow-up. Although a coincidental co-existence cannot be excluded, ghost cell calcifications mimicking pilomatricoma-like changes in an unusual odontogenic cyst combining OOC and KCOT features as seen in this patient with GS may be explained by the common molecular mechanisms underlying the pathogenesis of cutaneous pilomatricomas and GS.

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“…Positivity for p53 protein has been detected in rare aggressive thyroid tumours such as a mixed columnar and tall cell variant of PTC (81) and a squamous cell carcinoma associated with the tall cell variant of PTC (82). Positivity for p53 protein has also been reported in some aggressive cases of the cribriformmorular variant of PTC (83,84). Immunohistochemical evaluation of the columnar cell variant of PTC showed a predominantly weak nuclear p53 staining in both indolent and aggressive tumours (81).…”

Section: Tp53 Mutationsmentioning

confidence: 98%

“…Loss of cellular polarity/cohesiveness, hobnail features and micropapillary structures, either alone or in combination, are independent predictive factors for lymph node metastasis both in common PTC and in papillary microcarcinoma (82,83,84,85). All of these peculiar morphological features are characteristic of the so-called micropapillary/hobnail variant of PTC (85,86,87,88,89), an aggressive type of PTC carrying poor outcome, which is consistently positive for p53 (85,86,87,89) at the immunohistochemical level.…”

Section: Tp53 Mutationsmentioning

confidence: 99%

ENDOCRINE TUMOURS: Genetic predictors of thyroid cancer outcome

Tavares

Melo

Cameselle-Teijeiro³

et al. 2016

European Journal of Endocrinology

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Genetic predictors of outcome are reviewed in the context of a disease -cancer -that can be (too) simplistically described as a 'successful, invasive clone of our own tissues'. Context has many faces that determine a thyroid cancer patient's outcome beyond the influence of genetic markers. There is also plenty of evidence on the prognostic meaning of the interplay between genetics and context/microenvironment factors (encapsulation, degree of invasion, staging, etc.). This review addresses only genetic alterations detected by molecular methods in surgically resected specimens, thus ruling out immunohistochemistry and (F)ISH, despite their crucial relevance as topographically oriented methods. For the sake of the discussion, well-differentiated carcinomas were divided into two main morphologic types: papillary carcinoma (classic and most variants) displaying BRAFV600E mutations and RET/papillary thyroid carcinoma rearrangements and the group of follicular patterned carcinomas that encompasses follicular carcinoma and the encapsulated form of follicular variant of papillary carcinoma, displaying RAS mutations and PAX8/PPARg rearrangement. TERT promoter mutations have been recently described (and associated with distant metastases and reduced survival) in papillary and follicular carcinomas, as well as in poorly differentiated and undifferentiated carcinoma. TP53 mutations, previously thought to be restricted to less differentiated carcinomas, were also detected in papillary and follicular carcinoma and found to carry a guarded prognosis. Besides their putative importance for targeted therapies, the prognostic meaning of such mutations is discussed per se and in the setting of concurrent BRAF mutation.

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Cribriform-Morular Variant of Papillary Thyroid Carcinoma Displaying Poorly Differentiated Features

Cited by 35 publications

References 26 publications

Cribriform-morular variant of papillary thyroid carcinoma: a distinctive type of thyroid cancer

Cribriform-morular variant of papillary thyroid carcinoma: a distinctive type of thyroid cancer

Orthokeratinized Odontogenic Cyst with an Associated Keratocystic Odontogenic Tumor Component and Ghost Cell Keratinization and Calcifications in a Patient with Gardner Syndrome

ENDOCRINE TUMOURS: Genetic predictors of thyroid cancer outcome

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