Salajegheh A, Petcu EB, Smith RA, Lam AKFollicular variant of papillary thyroid carcinoma: a diagnostic challenge for clinicians and pathologists. Postgrad Med J 84(988): 78-82

Department of Pathology, Griffith Medical School, Gold Coast Campus, Gold Coast, Queensland 4222, Australia.
Postgraduate medical journal (Impact Factor: 1.45). 03/2008; 84(988):78-82. DOI: 10.1136/pgmj.2007.064881
Source: PubMed


The follicular variant of papillary thyroid carcinoma (FVPTC) presents a type of papillary thyroid cancer that has created continuous diagnosis and treatment controversies among clinicians and pathologists. In this review, we describe the nomenclature, the clinical features, diagnostic problems and the molecular biology of FVPTC. It is important for clinicians to understand this entity as the diagnosis and management of this group of patient may be different from other patients with conventional PTC. The literature suggests that FVPTC behaves in a way similar, clinically, to conventional papillary thyroid carcinoma. However, there are some genotypic differences which may characterise this neoplasm. These parameters may account for the phenotypic variation described by some scientists in this type of cancer. Further understanding can only be achieved by defining strict pathological criteria, in-depth study of the molecular biology and long term follow-up of the optional patients with FVPTC.

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    • "Our study has also shown association between FVPTC and distant metastasis when compared with the classical subtype. Therefore, inactivation of PTEN in this particular subtype of PTC could probably have several clinical implications as other studies have revealed the diagnostic and clinical challenges associated with FVPTC as its molecular features are shared by both papillary thyroid cancers and follicular neoplasms (Salajegheh et al, 2008; D et al, 2014). "
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    ABSTRACT: PTEN gene at chromosomes 10q23.3 is a tumour suppressor gene that is inactivated in many types of human cancers. The known mechanisms of PTEN inactivation are rendered to mutation, epigenetic silencing by aberrant methylation or gene deletion. Although PTEN role has been documented in many cancers, PTEN alteration in papillary thyroid carcinoma (PTC) has not been fully elucidated. The aim of this study is to comprehensively investigate PTEN alterations in a large cohort of Middle Eastern papillary thyroid cancer by immunohistochemistry and fluorescent in situ hybridisation (FISH). PTEN protein expression was analysed by immunohistochemistry in a tissue microarray (TMA) format in a large cohort of more than 1000 patients with papillary thyroid cancer. Copy number changes in PTEN were analysed by FISH and data were correlated with clinicopathological parameters along with survival analysis. PTEN inactivation reflected by complete absence of staining was seen in 24.5% of PTC samples, whereas PTEN deletion was seen only in 4.8% of the tested samples by FISH. No association was seen between PTEN loss of protein expression and PTEN gene deletion. However, interestingly, PTEN loss of expression was significantly associated with the follicular variant subset of papillary thyroid cancer. Our study confirmed that PTEN might have a role in pathogenesis in a subset of PTC. PTEN loss of protein expression is a more common event in follicular variant of papillary thyroid cancer. Lack of association between PTEN loss of protein expression and PTEN gene deletion might indicate that gene deletion may not be the sole cause for PTEN loss of expression and these results might raise the possibility of other mechanism such as promoter methylation-mediated gene silencing to be responsible for PTEN inactivation.British Journal of Cancer advance online publication, 19 May 2015; doi:10.1038/bjc.2015.169
    British Journal of Cancer 05/2015; 112(12). DOI:10.1038/bjc.2015.169 · 4.84 Impact Factor
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    • "Follicular variant of papillary thyroid carcinoma (FVPTC) is the third most common type of PTC, following conventional papillary thyroid carcinoma (CPTC) and papillary microcarcinoma [2]. Patients with FVPTC often present with larger tumor size and at a younger age than patients with CPTC [3]. FVPTC also shows less ☆ Disclosure/conflict of interest: The authors wish to state that they have no conflicts of interest or disclosures to make. "
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    ABSTRACT: Mutation of the BRAF gene is common in thyroid cancer. Follicular variant of papillary thyroid carcinoma is a variant of papillary thyroid carcinoma that has created continuous diagnostic controversies among pathologists. The aims of this study are to (1) investigate whether follicular variant of papillary thyroid carcinoma has a different pattern of BRAF mutation than conventional papillary thyroid carcinoma in a large cohort of patients with typical features of follicular variant of papillary thyroid carcinoma and (2) to study the relationship of clinicopathological features of papillary thyroid carcinomas with BRAF mutation. Tissue blocks from 76 patients with diagnostic features of papillary thyroid carcinomas (40 with conventional type and 36 with follicular variant) were included in the study. From these, DNA was extracted and BRAF V600E mutations were detected by polymerase chain reaction followed by restriction enzyme digestion and sequencing of exon 15. Analysis of the data indicated that BRAF V600E mutation is significantly more common in conventional papillary thyroid carcinoma (58% versus 31%, P = .022). Furthermore, the mutation was often noted in female patients (P = .017), in high-stage cancers (P = .034), and in tumors with mild lymphocytic thyroiditis (P = .006). We concluded that follicular variant of papillary thyroid carcinoma differs from conventional papillary thyroid carcinoma in the rate of BRAF mutation. The results of this study add further information indicating that mutations in BRAF play a role in thyroid cancer development and progression.
    Human pathology 12/2010; 42(4):500-6. DOI:10.1016/j.humpath.2009.09.023 · 2.77 Impact Factor
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    • "Prognosis of DTC is generally very good if the initial treatment is properly carried out, with an overall 10-year survival ranging from 80% to >90% in different series [14] [15]. As already mentioned, it is reassuring to note that, in spite of the recent increase in DTC incidence, DTC-related mortality has not increased [3]. It is beyond the scope of this article to review factors affecting the prognosis of DTC. "
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    ABSTRACT: Treatment with thyroid hormone is needed in patients with differentiated thyroid carcinoma (DTC) after the initial treatment (thyroidectomy followed, in most cases, by radioiodine remnant ablation) for two reasons: a) Correction of hypothyroidism in an athyreotic patient (replacement therapy); b) Blockade of thyrotropin (TSH) secretion in view of the TSH-dependence of DTC (TSH-suppressive therapy). Levothyroxine (L-T4) is the hormone of choice, since combina-tion with levotriiodothyronine does not add any clear advantage with respect to L-T4 monotherapy. While replacement therapy obviously is a lifelong requirement, duration of TSH-suppressive therapy depends on the tumor risk stratification after and the response to the initial treatment. According to recent European and American guidelines, in low-risk DTC L-T4 treatment should be carried out at TSH-suppressive doses until there is evidence that the patient is disease-free. In high-risk DTC, TSH suppression should be maintained for several years after such an evidence has been achieved. After-wards, the patient can be shifted to replacement doses, also to avoid the risks of iatrogenic thyrotoxicosis, especially in the elderly and/or in the presence of cardiovascular disease. The dose of L-T4 must be invidualized; particular attention must be given to the coexistence of pathophysiological conditions or drug treatments that may affect L-T4 absorption or me-tabolism.
    Current Cancer Therapy Reviews 11/2009; 5(4):296-302. DOI:10.2174/157339409789712717
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