Published in:
01-06-2016
Classic Architecture with Multicentricity and Local Recurrence, and Absence of TERT Promoter Mutations are Correlates of BRAF
V600E
Harboring Pediatric Papillary Thyroid Carcinomas
Authors:
Semen Onder, Sule Ozturk Sari, Gulcin Yegen, Ismail Cem Sormaz, Ismail Yilmaz, Sukran Poyrazoglu, Yasemin Sanlı, Yasemin Giles Senyurek, Yersu Kapran, Ozgur Mete
Published in:
Endocrine Pathology
|
Issue 2/2016
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Abstract
This study is aimed to investigate the BRAF
V600E
and TERT promoter mutation profile of 50 pediatric papillary thyroid carcinomas (PTCs) to refine their clinicopathological correlates. The median age at the time of surgery was 16 years (range, 6–18). No TERT promoter mutations were identified in this series. The BRAF
V600E
mutation was present in 15 (30 %) tumors. From genotype-histologic variant correlation perspective, 13 of 24 classic variant PTCs and 2 of 7 diffuse sclerosing variant PTCs were found to harbor BRAF
V600E
mutation. One cribriform-morular variant, 3 solid variant, and 15 follicular variant PTCs were BRAF wild type. While tumors with distant metastasis were BRAF wild type, two of five tumors with extrathyroidal extension (ETE) harbored BRAF
V600E
mutation. Nine of 15 BRAF
V600E
harboring tumors had central lymph node metastases. There was no significant correlation with BRAF
V600E
mutation and age, gender, tumor size, ETE, central lymph node metastasis, the status of pT, pN1a-b, and distant metastasis. An adverse correlation between BRAF
V600E
mutation and disease-free survival (DFS) was noted in the entire cohort; however, the predictive value of BRAF
V600E
mutation disappeared within the group of tumors displaying classic architecture as well as classic variant PTCs. The present cohort identifies that the classic architecture with multicentricity and local recurrence are correlates of BRAF
V600E
harboring pediatric PTCs. While the small size of this cohort is one of the limitations, neither the BRAF mutation status nor the classic tumor architecture does seem to be an independent prognosticator of DFS in this series. Evidence also suggests that TERT promoter mutations do not seem to play a major role in the pathogenesis of pediatric PTCs.