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Paediatric follicular thyroid carcinoma – indolent cancer with low prevalence of RAS mutations and absence of PAX 8– PPARG fusion in a Japanese population
Author(s) -
Vuong Huy Gia,
Kondo Tetsuo,
Oishi Naoki,
Nakazawa Tadao,
Mochizuki Kunio,
Miyauchi Akira,
Hirokawa Mitsuyoshi,
Katoh Ryohei
Publication year - 2017
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/his.13285
Subject(s) - kras , neuroblastoma ras viral oncogene homolog , medicine , thyroid carcinoma , follicular phase , thyroid , thyroid cancer , population , hras , thyroid neoplasm , pathology , oncology , cancer research , gastroenterology , cancer , colorectal cancer , environmental health
Aims Paediatric follicular thyroid carcinomas are uncommon, and their clinicopathological features and molecular profiles are still unknown. In the present study, we aimed to investigate the clinicopathological aspects of a large series of follicular thyroid carcinomas ( FTC s) in paediatric patients and to analyse the point mutations in codons 12, 13 and 61 of NRAS , HRAS and KRAS genes and the rearrangements of PAX 8 – PPARG . Methods and results A total of 41 paediatric FTC s less than 21 years of age were enrolled into the present study. We used direct sequencing and reverse transcription–polymerase chain reaction ( RT – PCR ) to detect RAS mutations and PAX 8 – PPARG fusions, respectively. The paediatric FTC s were 6:1 in a female to male ratio, with a mean tumour size of 52.7 mm. Distant metastasis was found in one case at the time of presentation. During a median follow‐up time of 69 months, two cases had lung metastasis and all patients were alive. Histologically, all cases were minimally invasive FTC s and varied in growth patterns: microfollicular (39%), follicular (14.6%), solid/trabecular (6%), oncocytic (4.9%) and mixed patterns (26.8%). The mean Ki67 index was 5.7% and it was not statistically different among the growth patterns. NRAS mutations were found in five cases (12.2%) and associated significantly with small tumour size ( P = 0.014). PAX 8 – PPARG fusion was not detected in our series. Conclusion Paediatric FTC s are indolent in clinical course in spite of their large tumour size and have a distinct genetic background. RAS mutations and PAX 8 – PPARG fusions may not play major roles in the tumorigenesis of paediatric FTC s.