Expression of PAX8-PPAR gamma 1 rearrangements in both follicular thyroid carcinomas and adenomas.
Expression of PAX8-PPAR gamma 1 rearrangements in both follicular thyroid carcinomas and adenomas.
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发表时间：
2002
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通讯作者：
A. Marques;C. Espadinha;A. Catarino;S. Moniz;T. Pereira;L. Sobrinho;V. Leite
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作者：
A. Marques;C. Espadinha;A. Catarino;S. Moniz;T. Pereira;L. Sobrinho;V. Leite
最近，在滤泡性甲状腺癌（FTC）中检测到导致PAX 8-过氧化物酶体增殖物激活受体（PPAR）γ 1癌基因嵌合体形成的t（2;3）（q13;p25）易位，但在滤泡性甲状腺腺瘤（FTA）、乳头状甲状腺癌（PTC）或多结节增生中未检测到。然而，以前的细胞遗传学研究已经确定了t（2;3）（q13;p25）易位也在某些情况下的FTA。在这项研究中，我们结合RT-PCR与引物在PAX 8的外显子4-8和PPAR γ 1的外显子1与PPAR γ免疫组化研究PAX 8-PPAR γ 1癌基因激活FTC（n = 9），FTA（n = 16），PTC（n = 9），未分化甲状腺癌（n = 4），和多结节增生（n = 2）。RT-PCR检测到9例FTC中5例（56%）和16例FTA中2例（13%）发生PAX 8-PPAR γ 1重排。相比之下，所有PTC、甲状腺未分化癌和多结节增生病例的RT-PCR均呈阴性。在9例FTC中的7例（78%）、16例FTA中的5例（31%）和9例PTC中的1例（11%）中观察到弥漫性核免疫反应性。3例为局灶性阳性（1例FTC，1例PTC和1例多结节增生）。在FTC（n = 3）、FTA（n = 3）和PTC（n = 1）的RT-PCR阴性病例中存在PPAR γ的弥漫性核染色，表明可能存在不同的PAX 8-PPAR γ 1断裂点、PPAR γ 1和非PAX 8伴侣之间的重排或天然蛋白的过表达。我们的研究结果表明，PAX 8-PPAR γ 1重排存在于滤泡癌和腺瘤，这表明该癌基因是不是一个可靠的标记，以区分FTC和FTA细针穿刺活检的甲状腺滤泡性肿瘤。
Recently, a translocation t(2;3)(q13;p25), leading to the formation of a chimeric PAX8-peroxisome proliferator-activated receptor (PPAR)gamma 1 oncogene, was detected in follicular thyroid carcinomas (FTC), but not in follicular thyroid adenomas (FTA), papillary thyroid carcinomas (PTC), or multinodular hyperplasias. However, previous cytogenetic studies have identified the t(2;3)(q13;p25) translocation also in some cases of FTA. In this study, we have combined RT-PCR with primers in exons 4-8 of PAX8 and in exon 1 of PPAR gamma 1 with PPAR gamma immunohistochemistry to study PAX8-PPAR gamma 1 oncogene activation in FTC (n = 9), FTA (n = 16), PTC (n = 9), anaplastic thyroid carcinomas (n = 4), and multinodular hyperplasias (n = 2). PAX8-PPAR gamma 1 rearrangements were detected by RT-PCR in 5 of 9 (56%) FTC and in 2 of 16 (13%) FTA. By contrast, all cases of PTC, anaplastic thyroid carcinomas, and multinodular hyperplasia were RT-PCR-negative. Diffuse nuclear immunoreactivity for PPAR gamma was observed in 7 of 9 (78%) FTC, 5 of 16 FTA (31%), and 1 of 9 PTC (11%). Positivity was focal in 3 cases (1 FTC, 1 PTC, and 1 multinodular hyperplasia). Diffuse nuclear staining for PPAR gamma was present in RT-PCR- negative cases of FTC (n = 3), FTA (n = 3), and PTC (n = 1), suggesting that a different PAX8-PPAR gamma 1 breakpoint, a rearrangement between PPAR gamma 1 and a non-PAX8 partner, or overexpression of the native protein might be present. Our findings that PAX8-PPAR gamma 1 rearrangements are present in both follicular carcinomas and adenomas suggest that this oncogene is not a reliable marker to differentiate between FTC and FTA in fine-needle aspiration biopsies of follicular neoplasms of the thyroid.