Department of Pathology, Faculty of Medical Sciences (FCM), University of Campinas (UNICAMP), 126, Tessalia Vieira de Camargo Street, Cidade Universitaria, Campinas, São Paulo, 13083887, Brazil.
Department of Oral Diagnosis, Piracicaba Dental School (FOP), University of Campinas (UNICAMP), Piracicaba, São Paulo, Brazil.
Sci Rep. 2024 Oct 9;14(1):23645. doi: 10.1038/s41598-024-63763-9.
The mechanisms involved with the pathogenesis of carcinoma ex pleomorphic adenoma (CXPA) seem to be associated with the accumulation of molecular alterations in the pleomorphic adenoma (PA). In this sense, using array-based comparative genomic hybridization (aCGH) a rare series of 27 cases of CXPA and 14 residual PA (rPA) adjacent to the transformation area, we investigated the profile of the copy number alterations (CNAs) comparing benign residual and transformed areas. The main findings were correlated with the histopathological classification by histologic subtype and degree of invasion. The distribution of losses (p = 0.187) and amplifications (p = 0.172) was not statistically different between rPA and CXPA. The number of gains was increased in the transformed areas compared to the benign residual areas (p = 0.005). PLAG1 gain was maintained along the malignant transformation, as it was observed in both residual PA and CXPA samples, likely being an earlier event during transformation. The amplification of GRB7 and ERBB2 may also be an initial step in the malignant transformation of PA to CXPA (salivary duct carcinoma subtype). Furthermore, the amplification of HMGA2 and RPSAP52 were the most prevalent alterations among the studied samples. It was noteworthy that amplified genes in the transformed areas of the tumors were enriched for biological processes related to immune signaling. In conclusion, our results underscored for the first-time crucial CNAs in CXPA, some of them shared with the residual benign area adjacent to the transformation site. These CNAs included PLAG1 gain, as well as amplification of GRB7, ERBB2, HMGA2, and RPSAP52.
癌在多形性腺瘤(CXPA)发病机制中涉及的机制似乎与多形性腺瘤(PA)中分子改变的积累有关。在这个意义上,我们使用基于阵列的比较基因组杂交(aCGH)技术,对 27 例罕见的 CXPA 和 14 例位于转化区附近的残留多形性腺瘤(rPA)进行了研究,以研究良性残留区和转化区的拷贝数改变(CNAs)谱。主要发现与组织学亚型和侵袭程度的组织病理学分类相关。在 rPA 和 CXPA 之间,缺失(p=0.187)和扩增(p=0.172)的分布没有统计学差异。与良性残留区相比,转化区的增益数增加(p=0.005)。PLAG1 增益在恶性转化过程中得以维持,因为在残留的多形性腺瘤和 CXPA 样本中均观察到了这一点,这可能是转化过程中的早期事件。GRB7 和 ERBB2 的扩增也可能是 PA 向 CXPA(涎腺导管癌亚型)恶性转化的初始步骤。此外,HMGA2 和 RPSAP52 的扩增也是研究样本中最常见的改变之一。值得注意的是,肿瘤转化区扩增的基因富集了与免疫信号相关的生物学过程。总之,我们的研究结果首次强调了 CXPA 中的关键 CNA,其中一些与转化部位相邻的良性残留区共享。这些 CNA 包括 PLAG1 增益,以及 GRB7、ERBB2、HMGA2 和 RPSAP52 的扩增。