Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY.
Institute of Pathology, Erlangen University Hospital, Comprehensive Cancer Center, European Metropolitan Area Erlangen-Nuremberg, Friedrich Alexander University of Erlangen-Nuremberg, Erlangen, Germany.
Am J Surg Pathol. 2024 Oct 1;48(10):1302-1317. doi: 10.1097/PAS.0000000000002272. Epub 2024 Jun 27.
GLI1 -altered mesenchymal tumor is a recently described distinct pathologic entity with an established risk of malignancy, being defined molecularly by either GLI1 gene fusions or amplifications. The clinicopathologic overlap of tumors driven by the 2 seemingly distinct mechanisms of GLI1 activation is still emerging. Herein, we report the largest series of molecularly confirmed GLI1 -altered mesenchymal neoplasms to date, including 23 GLI1- amplified and 15 GLI1 -rearranged new cases, and perform a comparative clinicopathologic, genomic, and survival investigation. GLI1- rearranged tumors occurred in younger patients (42 vs. 52 y) and were larger compared with GLI1 -amplified tumors (5.6 cm vs. 1.5 cm, respectively). Histologic features were overall similar between the 2 groups, showing a multinodular pattern and a nested architecture of epithelioid, and less commonly spindle cells, surrounded by a rich capillary network. A distinct whorling pattern was noted among 3 GLI1 -amplified tumors. Scattered pleomorphic giant cells were rarely seen in both groups. The immunoprofile showed consistent expression of CD56, with variable S100, CD10 and SMA expression. Genomically, both groups had overall low mutation burdens, with rare TP53 mutations seen only in GLI1- amplified tumors. GLI1 -amplified mesenchymal tumors exhibit mostly a single amplicon at the 12q13-15 locus, compared with dedifferentiated liposarcoma, which showed a 2-peak amplification centered around CDK4 (12q14.1) and MDM2 (12q15). GLI1 -amplified tumors had a significantly higher GLI1 mRNA expression compared with GLI1 -rearranged tumors. Survival pooled analysis of current and published cases (n=83) showed a worse overall survival in GLI1 -amplified patients, with 16% succumbing to disease compared with 1.7% in the GLI1- rearranged group. Despite comparable progression rates, GLI1 -amplified tumors had a shorter median progression-free survival compared with GLI1 -rearranged tumors (25 mo vs. 77 mo). Univariate analysis showed that traditional histologic predictors of malignancy (mitotic count ≥4/10 high-power fields, presence of necrosis, and tumor size ≥5 cm) are associated with worse prognosis among GLI1 -altered mesenchymal tumors.
GLI1 改变的间叶性肿瘤是一种最近描述的具有明确恶性风险的独特病理实体,其分子定义为 GLI1 基因融合或扩增。由 GLI1 激活的两种看似不同机制驱动的肿瘤的临床病理重叠仍在出现。在此,我们报告了迄今为止最大的一组分子证实的 GLI1 改变的间叶性肿瘤,包括 23 例 GLI1 扩增和 15 例 GLI1 重排的新病例,并进行了比较临床病理、基因组和生存研究。GLI1 重排肿瘤发生在年轻患者(42 岁 vs. 52 岁)中,并且与 GLI1 扩增肿瘤相比更大(分别为 5.6cm 和 1.5cm)。两组之间的组织学特征总体相似,显示出多结节模式和上皮样的巢状结构,以及较少见的梭形细胞,周围有丰富的毛细血管网络。在 3 例 GLI1 扩增肿瘤中观察到明显的漩涡状模式。两组均罕见散在的多形性巨细胞。免疫组化显示 CD56 一致表达,S100、CD10 和 SMA 表达可变。从基因组角度来看,两组的总突变负担均较低,仅在 GLI1 扩增肿瘤中观察到罕见的 TP53 突变。与去分化脂肪肉瘤相比,GLI1 扩增的间叶性肿瘤在 12q13-15 位点主要显示单个扩增子,而在 12q14.1 处的 CDK4 和 12q15 处的 MDM2 周围有两个峰扩增。与 GLI1 重排肿瘤相比,GLI1 扩增肿瘤的 GLI1 mRNA 表达显著更高。对当前和已发表病例(n=83)的生存汇总分析显示,GLI1 扩增患者的总生存率较差,16%的患者死于疾病,而 GLI1 重排组为 1.7%。尽管进展率相当,但与 GLI1 重排肿瘤相比,GLI1 扩增肿瘤的中位无进展生存期更短(25 个月 vs. 77 个月)。单因素分析显示,传统的恶性预测组织学指标(有丝分裂计数≥4/10 高倍视野、坏死存在和肿瘤大小≥5cm)与 GLI1 改变的间叶性肿瘤的预后不良相关。