Department of Pathology, Virginia Commonwealth University (VCU) School of Medicine, Richmond, Virginia.
Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York.
Cancer Cytopathol. 2018 Dec;126(12):992-1002. doi: 10.1002/cncy.22071. Epub 2018 Oct 19.
Fumarate hydratase (FH)-deficient renal cell carcinoma (RCC) is rare and highly aggressive and is believed to arise mostly in the setting of hereditary leiomyomatosis-RCC syndrome with a germline mutation of FH. Because of the aggressiveness of these tumors and a frequent lack of ascertainable family history, these tumors may first present as metastases and be sampled by cytology. The cytologic findings of FH-deficient RCC have not previously been reported.
Cytologic and limited biopsy samples from patients with FH-deficient RCC were reviewed retrospectively.
In total, 24 cytologic and limited biopsy samples from 19 patients (6 women and 13 men; age range, 22-69 years) who had FH-deficient RCC and metastasis at presentation were evaluated. These included 21 cytology samples ranging from malignant effusions (n = 7) to metastases (n = 11), to samples of primary kidney tumors (n = 3). The samples exhibited cells, often in clusters and abortive papillae, with voluminous, finely vacuolated cytoplasm and large, pleomorphic nuclei with prominent, viral inclusion-like nucleoli. A distinctive finding of peripheral cytoplasmic clearing frequently was apparent, and intranuclear cytoplasmic pseudoinclusions were less frequent. Of 7 cell block and biopsy samples, several of which represented sampling from the same patient, all demonstrated tissue fragments that had discernable morphologic patterns associated with FH-deficient RCC, including tubulocystic and intracystic papillary growth.
Features characteristic and suggestive of FH-deficient RCC may be identified in cytologic and small biopsy samples. Although the current samples were identified retrospectively in well characterized cases of FH-deficient RCC, the authors argue that, with appropriate clinical correlation, these features are sufficiently distinctive to trigger recognition and confirmatory workup.
富马酸水合酶(FH)缺陷型肾细胞癌(RCC)较为罕见,侵袭性强,主要发生于伴 FH 种系突变的遗传性平滑肌瘤病-RCC 综合征背景下。由于这些肿瘤侵袭性强,且家族史常难以明确,因此这些肿瘤可能首先表现为转移,通过细胞学检查取样。FH 缺陷型 RCC 的细胞学表现尚未见报道。
回顾性分析 FH 缺陷型 RCC 患者的细胞学和有限活检样本。
共评估了 19 例 FH 缺陷型 RCC 伴初诊转移患者的 24 例细胞学和有限活检样本(6 例女性,13 例男性;年龄 22-69 岁)。这些样本包括 21 例细胞学样本,范围从恶性积液(7 例)到转移灶(11 例),再到原发性肾肿瘤(3 例)。这些样本表现为细胞,常呈簇状和发育不良的乳头样结构,细胞质丰富,呈细颗粒状空泡,细胞核大,多形性,核仁明显,类似包涵体。外周细胞质空泡化常常明显,核内细胞质假包涵体较少见。7 例细胞块和活检样本中,其中一些代表同一患者的取样,均显示与 FH 缺陷型 RCC 相关的可识别形态模式的组织碎片,包括小管状囊状和囊内乳头状生长。
在细胞学和小活检样本中可识别出 FH 缺陷型 RCC 的特征性和提示性表现。尽管目前的样本是在 FH 缺陷型 RCC 的特征明确的病例中进行回顾性识别的,但作者认为,结合适当的临床相关性,这些特征具有足够的特异性,可以触发识别并进行确认性检查。