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  • Author: Jian Pang x
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Boju Pan, Anqi Wang, Junyi Pang, Yuhan Zhang, Ming Cui, Jian Sun and Zhiyong Liang


PD-L1 is associated with prognosis and immunotherapeutic response in patients with malignancies. In previous studies, PD-L1 expression was detected in many endocrine tumors. However, the PD-L1 expression status in parathyroid tumors is unknown.


We included 26 parathyroid carcinoma and 37 adenoma samples, as well as the corresponding patient information. PD-L1 was stained using the FDA-approved PD-L1 IHC 22C3 pharmDx and Ventana PD-L1 (SP263) assays, and staining was assessed by the estimated percentages of positive tumor cells and immune cells, respectively.


We classified the PD-L1 expression in the parathyroid tumors into four groups: (0) <1%, (1) 1–4%, (2) 5–9% and (3) ≥10% positive. With the SP263 clone, 37 (carcinoma:adenoma = 18:19) samples scored 0, 13 (carcinoma:adenoma = 4:9) scored 1, 7 (carcinoma:adenoma = 1:6) scored 2 and 6 (carcinoma:adenoma = 3:3) scored 3. However, in the series of cases using the 22C3 clone, 45 (carcinoma:adenoma = 20:25) samples scored 0, 10 (carcinoma: adenoma = 3:7) scored 1, 5 (carcinoma:adenoma = 1:4) scored 2, and 3 (carcinoma:adenoma = 2:1) scored 3. Concerning tumor-infiltrating immune cells, 57 samples were negative and six were positive with SP263, and 59 were negative and four were positive with 22C3. Moreover, PD-L1 expression was negatively correlated with the Ki-67 index and mitotic rate in parathyroid tumors depending on the different clones. However, the results indicated only moderate consistency between the SP263 and 22C3 clones in parathyroid tumors.


We found deficient PD-L1 expression in the majority of parathyroid tumors. However, the PD-L1 expression score in parathyroid tumors depended greatly on the antibody clone used.

Open access

Yiqiang Huang, Lin-ang Wang, Qiubo Xie, Jian Pang, Luofu Wang, Yuting Yi, Jun Zhang, Yao Zhang, Rongrong Chen, Weihua Lan, Dianzheng Zhang and Jun Jiang

Pheochromocytoma and paragangliomas (PCC/PGL) are neuroendocrine tumors that arise from chromaffin cells of the adrenal medulla and sympathetic/parasympathetic ganglia, respectively. Of clinical relevance regarding diagnosis is the highly variable presentation of symptoms in PCC/PGL patients. To date, the clear-cut correlations between the genotypes and phenotypes of PCC/PGL have not been entirely established. In this study, we reviewed the medical records of PCC/PGL patients with pertinent clinical, laboratory and genetic information. Next-generation sequencing (NGS) performed on patient samples revealed specific germline mutations in the SDHB (succinate dehydrogenase complex iron-sulfur subunit B) and SDHD (succinate dehydrogenase complex subunit D) genes and these mutations were validated by Sanger sequencing. Of the 119 patients, two were identified with SDHB mutation and one with SDHD mutation. Immunohistochemical (IHC) staining was used to analyze the expression of these mutated genes. The germline mutations identified in the SDH genes were c343C>T and c.541-542A>G in the SDHB gene and c.334-337delACTG in the SDHD gene. IHC staining of tumors from the c.343C>T and c.541-2A>G carriers showed positive expression of SDHB. Tumors from the c.334-337delACTG carrier showed no expression of SDHD and a weak diffused staining pattern for SDHB. We strongly recommend genetic testing for suspected PCC/PGL patients with a positive family history, early onset of age, erratic hypertension, recurrence or multiple tumor sites and loss of SDHB and/or SDHD expression. Tailored personal management should be conducted once a patient is confirmed as an SDHB and/or SDHD mutation carrier or diagnosed with PCC/PGL.