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Progesteron receptor expression in insulin producing cells of neuroendocrine neoplasms.
The Journal of Steroid Biochemistry and Molecular Biology ( IF 2.7 ) Pub Date : 2020-05-11 , DOI: 10.1016/j.jsbmb.2020.105694
Tomoyoshi Tachibana 1 , Atsuko Kasajima 2 , Takeshi Aoki 3 , Tomoaki Tabata 4 , Keely McNamara 4 , Samaneh Yazdani 4 , Sato Satoko 4 , Fumiyoshi Fujishima 4 , Fuyuhiko Motoi 3 , Michiaki Unno 3 , Hironobu Sasano 4
Affiliation  

Progesterone receptor (PgR) inhibits cell proliferation in pancreatic neuroendocrine neoplasms (PanNEN). In non-neoplastic pancreas, loss of PgR induces β-cell proliferation and insulin production. However, detailed association between PgR and insulin producing PanNENs is poorly understood. Insulin, proinsulin, and PgR were immunolocalized in 82 PanNENs (54 non-functioning PanNENs: NF-PanNENs and 28 insulinomas). The status of immunoreactivity was compared to the clinicopathological factors of the patients. Immunoreactivity was also confirmed by employing the double-immunohistochemistry. These results were also compared with those in non-neoplastic Langerhans islets. PgR immunoreactivity was significantly higher in insulinomas than that in NF-PanNENs (p < 0.001). Insulin and proinsulin immunoreactivity was also detected in 20 (37 %) of (single cell) insulin positive NFs (Inspos-NF-PanNEN), in which PgR expression was higher than in insulin negative NF-PanNENs (Insneg-NF-PanNEN, p = 0.03). The ratio of PgR-insulin double positive cells to overall insulin positive cells, as well as PgR-proinsulin double positive cells to proinsulin positive cells, was detected to the same degree in insulinoma (PgR-insulin 70 %, PgR-proinsulin 66 %), Inspos-NF-PanNENs (PgR-insulin 65 %, PgR-proinsulin 68 %) and normal islet (PgR-insulin 80 %, PgR-proinsulin 72 %). PgR and insulin expressing cells colocalize in tumor cells of the PanNENs regardless of the hormone-related symptoms of the patients. Inhibitory effect of PgR on tumor cells might be associated with the favourable clinical outcome of insulinoma patients.

中文翻译:

孕激素受体在神经内分泌肿瘤的胰岛素产生细胞中的表达。

孕酮受体(PgR)抑制胰腺神经内分泌肿瘤(PanNEN)中的细胞增殖。在非肿瘤性胰腺中,PgR的丢失会诱导β细胞增殖和胰岛素产生。然而,人们对PgR与产生胰岛素的PanNENs之间的详细联系知之甚少。将胰岛素,胰岛素原和PgR免疫定位在82个PanNEN中(54个非功能性PanNEN:NF-PanNEN和28个胰岛素瘤)。将免疫反应性的状况与患者的临床病理因素进行比较。通过采用双重免疫组织化学也证实了免疫反应性。还将这些结果与非肿瘤性朗格罕氏胰岛中的结果进行了比较。胰岛素瘤中的PgR免疫反应性显着高于NF-PanNENs(p <0.001)。在20个(37%)(单细胞)胰岛素阳性NFs(Inspos-NF-PanNEN)中也检测到胰岛素和胰岛素原免疫反应性,其中PgR表达高于胰岛素阴性NF-PanNENs(Insneg-NF-PanNEN,p = 0.03)。在胰岛素瘤中检测到PgR-胰岛素双阳性细胞与总胰岛素阳性细胞的比率以及PgR-胰岛素双阳性细胞与胰岛素原阳性细胞的比例相同(PgR-胰岛素70%,PgR-胰岛素66%) ,Inspos-NF-PanNENs(PgR-胰岛素65%,PgR-胰岛素原68%)和正常胰岛(PgR-胰岛素80%,PgR-胰岛素72%)。无论患者的激素相关症状如何,PgR和胰岛素表达细胞共定位在PanNENs的肿瘤细胞中。PgR对肿瘤细胞的抑制作用可能与胰岛素瘤患者的良好临床预后有关。
更新日期:2020-05-11
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