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本文引用的文献

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Ruxolitinib improves symptoms and quality of life in a patient with systemic mastocytosis.芦可替尼可改善系统性肥大细胞增多症患者的症状和生活质量。
Biomark Res. 2016 Feb 5;4:2. doi: 10.1186/s40364-016-0056-5. eCollection 2016.
2
Beneficial effects of JAK inhibitor therapy in Systemic Mastocytosis.JAK抑制剂疗法在系统性肥大细胞增多症中的有益作用。
Br J Haematol. 2017 Jan;176(2):324-327. doi: 10.1111/bjh.13951. Epub 2016 Feb 5.
3
Targeting JAK kinase in solid tumors: emerging opportunities and challenges.靶向实体瘤中的JAK激酶：新出现的机遇与挑战。
Oncogene. 2016 Feb 25;35(8):939-51. doi: 10.1038/onc.2015.150. Epub 2015 May 18.
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Polycythemia vera and essential thrombocythemia: 2015 update on diagnosis, risk-stratification and management.真性红细胞增多症和原发性血小板增多症：2015 年诊断、风险分层和治疗更新。
Am J Hematol. 2015 Feb;90(2):162-73. doi: 10.1002/ajh.23895.
5
Co-operating STAT5 and AKT signaling pathways in chronic myeloid leukemia and mastocytosis: possible new targets of therapy.慢性粒细胞白血病和肥大细胞增多症中协同作用的STAT5和AKT信号通路：可能的新治疗靶点。
Haematologica. 2014 Mar;99(3):417-29. doi: 10.3324/haematol.2013.098442.
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STAT5 in hematopoietic stem cell biology and transplantation.造血干细胞生物学与移植中的信号转导及转录激活因子5（STAT5）
JAKSTAT. 2013 Oct 1;2(4):e27159. doi: 10.4161/jkst.27159. Epub 2013 Nov 19.
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Identification of Ponatinib as a potent inhibitor of growth, migration, and activation of neoplastic eosinophils carrying FIP1L1-PDGFRA.鉴定泊那替尼是一种有效的抑制剂，可抑制携带 FIP1L1-PDGFRA 的肿瘤性嗜酸性粒细胞的生长、迁移和激活。
Exp Hematol. 2014 Apr;42(4):282-293.e4. doi: 10.1016/j.exphem.2013.12.007. Epub 2014 Jan 6.
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The inhibition of stat5 by a Peptide aptamer ligand specific for the DNA binding domain prevents target gene transactivation and the growth of breast and prostate tumor cells.肽适体配体特异性抑制 stat5 的 DNA 结合域可防止靶基因反式激活和乳腺癌及前列腺癌细胞的生长。
Pharmaceuticals (Basel). 2013 Aug 20;6(8):960-87. doi: 10.3390/ph6080960.
9
Synergistic growth-inhibitory effects of ponatinib and midostaurin (PKC412) on neoplastic mast cells carrying KIT D816V.达沙替尼和泊那替尼（PKC412）对携带 KIT D816V 的肿瘤性肥大细胞的协同生长抑制作用。
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10
5'-OH-5-nitro-Indirubin oxime (AGM130), an Indirubin derivative, induces apoptosis of Imatinib-resistant chronic myeloid leukemia cells.5'-羟基-5-硝基靛玉红肟（AGM130），一种靛玉红衍生物，诱导伊马替尼耐药慢性髓系白血病细胞凋亡。
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JAK2/STAT5信号通路作为犬肥大细胞瘤的潜在治疗靶点。

The JAK2/STAT5 signaling pathway as a potential therapeutic target in canine mastocytoma.

作者信息

Keller Alexandra, Wingelhofer Bettina, Peter Barbara, Bauer Karin, Berger Daniela, Gamperl Susanne, Reifinger Martin, Cerny-Reiterer Sabine, Moriggl Richard, Willmann Michael, Valent Peter, Hadzijusufovic Emir

机构信息

Department of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of Vienna, Vienna, Austria.

Ludwig Boltzmann Cluster Oncology, Medical University of Vienna, Vienna, Austria.

出版信息

Vet Comp Oncol. 2018 Mar;16(1):55-68. doi: 10.1111/vco.12311. Epub 2017 Apr 11.

DOI:10.1111/vco.12311
PMID:28397975
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5824979/
Abstract

BACKGROUND

Mastocytoma are frequently diagnosed cutaneous neoplasms in dogs. In non-resectable mastocytoma patients, novel targeted drugs are often applied. The transcription factor STAT5 has been implicated in the survival of human neoplastic mast cells (MC). Our study evaluated the JAK2/STAT5 pathway as a novel target in canine mastocytoma.

MATERIALS AND METHODS

We employed inhibitors of JAK2 (R763, TG101348, AZD1480, ruxolitinib) and STAT5 (pimozide, piceatannol) and evaluated their effects on 2 mastocytoma cell lines, C2 and NI-1.

RESULTS

Activated JAK2 and STAT5 were detected in both cell lines. The drugs applied were found to inhibit proliferation and survival in these cells with the following rank-order of potency: R763 > TG101348 > AZD1480 > pimozide > ruxolitinib > piceatannol. Moreover, synergistic anti-neoplastic effects were obtained by combining pimozide with KIT-targeting drugs (toceranib, masitinib, nilotinib, midostaurin) in NI-1 cells.

CONCLUSION

The JAK2/STAT5 pathway is a novel potential target of therapy in canine mastocytoma.

摘要

背景

肥大细胞瘤是犬类中常被诊断出的皮肤肿瘤。在不可切除的肥大细胞瘤患者中，常应用新型靶向药物。转录因子STAT5与人类肿瘤性肥大细胞（MC）的存活有关。我们的研究评估了JAK2/STAT5通路作为犬肥大细胞瘤的一个新靶点。

材料与方法

我们使用了JAK2抑制剂（R763、TG101348、AZD1480、鲁索替尼）和STAT5抑制剂（匹莫齐特、白皮杉醇），并评估它们对两种肥大细胞瘤细胞系C2和NI-1的作用。

结果

在两种细胞系中均检测到活化的JAK2和STAT5。发现所应用的药物可抑制这些细胞的增殖和存活，其效力排序如下：R763 > TG101348 > AZD1480 > 匹莫齐特 > 鲁索替尼 > 白皮杉醇。此外，在NI-1细胞中，匹莫齐特与KIT靶向药物（托西替尼、马斯itinib、尼洛替尼、米哚妥林）联合使用可获得协同抗肿瘤作用。

结论

JAK2/STAT5通路是犬肥大细胞瘤治疗的一个新的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbb9/5824979/45ed107f6fe0/emss-75951-f006.jpg
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