Merkel cell carcinoma-derived macrophage migration inhibitory factor (MIF) may promote persistence of Chronic Lymphocytic Leukemia

Gabriel F Alencar, Haroldo J Rodriguez, Thomas H Pulliam, Allison S Remington, Macy W Gilmour, Rian Alam, Austin J Jabbour, Logan J Mullen, Blair L DeBuysscher, Paul Nghiem, Justin J Taylor
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Abstract

While concurrent diagnoses of Merkel cell carcinoma (MCC) and other cancers, like Chronic lymphocytic leukemia (CLL), are rare, patients with MCC have a 30-fold higher incidence of CLL. While these increases have been attributed to the ability of CLL to suppress immune responses allowing for the emergence of MCC, here we found evidence that MCC could support the persistence of CLL. Using single cell sequencing approaches and computational analyses of MCC and CLL from a patient where both cancers were present in the same lymph node, we found that production of macrophage migration inhibitory factor (MIF) by MCC could promote the persistence of CLL through stimulation of CD74 and CXCR4. These results may explain why blood cell counts rapidly normalized after treatment for MCC and were maintained at normal levels despite the absence of treatment for CLL.
梅克尔细胞癌衍生的巨噬细胞迁移抑制因子(MIF)可能会促进慢性淋巴细胞白血病的持续发展
虽然梅克尔细胞癌(MCC)和其他癌症(如慢性淋巴细胞白血病(CLL))同时确诊的情况非常罕见,但梅克尔细胞癌患者的CLL发病率要高出30倍。虽然这些增长被归因于 CLL 能够抑制免疫反应,从而导致 MCC 的出现,但我们在这里发现了 MCC 可以支持 CLL 持续存在的证据。利用单细胞测序方法和计算分析法,我们发现 MCC 产生的巨噬细胞迁移抑制因子(MIF)可通过刺激 CD74 和 CXCR4 促进 CLL 的持续存在。这些结果可以解释为什么在治疗 MCC 后血细胞计数迅速恢复正常,并且在没有治疗 CLL 的情况下仍能维持在正常水平。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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