癌癥患者常遭受劇烈疼痛折磨，而現(xiàn)有藥物常常不能有效鎮(zhèn)痛,。德國(guó)研究人員日前報(bào)告說(shuō)找到了癌癥產(chǎn)生劇痛的原因,，有望幫助癌癥患者緩解疼痛。
德國(guó)海德堡大學(xué)藥理學(xué)研究所16日發(fā)表新聞公報(bào)說(shuō),，研究人員在檢查實(shí)驗(yàn)鼠身上的腫瘤釋放哪些信號(hào)物質(zhì)時(shí),，發(fā)現(xiàn)了兩種特殊的分子。通過(guò)電極檢測(cè),，發(fā)現(xiàn)癌變組織周?chē)纳窠?jīng)細(xì)胞與這些分子接觸后變得對(duì)壓力特別敏感,。
現(xiàn)實(shí)生活中，癌癥患者常常因?yàn)榕龅侥[瘤部位而感到疼痛,。腫瘤生長(zhǎng)本身也會(huì)產(chǎn)生壓力,，從而引發(fā)疼痛。此外,，癌細(xì)胞似乎也利用這些特殊分子來(lái)促進(jìn)自己的生長(zhǎng),。
在進(jìn)一步的動(dòng)物實(shí)驗(yàn)中，研究人員通過(guò)注射抗體蛋白質(zhì),，封鎖了神經(jīng)細(xì)胞與腫瘤釋放的信號(hào)物質(zhì)的接觸點(diǎn),，結(jié)果癌變組織周邊神經(jīng)細(xì)胞的敏感性和腫瘤的生長(zhǎng)速度都有所下降。
公報(bào)說(shuō),，下一步研究人員將驗(yàn)證在人體腫瘤部位采取類(lèi)似措施是否也能起到鎮(zhèn)痛的效果,。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature Medicine 7 June 2009 | doi:10.1038/nm.1976
Hematopoietic colony–stimulating factors mediate tumor-nerve interactions and bone cancer pain
Matthias Schweizerhof1, Sebastian St?sser1,6, Martina Kurejova1,6, Christian Njoo1,6, Vijayan Gangadharan1, Nitin Agarwal1, Martin Schmelz2, Kiran Kumar Bali1, Christoph W Michalski1,3,7, Stefan Brugger1,7, Anthony Dickenson4, Donald A Simone5 & Rohini Kuner1
Pain is one of the most severe and debilitating symptoms associated with several forms of cancer1, 2. Various types of carcinomas and sarcomas metastasize to skeletal bones and cause spontaneous bone pain and hyperalgesia, which is accompanied by bone degradation and remodeling of peripheral nerves2. Despite recent advances, the molecular mechanisms underlying the development and maintenance of cancer-evoked pain are not well understood2. Several types of non-hematopoietic tumors secrete hematopoietic colony-stimulating factors that act on myeloid cells3 and tumor cells4. Here we report that receptors and signaling mediators of granulocyte- and granulocyte-macrophage colony-stimulating factors (G-CSF and GM-CSF)3 are also functionally expressed on sensory nerves. GM-CSF sensitized nerves to mechanical stimuli in vitro and in vivo, potentiated CGRP release and caused sprouting of sensory nerve endings in the skin. Interruption of G-CSF and GM-CSF signaling in vivo led to reduced tumor growth and nerve remodeling, and abrogated bone cancer pain. The key significance of GM-CSF signaling in sensory neurons was revealed by an attenuation of tumor-evoked pain following a sensory nerve–specific knockdown of GM-CSF receptors. These results show that G-CSF and GM-CSF are important in tumor-nerve interactions and suggest that their receptors on primary afferent nerve fibers constitute potential therapeutic targets in cancer pain.
1 Pharmacology Institute, University of Heidelberg, Heidelberg, Germany.
2 Department of Anesthesiology and Intensive Care Medicine, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany.
3 Department of General Surgery, University of Heidelberg, Heidelberg, Germany.
4 Department of Pharmacology, University College London, London, UK.
5 Department of Diagnostic & Biological Sciences, University of Minnesota, School of Dentistry, Minneapolis, Minnesota, USA.
6 These authors contributed equally to this work.
7 Present addresses: Surgery Clinic, Klinikum Rechts der Isar, Technical University of Munich, Munich, Germany (C.W.M.); Anesthesiology and Intensive Medicine, University Clinic of Basel, Basel, Switzerland (S.B.).
