人們已知腫瘤會(huì)觸發(fā)新血管的生長(zhǎng)以促進(jìn)對(duì)其氧氣和營(yíng)養(yǎng)物質(zhì)的供應(yīng),。但是,，根據(jù)一項(xiàng)對(duì)小鼠的新的研究，這種所謂的腫瘤血管生成并非腫瘤利用其健康組織“微環(huán)境”來(lái)加速其生長(zhǎng)的唯一方法：研究人員說(shuō),，當(dāng)某些類(lèi)型的神經(jīng)纖維在前列腺腫瘤附近或腫瘤內(nèi)生長(zhǎng)時(shí),，前列腺癌會(huì)變得更加致命和富有侵略性。ClaireMagnon及其同事研究了前列腺癌的小鼠模型并發(fā)現(xiàn)，在腫瘤中及腫瘤周?chē)母呙芏鹊纳窠?jīng)生長(zhǎng)可幫助前列腺癌的生長(zhǎng)及擴(kuò)散,。研究人員觀察到,，手術(shù)性或化學(xué)性破壞前列腺內(nèi)的交感神經(jīng)——即那些與“戰(zhàn)或逃”有關(guān)的神經(jīng)——可防止腫瘤的早期生長(zhǎng)，而用藥理學(xué)的方法抑制副交感神經(jīng)——即那些發(fā)出“休息與消化”信號(hào)的神經(jīng)——則可抑制腫瘤的播散,。研究人員還分析了來(lái)自43位前列腺癌患者的腫瘤樣本并發(fā)現(xiàn),，在腫瘤內(nèi)及腫瘤周?chē)母呙芏鹊倪@種神經(jīng)纖維與不良的臨床轉(zhuǎn)歸有關(guān)。鑒于其發(fā)現(xiàn),，Magnon及她的同事提出,，抑制這些神經(jīng)發(fā)育的藥物作為一種可能的前列腺癌療法而值得人們研究。一則由JohnIsaacs撰寫(xiě)的《觀點(diǎn)欄目》文章更為詳細(xì)地討論了這些發(fā)現(xiàn),。（生物谷 Bioon.com）
生物谷推薦的英文摘要
Science DOI:10.1126/science.1236361
Autonomic Nerve Development Contributes to Prostate Cancer Progression
C. Magnon; J. Lin; X. Xue; P.S. Frenette at Albert Einstein College of Medicine in Bronx, NY; S.J. Hall at Mount Sinai School of Medicine in New York, NY; L. Gerber; S.J.
Nerves are a common feature of the microenvironment, but their role in tumor growth and progression remains unclear. We found that the formation of autonomic nerve fibers in the prostate gland regulates prostate cancer development and dissemination in mouse models. The early phases of tumor development were prevented by chemical or surgical sympathectomy and by genetic deletion of stromal β2- and β3-adrenergic receptors. Tumors were also infiltrated by parasympathetic cholinergic fibers that promoted cancer dissemination. Cholinergic-induced tumor invasion and metastasis were inhibited by pharmacological blockade or genetic disruption of the stromal type 1 muscarinic receptor, leading to improved survival of the mice. A retrospective blinded analysis of prostate adenocarcinoma specimens from 43 patients revealed that the densities of sympathetic and parasympathetic nerve fibers in tumor and surrounding normal tissue, respectively, were associated with poor clinical outcomes. These findings may lead to novel therapeutic approaches for prostate cancer.
