美國(guó)研究人員進(jìn)行的一項(xiàng)動(dòng)物實(shí)驗(yàn)顯示,，用一種簡(jiǎn)單的藥物混合劑可以阻止乳腺癌細(xì)胞在實(shí)驗(yàn)鼠體內(nèi)擴(kuò)散。
據(jù)《自然》雜志１２日?qǐng)?bào)道,，位于美國(guó)紐約的斯隆—凱特林癌癥研究所研究人員發(fā)現(xiàn),，在促使乳腺癌細(xì)胞向肺部轉(zhuǎn)移的過(guò)程中有４種基因起了顯著作用，它們分別是ＥＲＥＧ,、ＭＭＰ１,、ＭＭＰ２和ＣＯＸ２。這些基因?qū)Π┘?xì)胞的生長(zhǎng)和轉(zhuǎn)移都至關(guān)重要,。
研究人員發(fā)現(xiàn),，如果將現(xiàn)有經(jīng)核準(zhǔn)用于人體的能抑制基因活動(dòng)的藥物艾必妥和西樂(lè)葆以及試驗(yàn)藥物ＧＭ６００１混合用藥，就能有效抑制上述基因發(fā)揮作用,，從而能阻止實(shí)驗(yàn)鼠體內(nèi)的乳腺癌細(xì)胞生長(zhǎng),，同時(shí)也能阻止癌細(xì)胞向肺部轉(zhuǎn)移。
這項(xiàng)研究的負(fù)責(zé)人瓊·馬薩格說(shuō),，他們下一步計(jì)劃進(jìn)行人體試驗(yàn),，以確認(rèn)這種藥物混合劑對(duì)人體是否有效。
部分英文原文：
Article
Nature 446, 765-770 (12 April 2007) | doi:10.1038/nature05760; Received 19 December 2006; Accepted 21 March 2007
Mediators of vascular remodelling co-opted for sequential steps in lung metastasis
Gaorav P. Gupta1,5, Don X. Nguyen1,5, Anne C. Chiang1,2, Paula D. Bos1, Juliet Y. Kim1, Cristina Nadal1,6, Roger R. Gomis1,6, Katia Manova-Todorova3 & Joan Massagué1,4
Cancer Biology and Genetics Program,
Department of Medicine,
Molecular Cytology Core Facility, and,
Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA
These authors contributed equally to this work.
Present addresses: Hemato-Oncology Institute, Hospital Clinic de Barcelona, 08036 Barcelona, Spain (C.N.); Oncology Programme, Institute for Research in Biomedecine, Barcelona Science Park and University of Barcelona, 08028 Barcelona, Spain (R.R.G.).
Correspondence to: Joan Massagué1,4 Correspondence and requests for materials should be addressed to J.M. (Email: [email protected]).
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Abstract
Metastasis entails numerous biological functions that collectively enable cancerous cells from a primary site to disseminate and overtake distant organs. Using genetic and pharmacological approaches, we show that the epidermal growth factor receptor ligand epiregulin, the cyclooxygenase COX2, and the matrix metalloproteinases 1 and 2, when expressed in human breast cancer cells, collectively facilitate the assembly of new tumour blood vessels, the release of tumour cells into the circulation, and the breaching of lung capillaries by circulating tumour cells to seed pulmonary metastasis. These findings reveal how aggressive primary tumorigenic functions can be mechanistically coupled to greater lung metastatic potential, and how such biological activities may be therapeutically targeted with specific drug combinations.
