美国研究人员进行的一项动物实验显示，用一种简单的药物混合剂可以阻止乳腺癌细胞在实验鼠体内扩散。
据《自然》杂志１２日报道，位于美国纽约的斯隆—凯特林癌症研究所研究人员发现，在促使乳腺癌细胞向肺部转移的过程中有４种基因起了显著作用，它们分别是ＥＲＥＧ、ＭＭＰ１、ＭＭＰ２和ＣＯＸ２。这些基因对癌细胞的生长和转移都至关重要。
研究人员发现，如果将现有经核准用于人体的能抑制基因活动的药物艾必妥和西乐葆以及试验药物ＧＭ６００１混合用药，就能有效抑制上述基因发挥作用，从而能阻止实验鼠体内的乳腺癌细胞生长，同时也能阻止癌细胞向肺部转移。
这项研究的负责人琼·马萨格说，他们下一步计划进行人体试验，以确认这种药物混合剂对人体是否有效。
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: j-massague@ski.mskcc.org).
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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.
