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However, some MSCs may appear as unusual in the sense of vascular dissemination pattern and therefore be explained by alternative metastasis models or even by non-metastatic independent formation mechanisms.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Through literature review and incorporation of recent advance in understanding aging and development, we identified two alternative mechanisms for the independent formation of MSCs: 1) formation of separate tumors from cancer-initiating cells (CICs) mutated at an early stage of development and then diverging as to their physical locations upon further development, 2) formation of separate tumors from different CICs that contain mutations in some convergent ways. Either of these processes does not require long-distance migration and\/or vascular dissemination of cancer cells from a primary site to a secondary site. Thus, we classify the formation of these MSCs from indigenous CICs (iCICs) into a new mechanistic category of tumor formation \u2013 multigenesis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>A multigenesis view on multi-site cancer (MSCs) may offer explanations for some \"unusual metastasis\" and has important implications for designing expanded strategies for the diagnosis and treatment of cancers.<\/jats:p><\/jats:sec><jats:sec><jats:title>Reviewers<\/jats:title><jats:p>This article was reviewed by Carlo C. Maley nominated by Laura F. Landweber and Razvan T. Radulescu nominated by David R. Kaplan. For the full reviews, please go to the Reviewers' comments section.<\/jats:p><\/jats:sec>","DOI":"10.1186\/1745-6150-3-14","type":"journal-article","created":{"date-parts":[[2008,4,11]],"date-time":"2008-04-11T18:13:46Z","timestamp":1207937626000},"update-policy":"http:\/\/dx.doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Occurrence of cancer at multiple sites: Towards distinguishing multigenesis from metastasis"],"prefix":"10.1186","volume":"3","author":[{"given":"Wei-Kang","family":"Zhang","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chun","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jing J","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shi V","family":"Liu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2008,4,11]]},"reference":[{"key":"92_CR1","doi-asserted-by":"publisher","first-page":"600","DOI":"10.1126\/science.1139851","volume":"316","author":"F Barabe","year":"2007","unstructured":"Barabe F, Kennedy JA, Hope KJ, Dick JE: Modeling the initiation and progression of human acute leukemia in mice. 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