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  1. Cancer Metastasis Reviews
  2. Year: 2012, Volume: 31
  3. Year: 2012, Volume: 31, Issue: 1-2
  4. A new hypothesis for the cancer mechanism
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Year: 2016, Volume: 35
Year: 2015, Volume: 34
Year: 2014, Volume: 33
Year: 2013, Volume: 33
Year: 2013, Volume: 32
Year: 2012, Volume: 31
Year: 2012, Volume: 31, Issue: 3-4
Year: 2012, Volume: 31, Issue: 1-2
Potential roles for prions and protein-only inheritance in cancer
Significance of vascular endothelial growth factor in growth and peritoneal dissemination of ovarian cancer
A new hypothesis for the cancer mechanism
DISCOIDIN DOMAIN RECEPTOR TYROSINE KINASES: NEW PLAYERS IN CANCER PROGRESSION
Biological influence of Hakai in cancer: a 10-year review
Cell–cell and cell–matrix dynamics in intraperitoneal cancer metastasis
Year: 2012, Volume: 31, Issue: 0
Year: 2011, Volume: 30
Year: 2010, Volume: 29
Year: 2009, Volume: 28
Year: 2008, Volume: 27
Year: 2007, Volume: 26
Year: 2006, Volume: 25
Year: 2005, Volume: 24

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A new hypothesis for the cancer mechanism

Content Provider PubMed Central
Author Meng, Xiaolong Zhong, Jie Liu, Shuying Murray, Mollianne Gonzalez-angulo, Ana M.
Abstract Several observations have led us to a new hypothesis for cancer mechanism. First, that cancer appears only on those multicellular organisms with complicated wound-healing capacities. Second, that wounds considered as risk factors can be identified in all cancers in clinics. And finally, that oncogene activation appears not only in cancer, but also in normal physiology and noncancer pathology processes. Our proposed hypothesis is that cancer is a natural wound healing-related process, which includes oncogene activations, cytokine secretions, stem cell recruitment differentiation, and tissue remodeling. Wounds activate oncogenes of some cells and the latter secrete cytokines to recruit stem cells to heal the wounds. However, if the cause of the wound or if the wound persists, such as under the persistent UV and carcinogen exposures, the continuous wound healing process will lead to a clinical cancer mass. There is no system in nature to stop or reverse the wound healing process in the middle stage when the wound exists. The outcome of the cancer mechanism is either healing the wound or exhausting the whole system (death). The logic of this cancer mechanism is consistent with the rationales of the other physiological metabolisms in the body—for survival. This hypothesis helps to understand many cancer mysteries derived from the mutation theory, such as why cancer only exists in a small proportion of multicellular organisms, although they are all under potential mutation risks during DNA replications. The hypothesis can be used to interpret and guide cancer prevention, recurrence, metastasis, in vitro and in vivo studies, and personalized treatments.
Related Links http://dx.doi.org/10.1007/s10555-011-9342-8
Ending Page 268
Page Count 22
Starting Page 247
File Format PDF
ISSN 01677659
e-ISSN 15737233
Journal Cancer Metastasis Reviews
Issue Number 1-2
Volume Number 31
Language English
Publisher Springer US
Publisher Date 2012-06-01
Access Restriction Open
Rights Holder Springer US
Subject Keyword Cancer Research Oncology Research in Higher Education
Content Type Text
Resource Type Article
Subject Cancer Research Oncology
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