Why Us? >>

  • - Open Access
  • - Peer-reviewed
  • - Rapid publication
  • - Lifetime hosting
  • - Free indexing service
  • - Free promotion service
  • - More citations
  • - Search engine friendly

Free SCIRP Newsletters>>

Add your e-mail address to receive free newsletters from SCIRP.

 

Contact Us >>

WhatsApp  +86 18163351462(WhatsApp)
   
Paper Publishing WeChat
Book Publishing WeChat
(or Email:book@scirp.org)

Article citations

More>>

Eming, S.A., Krieg, T. and Davidson, J.M. (2007) Inflammation in Wound Repair: Molecular and Cellular Mechanisms. Journal of Investigative Dermatology, 127, 514-525.
http://dx.doi.org/10.1038/sj.jid.5700701

has been cited by the following article:

  • TITLE: Cancers in Children Ages 8 to 12 Are Injury-Related

    AUTHORS: Kirsten H. Walen

    KEYWORDS: Endomitosis, Endotetraploidization, Diplochromosomes, Reductive Division, Genomic Change, Proliferative Advantage, Wound Healing

    JOURNAL NAME: Journal of Cancer Therapy, Vol.6 No.2, February 9, 2015

    ABSTRACT: Cancers in young children in early growing age was a short PBS (KQED) report (11/21/2014), but without informational source, which prompted a Google search. Sports-associated injuries with medical healing treatments concluded that there were no association between these body traumas and cancer development. But there are other activities from young children, such as “dare-devil” skateboard and bicycling meter-high jumping with potential high energy falls, to serious broken-bone injuries. Falls of children are among the most common causes of US emergency response. The question is why bodily injury is associated with cancer-development? An answer to this question was exemplified by osteosarcoma in young children, which suggested that injury to growing points of bone and surrounding soft tissue cells would elicit a repair process (wound healing process) producing polyploidy with diplochromosomes. The non-mitotic reductive division of such 4-chromatid chromosomes has been shownin vitroto produce pathological cancer-like phenotypes, including gain of a proliferative advantage.