Cancers in Children Ages 8 to 12 Are Injury-Related

Author(s): Kirsten H. Walen

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 shown in vitro to produce pathological cancer-like phenotypes, including gain of a proliferative advantage.

Over hundred years ago renowned pathologist von Hansemann concluded that cancers arose “—from non-specific injury to a cell—”, not believed at that time and sparingly believed today [1].

Specifically, broken bones in childhood, a time when bones grow very rapidly from cell division (mitosis), the cancer cells were located inside and around ends of growing bones (osteo-sarcomas: thigh, arm, pelvic bone etc.). With von Hansemann in mind, the bone injuries trickle down to the cell level with an initial production of dead and sick, injured bone and soft tissue cells. Sick cells with genomic (DNA) damage must for survival-associated propagative ability repair the damage. Such cells from natural (dysfunctional telomeres) and induced sources (chemical, X-ray) showed changes to endo-tetraploidization (not regular doubling to 92 chromosomes) that could undergo a transient, mechanistic, genome reductive division (meiotic-like) to genome, altered progeny cells [2]-[5]. Inn passage-growth these altered cells expressed neoplastic-like phenotypes, including gain of a proliferative advantage (GPA) [3]. The notable biomarker for these divisions is 46 diplochromosomes, each chromosome with 4-chromatids, recently verified for “genome damaged” telomere-associated immortalization.

In conclusion from the facts of osteosarcoma occurrence in young children with broken bones, which must go through a wound healing process, it makes sense that a potential neoplastic process can be a wrong cellular route in the healing process. Wounds heal by unscheduled cell proliferation, inter-linked with repair of cells with genomic damage, which is the trigger for initiation of irregular endopolyploid cell division. Was von Hansemann right in his intuitive suggestion of “non-specific injury to a cell” in the origin of cancers? Avoidance of such injuries in the young children would be reduction in activities with chance of falling, which becomes a parent issue.


Journal: Journal of Cancer Therapy
DOI: 10.4236/jct.2015.62020 (PDF)
Paper Id: 53881 (metadata)

See also: Comments to Paper

About scirp

(SCIRP: is an academic publisher of open access journals. It also publishes academic books and conference proceedings. SCIRP currently has more than 200 open access journals in the areas of science, technology and medicine. Readers can download papers for free and enjoy reuse rights based on a Creative Commons license. Authors hold copyright with no restrictions. SCIRP calculates different metrics on article and journal level. Citations of published papers are shown based on Google Scholar and CrossRef. Most of our journals have been indexed by several world class databases. All papers are archived by PORTICO to guarantee their availability for centuries to come.
This entry was posted in JCT and tagged , , , , , , . Bookmark the permalink.

Comments are closed.