Cancers in Children Ages 8 to 12 Are Injury-Related

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 brokenbone 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.

Wound Healing Is a First Response in a Cancerous Pathway: Hyperplasia Developments to 4n Cell Cycling in Dysplasia Linked to Rb-Inactivation

“…In the cover-glass experiments the sequence of wound healing with a polyploid-phase also likely happened with the appearance of "transformed cells". Recently, bone cancers, claimed to be injury related in young children were evaluated [24]. The fact that their bones were still growing appeared to be a strong risk factor for advancement to cancer (sarcoma), which agrees with the fact that cancer in general, occurs in tissues that are growing (e.g., re-placement growth in intestine and skin).…”

Mitotic Slippage Process Concealed Cancer-Sought Chromosome Instability Mechanism (S-CIN)

“…Genomic damage "then" and now, in a repair process, today visualized from stained ᵞH2AX foci [63] in pre-neoplasia (before p53 inactivation), can have many causes, for example, naturally aging "broken" telomeres, tissue reactive oxygen species causing genomic damage, genotoxic lesion associated with phagocytic "garbage-bags" not properly discarded in tissues [64], and surprisingly, from injury of bone breaks in growing bone tips, which could be linked to osteosarcoma [27]. Furthermore, all life's molecule, DNA, is not a stable molecule [65].…”

“…Presently, the core principle for a paradigm different from "simple" MT, but inclusive of CIN inheritance, is "difficult" repair of DNA double strand breakage (DSBs), and how such a process can lead to genome and chromosomal CIN, derived from polyploid cells reversing to mildly, unstable, aneuploid, diploid CIN cells, an evolutionary conserved process. The origin of this thesis is based on a series of in vitro experiments from observations associated with natural telomere "breakage" and carcinogen-free, induced chromosomal breakage with a visual response of induced tetra-and endo-polyploid cells [18]- [27]. These polyploid cells mechanistically, underwent genome reductive divisions, culminating in fitness increase (KW) of near-diploid human cells, as mentioned, a first required hallmark for tumorigenesis [1].…”