Cancers in Children Ages 8 to 12 Are Injury-Related
Kirsten H. Walen*
CROMOS, Richmond, USA.
DOI: 10.4236/jct.2015.62020   PDF    HTML   XML   2,869 Downloads   3,671 Views   Citations


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.

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Walen, K. (2015) Cancers in Children Ages 8 to 12 Are Injury-Related. Journal of Cancer Therapy, 6, 177-181. doi: 10.4236/jct.2015.62020.

Conflicts of Interest

The authors declare no conflicts of interest.


[1] Bignold, L.P., Coghlan, B.L.D. and Jersmann, H.P.A. (2007) David von Hansemann: Contributions to Oncology: Context, Comments and Translations. Birkhauser Verlag, Basel, 83, 108.
[2] Walen, K.H. (2012) Genome Reversion Process of Endopolyploidy Confers Chromosome Instability on the Descendent Diploid Cells. Cell Biology International, 36, 1-9.
[3] Walen, K.H. (2013) Normal Human Cells Acquiring Proliferative Advantage to Hyperplasia-Like Growth Morphology: Aberrant Progeny Cells Associated with Endopolyploid and Haploid Divisions. Cancer and Clinical Oncology, 2, 1-15.
[4] Huna, A., Salmina, K., Jascenko, E., Duburs, G., Inashkina, I. and Erenpreisa, J. (2011) Self-Renewal Signaling in Pre-Senescent Tetraploid IMR90 Cells. Journal of Aging Research, 2011, Article ID: 103253.
[5] Shwarz-Finsterle, J., Scherthan, H., Huna, A., Gonzalez, P., Mueller, P., Schmitt, E., Erenpreisa, J. and Hausmann, M. (2013) Volume Increase and Spatial Shifts of Chromosome Territories in Nuclei of Radiation-Induced Polyploidizing Tumor Cells. Mutation Research/Genetic Toxicology and Environmental Mutagenesis, 756, 56-65.
[6] Walen, K.H. (2006) Human Diploid Fibroblast Cells in Senescence: Cycling through Polyploidy to Mitotic Cells. In Vitro Cellular & Developmental Biology. Animal, 42, 43-50.
[7] Walen, K.H. (2007) Bipolar Genome Reductional Division of Human Near-Senescent Polyploid Fibroblast Cells. Cancer Genetics and Cytogenetics, 173, 43-50.
[8] Davoli, T. and de Lange, T. (2011) The Causes and Consequences of Polyploidy in Normal Development and Cancer. Annual Review of Cell and Developmental Biology, 27, 585-610.
[9] Ermis, A., Oberringer, M., Wirbel, R., Kochnick, M., Mutschler, W. and Hanselmann, R.G. (1998) Tetraploidization Is a Physiological Enhancer of Wound Healing. European Surgical Research, 30, 385-392.
[10] 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.
[11] Walen, K.H. (2011) Normal Human Cell Conversion to 3-D Cancer-Like Growth: Genome Damage, Endopolyploidy, Senecence Escape, and Cell Polarity Change/Loss. Journal of Cancer Therapy, 2, 181-189.
[12] Weinert, T. (2007) What a Cell Should Know (but May Not). Science, 315, 1374-1375.
[13] Unal, E., Heidinger-Pauli, J.M. and Koshland, D. (2007) DNA Double-Strand Breaks Trigger Genome-Wide Sister Chromatid Cohesion through Eco1 (Ctf7). Science, 317, 245-248.
[14] Uhlmann, F. (2009) A Matter of Choice: The Establishment of Sister Chromatid Cohesion. EMBO Reports, 10, 1095-1102.
[15] Ishida, R., Sato, M., Narita, T., Utsumi, K.R., Nishimoto, T., Morita, T., Nagata, H. and Andoh, T. (1994) Inhibition of DNA Topoisomerase II by ICRF-193 Induces Polyploidization by Uncoupling Chromosome Dynamics from Other Cell Cycle Events. Journal of Cell Biology, 126, 1341-1351.
[16] Brito, D. and Rieder, C.L. (2006) Mitotic Checkpoint Slippage in Human Occurs via Cyclin B Destruction in the Presence of an Active Checkpoint. Current Biology, 16, 1194-1200.
[17] Gasgoigne, K.E. and Taylor, S.S. (2008) Cancer Cells Display Profound Intra- and Interline Variation Following Prolonged Exposure to Antimitotic Drugs. Cancer Cell, 14, 111-122.
[18] Zhang, S., Mercado-Uribe, I., Xing, Z., Sun, B., Kuang, J. and Liu, J. (2013) Generation of Cancer-Stem-Like Cells through the Formation of Polyploidy Giant Cancer Cells. Oncogene, 33, 116-128.
[19] Coshi, C.H. and Dick, F.A. (2012) Chromosome Instability and Deregulated Proliferation: An Unavoidable Duo. Cellular and Molecular Life Sciences, 69, 2009-2024.
[20] Walen, K.H. (2014) Haploidization of Human Diploid Metaphase Cells: Is This Genome Reductive Mechanism Operational in Near-Haploid Leukemia? Journal of Cancer Therapy, 5, 101-114.
[21] Huang, S., Ernberg, I. and Kauffman, S. (2009) Cancer Attractors: A Systems View of Tumors from a Gene Network Dynamics and Developmental Perspective. Seminars in Cell & Developmental Biology, 20, 869-876.
[22] Heng, H.H., Bremer, S.W., Stevens, J.B., Horne, S.D., Liu, G., Abdallah, B.Y., Ye, K.J. and Ye, C.J. (2013) Chromosomal Instability (CIN): What It Is and Why It Is Crucial to Cancer Evolution. Cancer and Metastasis Reviews, 32, 325-340.
[23] Vogelstein, B. and Kinzler, K.W. (1993) The Multistep Nature of Cancer. Trends in Genetics, 9, 138-141.
[24] Rodier, F. and Campisi, J. (2011) Four Faces of Cellular Senescence. Journal of Cell Biology, 192, 547-556.
[25] Hanahan, D. and Weinberg, R.A. (2011) Hallmarks of Cancer: The Next Generation. Cell, 144, 646-674.
[26] Mosieniak, G. and Sikora, E. (2010) Polyploidy: The Link between Senescence and Cancer. Current Pharmaceutical Design, 16, 734-740.
[27] Steinbeck, R.G. (2004) Dysplasia in View of the Cell Cycle. European Journal of Histochemistry, 48, 203-211.
[28] Collado, M. and Serrano, M. (2010) Senescence in Tumors: Evidence from Mice and Humans. Nature Reviews Cancer, 10, 51-57.
[29] Walen, K.H. and Brown, S.W. (1962) Chromosomes in a Marsupial (Potorous tridactylis) Tissue Culture. Nature, 194, 406.
[30] Haig, D. (1993) Alternatives to Meiosis: The Unusual Genetics of Red Algae, Microsporidia and Others. Journal of Theoretical Biology, 163, 15-31.
[31] Walen, K.H. (2014) Neoplastic-Like Cell Changes of Normal Fibroblast Cells Associated with Evolutionary Conserved Maternal and Paternal Genomic Autonomous Behavior (Gonomery). Journal of Cancer Therapy, 5, 860-877.
[32] Li, R., Sonik, A., Stindl, R., Rasnik, D. and Duesberg, P. (2000) Aneuploidy vs. Gene Mutation Hypothesis of Cancer: Recent Study Claims Mutation but Is Found to Support Aneuploidy. Proceedings of the National Academy of Sciences of the United States of America, 97, 3236-3241.
[33] Storckova, Z. and Pellman, D. (2004) From Polyploidy to Aneuploidy, Genomic Instability and Cancer. Nature Reviews Molecular Cell Biology, 5, 45-54.
[34] Williams, B.R., Prabhu, V.R., Hunter, K.E., Glazier, C.M., Whittaker, C.A., Housman, D.E. and Amon, A. (2008) Aneuploidy Affects Proliferation and Spontaneous Immortalization in Mammalian Cells. Science, 322, 703-709.
[35] Erenpreisa, Je., Cragg, M.S., Anisimov, A.P. and Illidge, T.M. (2011) Tumor Cell Immortality and the Ploidy Number 32n? Is It a Developmental Checkpoint? Cell Cycle, 10, 1873-1874.
[36] Bar-Joseph, Z., Siegfried, Z., Brandeis, Z.B., Brors, B., Lu, Y., Eils, R., Dynlacht, B.D. and Simon, I. (2008) Genome-Wide Transcriptional Analysis of the Human Cell Cycle Identifies Genes Differentially Regulated in Normal and Cancer Cells. Proceedings of the National Academy of Sciences of the United States of America, 105, 955-960.
[37] Bozic, I., Antal, T., Ohtsuki, H., Carter, H., Kim, D., Chen, S., Karchin, R., Kinzler, K.W., Vogelstein, B. and Nowak, M.A. (2010) Accumulation of Driver and Passenger Mutations during Tumor Progression. Proceedings of the National Academy of Sciences of the United States of America, 107, 18545-18550.
[38] Stern, C. (1958) The Nucleus and Somatic Cell Variation. Journal of Cellular and Comparative Physiology, 52, 1-34.

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