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Flexible Cancer-Associated Chromatin Configuration (CACC) Might Be the Fundamental Reason Why Cancer Is So Difficult to Cure

DOI: 10.4236/oalib.1105531, PP. 1-8

Subject Areas: Genomics, Molecular Biology, Cell Biology

Keywords: Cancer, Cancer Heterogeneity, Cancer-Associated Chromatin Configuration (CACC), Cell Differentiation, Cell Type Transition, Rivet Proteins, Plasmodium falciparum Chloroquine Resistance Marker Protein (Pfcrmp)

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Abstract

We once proposed that cell-type-associated chromatin configurations determine cell types and that cancer cell type is determined by cancer-associated chromatin configuration (CACC). In this paper, we hypothesize that flexible cell-type-associated chromatin configuration is associated with cell potency and has an advantage over inflexible one in regulating genome related activities, such as DNA replication, DNA transcription, DNA repair, and DNA mutagenesis. The reason why cancer is so difficult to treat is because CACC is flexible, which enables cancer cells not only to produce heterogeneous subclones through limited cell differentiation, but also to maximally and efficiently use genome related resources to survive environmental changes. Therefore, to beat cancer, more efforts should be made to restrict the flexibility of CACC or to change CACC so that cancer cells can be turned back to normal or become less malignant.

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Li, G. (2019). Flexible Cancer-Associated Chromatin Configuration (CACC) Might Be the Fundamental Reason Why Cancer Is So Difficult to Cure. Open Access Library Journal, 6, e5531. doi: http://dx.doi.org/10.4236/oalib.1105531.

References

[1]  McGranahan, N. and Swanton, C. (2017) Clonal Heterogeneity and Tumor Evolution: Past, Present, and the Future. Cell, 168, 613-628.
https://doi.org/10.1016/j.cell.2017.01.018
[2]  Dagogo-Jack, I. and Shaw, A.T. (2018) Tumour Heterogeneity and Resistance to Cancer Therapies. Nature Reviews Clinical On-cology, 15, 81-94.
https://doi.org/10.1038/nrclinonc.2017.166
[3]  Burrell, R.A., McGranahan, N., Bartek, J. and Swanton, C. (2013) The Causes and Consequences of Ge-netic Heterogeneity in Cancer Evolution. Nature, 501, 338-345.
https://doi.org/10.1038/nature12625
[4]  Bakhoum, S.F. and Landau, D.A. (2017) Chromosomal Instability as a Driver of Tumor Heterogeneity and Evolution. Cold Spring Harbor Perspectives in Medicine, 7, a029611. https://doi.org/10.1101/cshperspect.a029611
[5]  Li, G.D. (1986) Abnormal Chromatin Configuration and Oncogenesis. Medicine and Philosophy, 7, 12-14.
[6]  Li, G.D. (2019) Further Thoughts on Abnormal Chromatin Configuration and Oncogenesis. Open Access Library Journal, 6, e5185.
[7]  Corces, M.R. and Corces, V.G. (2016) The Three-Dimensional Cancer Genome. Current Opinion in Genetics & Development, 36, 1-7.
https://doi.org/10.1016/j.gde.2016.01.002
[8]  Flavahan, W.A., Drier, Y., Liau, B.B., Gillespie, S.M., Venteicher, A.S., Stem-Mer-Rachamimov, A.O., Suvà, M.L. and Bernstein, B.E. (2016) Insulator Dysfunction and Oncogene Activation in IDH Mutant Gliomas. Nature, 529, 110-114. https://doi.org/10.1038/nature16490
[9]  Li, G.D. (2019) Formation of Cell-Type-Associated Chromatin Configurations: A Hypothesis. Open Access Library Journal, 6, e5246.
[10]  Hanahan, D. and Weinberg, R.A. (2000) The Hallmarks of Cancer. Cell, 100, 57-70.
https://doi.org/10.1016/S0092-8674(00)81683-9
[11]  Umlauf, D. and Mourad, R. (2019) The 3D Genome: From Fundamental Principles to Disease and Cancer. Seminars in Cell & Developmental Biology, 90, 128-137.
https://doi.org/10.1016/j.semcdb.2018.07.002
[12]  Kang, H.C., Kim, I.J., Park, J.H., Shin, Y., Ku, J.L., Jung. M.S., Yoo, B.C., Kim, H.K. and Park, J.G. (2004) Identification of Genes with Differential Expression in Acquired Drug-Resistant Gastric Cancer Cells Using High-Density Oligonucleotide Microarrays. Clinical Cancer Research, 10, 272-284.
https://doi.org/10.1158/1078-0432.CCR-1025-3
[13]  Loeb, L.A., Loeb, K.R. and Anderson, J.P. (2003) Multiple Mutations and Cancer. roceedings of the National Academy of Sciences of the United States of America, 100, 776-781. https://doi.org/10.1073/pnas.0334858100
[14]  Campbell, B.B., Light, N., Fabrizio, D., Zatzman, M., Fuligni, F., et al. (2017) Comprehensive Analysis of Hypermutation in Human Cancer. Cell, 171, 1042-1056.E10.
https://doi.org/10.1016/j.cell.2017.09.048
[15]  de Thé, H. (2018) Differentiation Therapy Revisited. Nature Reviews Cancer, 18, 117-127. https://doi.org/10.1038/nrc.2017.103

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