The “Multicellular Origin” of Cancer and the Clonal Evolution of Oncogenesis

AJBM crossMark

 

 

Abstract

Cancer cells are the result of the multi-step, multi-dimensional and multi-generational process of oncogenesis, but they are never the products of cellular transformation. When a stem cell divides, asymmetrically or symmetrically, it produces two new (new generation) cells, a differentiated daughter cell and a daughter which is a parent-identical stem-cell, or two identical daughter stem cells, respectively. In either case, the daughter cells, differentiated or parent-identical, have their own individuality and character. A daughter cell is not a transformed parent cell; it has its own cellular identity, genotype and phenotype although it carries its parent’s genotypical and phenotypical features. The term “Cellular Transformation” in today’s Medical Research Literature, which refers to neoplastic cellular changes, is unintentionally amiss, but scientifically delusive; it implies a solitary cellular reign that misleadingly suggests a “single cell” origin for oncogenesis. In any living multicellular organism, whose multicellular existence and functionality is totally based on intercellular subsistence, a multicellular act or happening is absolutely impossible to start with or from a solitary cell action. In multicellular organisms, in vivo, malignant neoplasms, including leukemias, which all are the products of highly organized cellular teamwork from the very beginning, never arise from single cells; they arise from groups of cells.

Keywords: Oncogenesis; Evolution of oncogenesis; Malignant transformation; Multicellular origin of cancer; Cancer stem cell; Dormancy; Microenvironment; Metastasis

Copyright © 2014 by The American Society for BioMedicine and BM-Publisher, Inc.

Article citationReferencesFull-Text/PDFBecome reviewer
The citation data is computed by the following citation measuring services:

Cited by (CrossRef)
Google Scholar

  1. Darnwin On the Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life. John Murray 1859 London.
  2. Merlo LM, Pepper JW, Reid BJ, Maley CC. Cancer as an evolutionary and ecological process. Nat Rev Cancer 2006;6:924–935.
  3. Pepper J, Scott Findlay C, Kassen R, Spencer S, Maley C. Cancer research meets evolutionary biology. Evolutionary Applications 2009;2:62–70.
  4. Graves M, Maley CC. Clonal evolution in cancer. Nature 2012;481:306-313.
  5. Campbell PJ et al. The patterns and dynamics of genomic instability in metastatic pancreatic cancer. Nature 2010;467:1109–1113.
  6. Yachida S et al. Distant metastasis occurs late during the genetic evolution of pancreatic cancer. Nature 2010;467:1114–1117.
  7. Klein G. Toward a genetics of cancer resistance. PNAS 2009; 106: 859-863.
  8. Podlaha O, Riester M, De S, Michor F. Evolution of the cancer genome. Trends in Genetics 2012;28(4):155-163.
  9. Malaise EP, Chavaudra N, Tubiana M. The relationship between growth rate, labelling index and histological type of human solid tumours. Eur J Cancer 1973;9(4):305-12.
  10. Luzzi KJ, MacDonald IC, Schmidt EE, Groom AC. Multistep Nature of Metastatic Inefficiency. Am J Pathol 1998;153(3): 865–873.


READ THE FULL ARTICLE

For any technique error please contact us and will be response to sending purchase article by email.

Who Can Become a Reviewer?
Any expert in the article's research field can become a reviewer with American Journal of BioMedicine. Editors might ask you to look at a specific aspect of an article.

Find out more

Research Article
DOI: http://dx.doi.org/10.18081/ajbm/2333-5106-014-01/1-14
American Journal of BioMedicine Volume 2, Issue 1, pages 57-68
Received 30 November 2013; accepted 27 March 2014; published 19 April 2014

How to cite this article
Karindas MM. The “Multicellular Origin” of Cancer and the Clonal Evolution of Oncogenesis. American Journal of BioMedicine 2014;2(2):37-45.

Case report outline
1. Abstract
2. Keywords
3. Introduction
4. Methods
5. Results
6. Discussion
7. References

Article metric