Response to “The tissue organization field theory of cancer: A testable replacement for the somatic mutation theory” DOI: 10.1002/bies.201100025

BioEssays ◽  
2011 ◽  
Vol 33 (9) ◽  
pp. 660-661 ◽  
Author(s):  
David L. Vaux
Keyword(s):  
Field Theory ◽  
Somatic Mutation ◽  
Somatic Mutation Theory ◽  
Tissue Organization ◽  
Mutation Theory ◽  
Tissue Organization Field Theory

Somatic Mutation Theory/Tissue Organization Field Theory: Has the Premise been Wrong All along?

2016 ◽  
Vol 7 (4) ◽  
pp. 167-168
Author(s):  
Rahul Anand
Keyword(s):  
Field Theory ◽  
Somatic Mutation ◽  
Somatic Mutation Theory ◽  
Tissue Organization ◽  
Mutation Theory ◽  
Tissue Organization Field Theory

ABSTRACT How to cite this article Sarode SC, Anand R, Sarode GS, Patil S. Somatic Mutation Theory/Tissue Organization Field Theory: Has the Premise been Wrong All along? World J Dent 2016;7(4):167-168.

scholarly journals One hundred years of somatic mutation theory of carcinogenesis: Is it time to switch?

BioEssays ◽  
2013 ◽  
Vol 36 (1) ◽  
pp. 118-120 ◽  
Author(s):  
Ana M. Soto ◽  
Carlos Sonnenschein
Keyword(s):  
Somatic Mutation ◽  
Somatic Mutation Theory ◽  
Mutation Theory

scholarly journals Real world in cancer? Epistemology of the origin of cancer: new paradigm for the majority of cancers

2015 ◽  
Author(s):  
Björn LDM Brücher ◽  
Ijaz S Jamall
Keyword(s):  
Somatic Mutation ◽  
Cancer Biology ◽  
Preventive Measures ◽  
Chemical Stimulus ◽  
Cancer Model ◽  
New Paradigm ◽  
Somatic Mutation Theory ◽  
Mutation Theory ◽  
Passenger Mutations ◽  
Cancerous Cells

Background: The somatic mutation theory as the origin of cancer (carcinogenesis) was born some 100 years ago, when Theodor Boveri 1914 suggested that a combination of chromosomal defects may result in cancer. This was followed by Karl-Heinrich Bauer in 1928 suggesting that mutations could cause cancer. Subsequently, in 1953 Carl Nordling proposed that a number of mutated genes could cause cancer. Alfred Knudson in 1971 proposed that one hit (one mutation) would result in a clone of cancerous cells. This was modified to a 2-hit-theory later and it seems that cancer biology has continued to try to bolster the somatic mutation theory by recently suggesting that ‘driver’ and ‘passenger’ mutations were necessary and when this proved insufficient, others proposed the hyper-mutation theory in 2014. In the attempt to clothe the Emperor, it was forgotten that mutations found in advanced cancers are either late events or epiphenomena that occur after carcinogenesis (cancer development) and especially after the appearance of a pre-cancerous niche. Reality: Fewer than 10% of cancers are proven to be hereditary (i.e., causally related to germline mutations) and this ratio is even lower in cancers of the stomach (<1%), the colorectum (3-8%) and breast (8%). Infection-triggered cancers constitute some 15% of all cancers and the remaining about some 80% cancers are sporadic, meaning their cause is unknown. New cancer paradigm: Findings from the plant and animal kingdoms, molecular and clinical data over the last 250 years were critically reviewed and gave rise to a new cancer hypothesis containing a multi-step process of 6 sequences. These include, (1) a pathogenic biological or chemical stimulus is followed by (2) chronic inflammation, from which develops (3) fibrosis with associated changes in the cellular microenvironment. These remodeling changes result in a (4) pre-cancerous niche, which triggers the deployment of (5) a chronic stress escape strategy, and when this fails to resolve, (6) a transition of a normal cell to a cancer cell occurs. Consequences: This recently proposed cancer model explains the origins of the vast majority of cancers which are until now were referred to as ‘sporadic’ cancers. Furthermore, this theory points out the need to establish preventive measures long before a cancer becomes clinically apparent. The epistemology of the origin of cancer is reviewed and presented.

scholarly journals Are the Somatic Mutation and Tissue Organization Field Theories of Carcinogenesis Incompatible?

2013 ◽  
Vol 12 ◽  
pp. CIN.S13013 ◽  
Author(s):  
Simon Rosenfeld
Keyword(s):  
Somatic Mutation ◽  
Large Scale ◽  
Control Cell ◽  
Tissue Level ◽  
Dna Mutations ◽  
Tissue Organization ◽  
Tissue Organization Field Theory ◽  
Wide Range ◽  
Carcinogenic Agents ◽  
Successful Resolution

Two drastically different approaches to understanding the forces driving carcinogenesis have crystallized through years of research. These are the somatic mutation theory (SMT) and the tissue organization field theory (TOFT). The essence of SMT is that cancer is derived from a single somatic cell that has successively accumulated multiple DNA mutations, and that those mutations occur on genes which control cell proliferation and cell cycle. Thus, according to SMT, neoplastic lesions are the results of DNA-level events. Conversely, according to TOFT, carcinogenesis is primarily a problem of tissue organization: carcinogenic agents destroy the normal tissue architecture thus disrupting cell-to-cell signaling and compromising genomic integrity. Hence, in TOFT the DNA mutations are the effect, and not the cause, of the tissue-level events. Cardinal importance of successful resolution of the TOFT versus SMT controversy dwells in the fact that, according to SMT, cancer is a unidirectional and mostly irreversible disease; whereas, according to TOFT, it is curable and reversible. In this paper, our goal is to outline a plausible scenario in which TOFT and SMT can be reconciled using the framework and concepts of the self-organized criticality (SOC), the principle proven to be extremely fruitful in a wide range of disciplines pertaining to natural phenomena, to biological communities, to large-scale social developments, to technological networks, and to many other subjects of research.

The somatic mutation theory of cancer: growing problems with the paradigm?

BioEssays ◽  
2004 ◽  
Vol 26 (10) ◽  
pp. 1097-1107 ◽  
Author(s):  
Ana M. Soto ◽  
Carlos Sonnenschein
Keyword(s):  
Somatic Mutation ◽  
Somatic Mutation Theory ◽  
Mutation Theory
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