scholarly journals THE FALLACY OF THE MUTATION THEORY

Science ◽  
1906 ◽  
Vol 23 (593) ◽  
pp. 746-748 ◽  
Author(s):  
A. E. ORTMANN
Keyword(s):  
Mutation Theory

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

The adaptation of Bact. coli mutabile to lactose

1954 ◽  
Vol 223 (1154) ◽  
pp. 420-420
Keyword(s):  
Inoculum Size ◽  
Colony Development ◽  
Lag Phase ◽  
Normal Cells ◽  
Adaptive Process ◽  
Large Numbers ◽  
Parent Culture ◽  
Mutation Theory ◽  
Special Circumstances ◽  
New Evidence

When Bact. coli mutabile not previously exposed to lactose is plated on lactose-ammonium sulphate agar the number of normal-sized colonies (lac + ) eventually formed is a complicated function of the inoculum size. For small numbers all the cells plated eventually form colonies; for large numbers the colony yield is determined not by a number of mutants in the parent culture but by plate exhaustion (for which the earlier developing colonies are chiefly responsible). The time of appearance of the lac + colonies is much longer than with a culture previously grown in lactose. Thus lac + mutants could not have been present from the start unless their growth is inhibited by an excess of normal cells. When, however, a small number of previously adapted cells are mixed with an excess of unadapted cells the presence of the latter does not impede the development on agar of lac + colonies from the former. When cells are first placed in a liquid lactose medium and samples are transferred at intervals during the ensuing lag phase, the time needed for colony development on lactose-agar progressively diminishes, once again showing that an adaptive process is occurring during the lag in the liquid medium. In certain special circumstances the adaptation to the liquid lactose medium may occur with abnormal speed. The growth rate of newly adapted strains is at first variable. If interpreted by a mutation theory the observations would demand the assumption of a complex polygenetic system for which current applications of the Luria-Delbrück and Lea-Coulson theories would be invalid. Recent arguments about the mutational nature of these phenomena are criticized in the light of the new evidence.

The Diagnostic Method of Concrete Dam Monitoring Information Valid Interval

2012 ◽  
Vol 226-228 ◽  
pp. 2072-2077
Author(s):  
Dong Qin ◽  
Xue Qin Zheng ◽  
Fa Meng Wang ◽  
He Zhi Liu
Keyword(s):  
Influential Factors ◽  
Arch Dam ◽  
Dynamical Structure ◽  
Concrete Dam ◽  
Concrete Arch Dam ◽  
Structural Mutation ◽  
Mutation Theory ◽  
Dam Monitoring ◽  
Mutation Sequence ◽  
Monitoring Information

On the basis of the analysis of the displacement of concrete dam and its related influential factors, based on the evolvement of nonlinear dynamics of concrete dam, it can effectively identify the mutations position of measured value and the attribute interval of dynamical system applied with the wavelet analysis, dynamic structural mutation theory and other numerical analysis methods. When detecting after separating structural mutation sequence, it can finally get the relative stable displacement time series of dynamical structure, so it can realize the diagnostic separation of the monitoring information effective interval. At the end of the paper, through applying a certain concrete arch dam, it is proved that the proposed method of concrete dam mutations diagnosis of is of great significance for the real-time monitoring of the workability state of a dam.

scholarly journals Mitochondrial changes in carcinogenesis as a goal of antitumor therapy (review)

2020 ◽  
pp. 65-73
Author(s):  
T. E. Potemina ◽  
E. V. Guzikov
Keyword(s):  
Malignant Tumors ◽  
Gene Mutations ◽  
Cancer Development ◽  
Antitumor Therapy ◽  
Mutation Theory ◽  
Main Variant

Causes and mechanisms of cancer development are currently one of the urgent problems of medicine. The main variant for today is the mutation theory. Identification of the system of gene mutations, including in mitochondria, leading to this or that type of tumors, made it possible to develop a personalized, so-called targeting, the therapy of malignant tumors.

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.

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