Interaction between oncogen activation and tumor suppressor gene activation in the genesis of five human neoplasias. A mathematical study.
The purpose of this study is to elucidate the nature of the mathematical regularity between the incidence of two particular neoplasia in their risk variations in space using world statistics. Our investigation covered 5 cancers in the tumor spectrum, 47 cancer registration units in space, and 1978 to 1982 in time. A 2 dimensional diagram was used to illustrate intercancer relationship, and log-transformed figures of the age-adjusted incidence rate (AAIR) in place of original (untransformed) figures were used as a measure of cancer risk for both statistical analysis and graphic illustration of data distribution. More specifically, the emphasis of study was on investigating the relation between the type of data distribution and the fitness of a given cancer pair to a mathematical equilibrium model under the control of the law of mass action. The results obtained are as follows: 1) A total of 7 tumor pairs investigated were divided into 3 elementary types according to their data distribution pattern-globular star cluster type, Galaxy-profile type, and open star cluster type. 2) Mathematically, the fitness of cancer pairs to the suggested equilibrium model decreased in the above order--a finding to indicate that a variety of interactions between centripetal force and centrifugal force are responsible for the production of the above data distribution types. 3) Evidence was presented to suggest that the activated oncogene system and the activated tumor suppressor gene system are the sources of the centripetal force and the centrifugal force, respectively, and that the equilibrium point of the former is very often different from the contra-equilibrium point of the latter in their locations. The pertinence of the above data interpretation is discussed in the light of recent information of oncogene/tumor suppressor gene studies.
Kodama
M
M
Kodama Research Institute of Preventive Medicine, Nagoya, Japan.
Kodama
T
T
D001943:Breast Neoplasms / Q000453:epidemiology / Q000235:genetics; D016889:Endometrial Neoplasms / Q000453:epidemiology / Q000235:genetics; D005260:Female; D005706:Gallbladder Neoplasms / Q000453:epidemiology / Q000235:genetics; D005786:Gene Expression Regulation; D016147:Genes, Tumor Suppressor; D014943:Global Health; D006801:Humans; D015994:Incidence; D007822:Laryngeal Neoplasms / Q000453:epidemiology / Q000235:genetics; D008297:Male; D008962:Models, Theoretical; D009369:Neoplasms / Q000453:epidemiology / Q000235:genetics*; D009857:Oncogenes; D012306:Risk; D013274:Stomach Neoplasms / Q000453:epidemiology / Q000235:genetics; D015533:Transcriptional Activation