RELATION BETWEEN THE CHANGES OF ONCOGENE VERSUS TUMOR-SUPPRESSOR GENEINTERACTION AND THE TRANSITION OF CANCER RISK FROM FEMALE DOMINANCE THROUGH NO SES DISCRIMINATION TO MALE-DOMINANCE, AS INVESTIGATED BY THERECIPROCAL REGRESSION-ANALYSIS OF 5 HUMAN NEOPLASIAS

We have been investigating the mathematical nature of intercancer link age that underlies the mutual regulation of cancer risks between any 2 tumors in their variations in time and space. Applications of both se quential regression test and topological manipulation of age-adjusted incidence rate (AAIR) data set enabled us to prepare the oncogene (Onc ) activation profile and the tumor suppressor gene (TSG) inactivation profile for each tumor. The purpose of this study was to investigate t he relation between the changes of 2 cancer gene profiles and the sex discrimination of cancer risk in 7 human neoplasias. Results obtained are as follows: i) The sex discrimination of cancer risk could better be defined by the use of log-transformed AAIR data rather than of untr ansformed AAIR data, ii) The sex discrimination of cancer risk, as cal culated with the AAIR data of 47 population units of the world, is as follows: a) breast cancer (Br), M:F=1:120.2; b) thyroid cancer (Thy), M:F=1:2.64; c) colon cancer (Co), M:F=1.18:1; d) liver cancer (Li), M: F=2.63:1; e) lung cancer (Lu), M:F=3.66:1; f) esophageal cancer (Eso), M:F=3.68:1; g) laryngeal cancer (Lar ) MF=7.26:1. iii) Female-dominan t cancers were associated with inversion (Br) or defectiveness (Thy) o f male oncogene profile, whereas male-dominant cancers were associated with inversion (Lar) or defectiveness (Li, Lu and Eso) of female One profiles. Sex-indifferent cancer, Co, was distinguished from other tum ors by the emergence of defectiveness in the TSG profiles of both sexe s. TSG defectiveness was also detectable in female (Br, Thy) and bisex ual (Lu) tumors, iv) The One vs TSG interaction, as assessed in terms of r value of the reciprocal regression analysis, was increasing in it s positivity rate from the top of the female-dominant family (Br) thro ugh the sex-indifferent tumor (Co) to the bottom of the male-dominant family (Lar). In conclusion, the emergence of sex discrimination of ca ncer risk was positively correlated to the extent of integrity of onco gene activation in the dominant gender relative to the recessive gende r. Findings with 6 sex-discriminant tumors are discussed in their rele vancy to tumorigenesis from the point of view of endocrinological epid emiology.