The purpose of the present study is to test the validity of our steroid carcinogenesis hypothesis that the outer environment is conditioning the risks of various human neoplasias by sending carcinogenic signals to their target tissues by way of the steroid generating system (the gonads and the adrenal). Practically, we attempted a case-control study for each of the 6 human neoplasia types as regards the excretions of 14 urinary steroids. From both mathematical and endocrinological reasons, case-control comparison was carried out by use of 13 log-transformed steroid ratios in place of 14 original steroid excretion data. The urinary steroid deviation profile was prepared for each of the 8 cancer populations in such a way as to include 13 t-values of the Student's t-test with the above 13 steroid parameters. The names and sizes (in parenthesis) of the normal- and cancer-populations used in this study are, given as follows: a) the male normal group (n=104); b) the female normal group (n=127); c) the female breast cancer group (n=245); d) the cervical cancer group (n=345); e) the endometrial cancer group (n=68); f) the ovarian cancer group (n=160); male gastric cancer group (n=421); h) the female gastric cancer group (n=615); i) the male esophageal cancer group (n=434); j) the female esophageal cancer group (n=123). The regression analysis technic was employed for the pattern analysis of the urinary steroid deviation profiles of the 8 cancer populations. The hormonal data were collated with the epidemiological data for each tumor population. The results obtained are as follows: a) the urinary steroid deviation profiles of 8 cancer populations were highly specific and were distinguishable from one another at the young age (20 years). The above specificities of the hormonal traits of the 8 cancer populations decreased with the progression of host age in the order of the young age, the middle age (40 years) and the old age (60 years). b) Evidence was presented to indicate that the difference of the hormonal trait between the male- and female-esophageal cancer groups was to be classified as qualitative, whereas the inter-sex difference of the hormonal trait of 2 gastric cancer populations was quantitative rather than qualitative, c) A parallelism between the epidemiological- and hormonal data of the 8 cancer groups was observed in that 3 high-morbidity cancer populations (the female breast cancer group and the gastric cancer groups of both sexes) were distinguished from other low morbidity cancer populations by their relative stability of both the steroid deviation pattern and the amplitude of steroid deviation. The significance of the observed findings was discussed with special emphasis on their relevance to the steroid carcinogenesis hypothesis in the light of recent information from our and other laboratories.

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