We have detected a <i>primate-specific</i> adrenal androgen-mediated tumor suppression system in which circulating DHEAS is converted to DHEA specifically in cells in which TP53 has been <i>inactivated</i> DHEA is an <i>uncompetitive</i> inhibitor of glucose-6-phosphate dehydrogenase (G6PD), an enzyme indispensable for maintaining reactive oxygen species within limits survivable by the cell.
When a single attenuation map was used for all individual PET frames, the normalized root-mean-square error (NRMSE) values in tumor region were 49.3% (STD: 8.3%), 50.5% (STD: 9.3%), 51.8% (STD: 10.8%) and 51.5% (STD: 12.1%) for 10-mm, 20-mm, 30-mm, and 40-mm tumors, respectively.
The lowered expression in tumor cells of SULT2A1 in HCC tissues involved in metabolism and/or inactivation of sex steroids is consistent with a regulatory role of the SULT2A1 gene product in the development and/or tumor cell differentiation and progression of human HCC.
The fact that we never observed amplification of HST & INT-2 independently of BCL-1, which in turn can be amplified solely, suggests the presence, between HST/INT-2 and BCL-1, of a genetic element which could be important in the development of a subset of mammary tumors.