Mh. Sohn et al., DISTRIBUTION OF GA-67 IN NORMAL AND HYPOTRANSFERRINEMIC TUMOR-BEARINGMICE, The Journal of nuclear medicine, 34(12), 1993, pp. 2135-2143
The mechanism by which Ga-67 accumulates in tumors is controversial. T
he most popular theory is that Ga-67 binds to transferrin and gains ac
cess to cells by the transferrin receptor. However, substantial eviden
ce suggests that uptake of Ga-67 may not be universally mediated by tr
ansferrin in tumors. To determine whether transferrin is required for
uptake of Ga-67 in vivo, we compared the uptake of Ga-67 by two types
of implanted tumors and by normal tissues in normal and severely hypot
ransferrinemic strains of Balb/C mice. One type of tumor was strongly
gallium-avid in normal mice; the other was not. Uptake of Ga-67 by nor
mal soft tissues was markedly less in hypotransferrinemic than in norm
al mice. Uptake of Ga-67 by bone was equivalent in the two types of mi
ce. For the more gallium-avid tumor, uptake of Ga-67 was similar and t
he ratio of tumor-to-background activity was substantially higher in t
he hypotransferrinemic than in the normal mice. For the less gallium-a
vid tumor, uptake was significantly less in hypotransferrinemic than i
n normal mice. These data suggest that uptake of Ga-67 by bone and by
some tumors may be a transferrin-independent process.