The effect of
lentinan on retardation and regression of transplanted
tumors was analysed in allogeneic and syngeneic
tumor-host systems. The effect of
lentinan treatment was most variable in random-bred Swiss albino mice bearing
sarcoma 180. With inbred host strains, it was most effective in A/PH and less, or not at all, in others (A.BY, A.CA, A.SW, DBA/2, BALB/c, C3H/Di, AKR, BIO, BIO.1, BIO.BR, BIO.D2). In order to eliminate the allogeneic differences, a syngeneic transplantable 3-methylcholanthrene-induced
sarcoma (A/PhMC.SI) has been developed in the A/Ph strain, previously found to be the most responsive to
lentinan. The growth of this
sarcoma was dramatically inhibited and regression was detected in all
lentinan-treated syngeneic recipients. Both the
lentinan-treated and untreated regressor animals exhibited a high degree of resistance to a secondary challenge. However, the growth of a spontaneous, transplantable syngeneic
adenocarcinoma in A/Ph mice was not influenced by
lentinan treatment. The results presented substantiate further the conclusion that the effect of
lentinan is mediated through host mechanisms, and show that these mechanisms are able to act against a syngeneic
tumor.