SummaryThe genetic control of hybrid resistance to BALB/c fibrosarcoma Meth‐A was investigated. A Meth‐A tumour grew slower in (BALB/c X C57BL/6)F1and reciprocal hybrid mice than in syngeneic BALB/c mice and was also found to grow slower in females than in males. Significant F1resistance was demonstrated after both subcutaneous and intraperitoneal injection of tumour cells. However, (BALB/c X DBA/2)F1mice did not show any significant resistance to Meth‐A. In H‐2 linkage studies of BALB/c X (BALB/c X C57BL/6) backcross mice, no statistically significant differences in the resistance of H‐2 heterozygotes and homozygotes to Meth‐A were observed. These results indicated that F1hybrid resistance to Meth‐A was controlled by non‐H‐2‐linked resistance factor(s). No linkage was observed between resistance to Meth‐A and coat
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