Transplantation immunity and isograft size of spontaneous mammary carcinomata in mice

A method was described for determining the size of palpable mammary tumors in a mice without removing the tumor or killing the host. A formula was worked out and nomographs were made for simple and direct use employing only 2 diameters, bisecting the palpable growth at right angles to each other. Small tumor implants [0.05 to 5 cu mm in size] of C 3H spontaneous mammary carcinomas developed palpable tumors with same growth rates and same times of appearance in young syngeneic hosts of C 3H virgin females irrespective of the initial implant size. On the other hand, large implants [25 and 50 cu mm in size] of same carcinomas underwent necrosis and/or regression after an initial retarded growth and delayed appearance in syngeneic hosts.However, animals with regressing tumors from large implants remained refractory to a second challenge implant [0.5 cu mm in size], those with progressing growing tumors from small implants developed large tumors at challenge site.Resistance to challenge implants apparently immunologic in nature could be passively transferred to normal syngeneic hosts by lymph node cells and peritoneal washing cells

Modified allogeneic immunity to Ehrlich ascites tumor with bacterial endotoxin [boivin's antigen] in mice

Allogenic immunity of young adult Swiss albino mice to their residual intraperitoneal tumors after aspiration of their initial ehrlich ascites tumor allografts 12 days post-implantation maintained these mice in complete remission for the rest of their lives.Yet, this solid resistance was depressed when 100 nanogram [ng] amounts of an endotoxinpreparation[Boivin'santigen] wasadministrated subcutaneously three times per week post-aspiration. Ascites tumors relapsed and developed rapidly in the allogenic hosts treated with endotoxin.On the other hand,administration of the endotoxin subcutaneously in ng amounts three times per week starting 24hours after intraperitoneal implantation of the ascites tumor heightened the resistance of the host to its tumor allograft for a week. This was marked by a delayed onset [seven days] and a slower growth rate than the controls.Such resistance was not observed when endotoxin was administrated in higher [10 and 100 ng] or lower [0.1 ng] doses. When endotoxin was administrated subcutaneously in amounts of 0.1 or 100 ng three times per week starting 12 days prior to the intraperitoneal implantation of the tumor allograft, no resistance was observed.The highest dose [100 ng] of the endotoxin had practically no effect on ehrlich ascites tumor cells after an in vitro incubation for one hour when the cells were inoculated back into normal young adult mice, except for a delay of 48 hours in the onset of the ascites tumor. The possibleuseofsystemicadjuvants of immunity in clinical immunotherapy of cancer patients conditioned by such factors as the dose and time of administration in relation to the amount of residual cancer left from a previous treatment was discussed

Australia antigen and anti-australia antibody in lymphomas, leukemias and breast cancer

The sera of 90 lymphoma and 60 leukemic patients were studied for the presence of either HBsAg or anti-HBs using counter-electrophoresis. In addition, the study included 40 breast cancer patients and 20 normal healthy subjects as controls. The findings indicated a close and specific association between hepatitis B infection and leukemia. The frequency of exposure in leukemia patients was 17% compared to 5% in the other groups. Acute leukemia cases with positive HBsAg or anti-HBs reactions indicated a group with very bad prognosis. The causal relationship of hepatitis B virus to certain types of leukemias was discussed