TY - JOUR
T1 - Oncogene-linked in situ immunotherapy of pre-B lymphoma arising in Eμ/ret transgenic mice
AU - Ichihara, M.
AU - Iwamoto, T.
AU - Isobe, K.
AU - Takahashi, M.
AU - Nakayama, A.
AU - Pu, M.
AU - Dai, Y.
AU - Parashar, A.
AU - Ohkus, K.
AU - Kato, M.
AU - Hotta, T.
N1 - Funding Information:
research from the Ministry of Education, Science and Culture of Japan. We thank Professor Hidehiko Saito, First Department of Internal Medicine, Nagoya University School of Medicine, for his encouragement throughout this work.
PY - 1995/4
Y1 - 1995/4
N2 - We attempted to induce anti-tumour immunity for rejecting pre-B lymphoma derived from Eu/ret transgenic mice (TGM). We established pre-B-lymphoma cell lines of C57BL/6 x Balb/c background (H-2b/d) into which H-2k alloantigen and C3H background were introduced (retLl-6 and retL6-6), and we inoculated BCF1, mice with these immunising tumour cells. After these tumours were rejected by alloantigen (H-k/C3H background)-specific effector cells, the mice were challenged with the pre-B-lymphoma cell line derived from the original Eμ/ret TGM (retO-2). All non-immunised control mice died within 80 days, whereas half the immunised mice survived for over 300 days. The immunity was also effective against primary pre-B-lymphoma cells from Eμ/ret TGM and the ret-driven melanoma cell line (MEL-ret), but not against the pre-B-lymphoma cell line from Eμ/myc TGM. This immunity was at least in part mediated by cell-mediated cytotoxicity that was specific to the ret oncogene product or ret-regulated antigen. Next we immunised Eμ/ret TGM by inoculating them with retL6-6 cells once every 2 weeks beginning at the age of 1 month. Interestingly, this immunisation enabled the TGM to survive longer than the non-immunised control group (P <0.05). Moreover, 2 of 11 transgenic mice receiving such immunisation were free from both macroscopic and microscopic tumours at the time when all of the 12 non-immunised control TGM had died from their tumour. This provides a new model for oncogene-linked immunotherapy research.
AB - We attempted to induce anti-tumour immunity for rejecting pre-B lymphoma derived from Eu/ret transgenic mice (TGM). We established pre-B-lymphoma cell lines of C57BL/6 x Balb/c background (H-2b/d) into which H-2k alloantigen and C3H background were introduced (retLl-6 and retL6-6), and we inoculated BCF1, mice with these immunising tumour cells. After these tumours were rejected by alloantigen (H-k/C3H background)-specific effector cells, the mice were challenged with the pre-B-lymphoma cell line derived from the original Eμ/ret TGM (retO-2). All non-immunised control mice died within 80 days, whereas half the immunised mice survived for over 300 days. The immunity was also effective against primary pre-B-lymphoma cells from Eμ/ret TGM and the ret-driven melanoma cell line (MEL-ret), but not against the pre-B-lymphoma cell line from Eμ/myc TGM. This immunity was at least in part mediated by cell-mediated cytotoxicity that was specific to the ret oncogene product or ret-regulated antigen. Next we immunised Eμ/ret TGM by inoculating them with retL6-6 cells once every 2 weeks beginning at the age of 1 month. Interestingly, this immunisation enabled the TGM to survive longer than the non-immunised control group (P <0.05). Moreover, 2 of 11 transgenic mice receiving such immunisation were free from both macroscopic and microscopic tumours at the time when all of the 12 non-immunised control TGM had died from their tumour. This provides a new model for oncogene-linked immunotherapy research.
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U2 - 10.1038/bjc.1995.156
DO - 10.1038/bjc.1995.156
M3 - Article
C2 - 7710948
AN - SCOPUS:0028944505
SN - 0007-0920
VL - 71
SP - 808
EP - 813
JO - British Journal of Cancer
JF - British Journal of Cancer
IS - 4
ER -
