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At least 19 recordsLinked to original sources
PubMed1976

A comparison of in vitro cell-mediated reactivity against syngeneic tumor cells by various lymphoid cell populations from Bacillus Calmette-Guérin-tumor-cured, tumor-sensitized, tumor-bearing, and normal inbred guinea pigs.

The cell-mediated reactivity (CMR) in vitro of normal, line 10 hepatocardinoma tumor-bearing, Bacillus Calmette Guérin (BCG)-line 10 tumor-cured, and line 1 sensitized guinea pigs against synegeneic line 10 hepatocarcinma was measured. This study was designed to determine whether the in vitro CMR correlates with the clinical stage of disease in a guinea pig immunotherapy model. A comparison was also made between the CMR of effector cells from active regional lymph nodes, pooled distant lymph nodes and spleen non-glass-adherent mononuclear cells (lymphocytes), peritoneal exudate macrophages (PEM), and peripheral blood leukocytes. In addition, the immunological specificity of the in vitro cytotoxicity was investigated by comparing the reactivities against line 10 and the highly antigenic syngeneic line 1 hepatocarcinoma as well as normal syngeneic guinea pig embryo cells. Pooled lymphocytes and PEM from normal guinea pigs were cytotoxic to line 1 hepatocarcinoma cells but not to line 10 hepatocarcinoma cells. Pooled lymphocytes and PEM obtained from animals sensitized in vivo to line 1 tumor exhibited in vitro cytotoxicity against line 1 cells, which was comparable to that cytotoxicity obtained from normal, naive donors. Various effector cells from BCG-tumor-cured guinea pigs destroyed line 10 cells but to different degrees. In the order of their decreasing cytotoxic effect against line 10 cells, the effector cells from BCG-tumor-cured guinea pigs were: glass-adherent regional lymph node cells and PEM, followed by non-glass-adherent regional lymph node cells, peripheral blood leukocytes, and pooled spleen and lymph node lymphocytes. Effector cells obtained from animals bearing line 10 tumors were all cytotoxic in vitro against line 10 cells. There were no qualitative differences in CMR between effector cells of tumor-bearing and BCG-tumor-cured guinea pigs. Although some quantitative differences between tumor-bearing and tumor-cured guinea pigs were observed, these differences were not large enough to reliably predict the clinical status of the donor in a blind test.

Animals↗
PubMed1977

Tumor immunity to murine plasma cell tumors. III. Detection of common and unique tumor-associated antigens on BALB/c, C3H, and NZB plasmacytomas by in vivo and in vitro induction of tumor-immune responses.

Tumor-associated antigens (TAA) were demonstrated on plasmacytomas derived from BALB/c, NZB, and C3H mouse strains, by in vivo and in vitro techniques. By immunizing the appropriate F1 hybrid mice with these tumors, it was possible to show that all the plasmacytomas expressed cross-reactive tumor-associated transplantation antigens. When cytotoxic lymphocytes (CL) were induced in vitro by the coculturing of syngeneic or F1 hybrid spleen cells with irradiated plasmacytoma cells, "shared" and "unique" plasmacytoma TAA were demonstrable. This was accomplished by inducing CL in vitro against one syngeneic plasmacytoma and assaying for lytic activity on a range of 51Cr-labeled BALB/c, NZB and C3H plasmacytoma cells in vitro. In a second in vitro assay, unlabeled plasmacytoma cells were tested for their ability to inhibit the lysis of a particular 51Cr-labeled plasmacytoma, with the use of CL induced in vitro against it. The possibility that these TAA were "self" antigens was excluded by demonstrating in the inhibition assay that they were not present on T lymphomas and spleen cells of the same strain, and that CL "autosensitized" in vitro could not significantly lyse 51Cr-labeled plasmacytoma cells in vitro. From both in vivo and in vitro studies of immunity to these tumors, it was concluded that any one plasmacytoma line possesses multiple TAA of both shared and unique types.

Animals↗
PubMed1979

Assessment of host immune status during progressive growth and after excision of DNA virus (simian virus 40) tumors in hamsters: comparison of tumor-specific and tumor-unrelated parameters of immune responsiveness.

The kinetics of cell-mediated immunity to simian virus 40 (SV40) tumor-specific transplantation antigen (TSTA) were compared to the kinetics of tumor-unrelated parameters of immune responsiveness in the assessment of the immune statuses of inbred MHA/SsLAK hamsters during the course of progressive syngeneic SV40 tumor growth and after tumor excision. With the use of the tumor cell neutralization test in vivo and the macrophage migration inhibition assay in vitro, specific cellular immunity to SV40 TSTA was detected by 4 days after tumor cell inoculation, when the tumor was small. This tumor-specific immune response was no longer detected at 7 days after tumor cell inoculation, when the tumor had reached a mean diameter of 12.5 mm, but it returned by 14 days after surgical excision of the tumor. The patterns of host responsiveness to mitogens in spleen cells derived from tumor-bearing animals or from tumor-excised animals generally showed little or no correlation with the kinetics of tumor-specific cellular immunity. The kinetics of the humoral immune response to murine erythrocytes, as determined by hemagglutination assays, correlated much more closely with the kinetics of tumor-specific immunity than did the responses to mitogens. IgG antibody (T-dependent) responses were more affected by progressive tumor growth than were IgM antibody (T-independent) responses. The data suggest that results of tests with the use of tumor-unrelated parameters of immune responsiveness for the assessment of the immune status of cancer patients should be interpreted with caution.

Animals↗
PubMed1976

Detection of anti-tumor antibody in virally induced tumors and its relationship to tumor growth.

The humoral antibody response to virally induced tumors insyngeneic hosts has been studied. The tumors include an SV40 tumor SVT2, the Friend virus-induced leukemias FBL-3 and FLC; and Moloney sarcoma virus-induced tumors. It was found that antitumor antibodies could be detected by the isotopic antiglobulin technique in these tumor systems at a relatively early stage of tumor growth. The kinetics of the antibody response in relation to the status of tumor growth varied between different tumors. In geneumor growth than in the regressors of tumor-free hosts. Reinoculation of tumor cells or recurrence of tumor growth produced elevation of antibody levels (secondary response). The specificity of the antibody reactions also varied in different tumor systems: some antibodies were truly tumor-specific and thus might produce a biological effect on in vivo tumor immunity, whereas others were not. These studies indicated that a sensitive antibody assay could be used for early detection of tumor growth. However, its usefulness in evaluation of the status of tumor growth should be carefully studied in each tumor system.

Animals↗
PubMed1977

Character of the tumors developing in young hamsters by the mixed cell transplantation of para-adeno-virus 12 and SV40 tumors-the similarity to the tumors induced by para-adenovirus 7.

Two mixtures of either allogeneic PARA-adenovirus 12 tumor cells or adenovirus (Adeno) 12 tumor cells and SV40 tumor cells in an equal number of 1 multiplied by 10(7) cells were transplanted subcutaneously at two sites of 10 young hamsters. The former two tumor cells were transplantable in nearly half of the transplants and the latter tumor cells in all of the transplants. By the mixture of PARA-Adeno 12 and SV40 tumor cells, 10 tumors were grown, 7 of which were mixed with Adeno and SV40 types and 3 were solely SV40 type. The other 10 tumors produced by the mixture of Adeno 12 and SV40 tumor cells revealed SV40 type only. Morphologically, Adeno type resembled the tumor induced by Adeno, and SV40 type by SV40. The results suggest that the existence of SV40 genetic information in Adeno type tumor cells is indispensable to the formation of mixed tumor in allogeneic tumor cell system. The similarity between the tumors developed by the mixed cell transplantation and those induced by PARA-adeno 7 was discussed both viro-immunologically and morphologically.

Adenoviridae↗
PubMed1979

Mouse mammary tumor virus genome expression in chemical carcinogen-induced mammary tumors in low- and high-tumor-incidence mouse strains.

Involvement of mouse mammary tumor virus (MMTV) in 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary tumorigenesis was investigated in low- (BALB/c) and high- (BALB/cfC3H) mammary-tumor-incidence mouse strains. Both strains contain endogenous MMTV integrated into the cellular genome. Additionally, BALB/cfC3H mice are infected with exogenous MMTV-S which is responsible for a higher incidence of mammary tumors in breeding females. Administration of DMBA to virgin mice of both strains resulted in a moderate frequency of mammary tumors within 40 wk after treatment. No differences were found in DMBA-induced tumor incidences at 18 wk (6% and 7%) or at 38 wk (29% and 36%) after treatment of BALB/c and BALB/cfC3H mice, respectively. Expression of MMTV in these tumors was examined by assaying for the presence of MMTV RNA by hybridization using MMTV-specific cDNA and by immunohistochemical staining utilizing antibodies against MMTV 52,000-dalton glycoprotein, gp52, and 28,000-dalton internal protein, p28. Of 16 BALB/c tumors assayed, 11 did not contain detectable levels of MMTV RNA and the remaining 5 tumors contained only low levels (0.0005-0.0010%) of viral RNA. Importantly, MMTV RNA was not detected in 5 of 27 BALB/cfC3H tumors. The other BALB/cfC3H tumors contained quantities of MMTV RNA ranging from 0.0006 to 0.4170%. Most BALB/cfC3H tumors with detectable levels of MMTV RNA also synthesized viral proteins gp52 and p28. Thus, expression of the complete MMTV genome is not requisite for maintenance of the tumor phenotype in DMBA-induced mammary tumors in either BALB/c or BALB/cfC3H virgin mice under 1 year of age.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2025

Tumor-immune partitioning and clustering algorithm for identifying tumor-immune cell spatial interaction signatures within the tumor microenvironment.

BACKGROUND: Growing evidence supports the importance of characterizing the organizational patterns of various cellular constituents in the tumor microenvironment in precision oncology. Most existing data on immune cell infiltrates in tumors, which are based on immune cell counts or nearest neighbor-type analyses, have failed to fully capture the cellular organization and heterogeneity. METHODS: We introduce a computational algorithm, termed Tumor-Immune Partitioning and Clustering (TIPC), that jointly measures immune cell partitioning between tumor epithelial and stromal areas and immune cell clustering versus dispersion. As proof-of-principle, we applied TIPC to a prospective cohort incident tumor biobank containing 931 colorectal carcinoma cases. TIPC identified tumor subtypes with unique spatial patterns between tumor cells and T lymphocytes linked to certain molecular pathologic and prognostic features. T lymphocyte identification and phenotyping were achieved using multiplexed (multispectral) immunofluorescence. In a separate hepatocellular carcinoma cohort, we replaced the stromal component with specific immune cell types-CXCR3+CD68+ or CD8+-to profile their spatial relationships with CXCL9+CD68+ cells. RESULTS: Six unsupervised TIPC subtypes based on T lymphocyte distribution patterns were identified, comprising two cold and four hot subtypes. Three of the four hot subtypes were associated with significantly longer colorectal cancer (CRC)-specific survival compared to a reference cold subtype. Our analysis showed that variations in T-cell densities among the TIPC subtypes did not strictly correlate with prognostic benefits, underscoring the prognostic significance of immune cell spatial patterns. Additionally, TIPC revealed two spatially distinct and cell density-specific subtypes among microsatellite instability-high colorectal cancers, indicating its potential to upgrade tumor subtyping. TIPC was also applied to additional immune cell types, eosinophils and neutrophils, identified using morphology and supervised machine learning; here two tumor subtypes with similarly low densities, namely 'cold, tumor-rich' and 'cold, stroma-rich', exhibited differential prognostic associations. Lastly, we validated our methods and results using The Cancer Genome Atlas colon and rectal adenocarcinoma data (n = 570). Moreover, applying TIPC to hepatocellular carcinoma cases (n = 27) highlighted critical cell interactions like CXCL9-CXCR3 and CXCL9-CD8. CONCLUSIONS: Unsupervised discoveries of microgeometric tissue organizational patterns and novel tumor subtypes using the TIPC algorithm can deepen our understanding of the tumor immune microenvironment and likely inform precision cancer immunotherapy.

Humans↗
PubMed1978

Immune responses to weakly immunogenic virally induced tumors. I. Overcoming low responsiveness by priming mice with a syngeneic in vitro tumor line or allogeneic cross-reactive tumor.

This report describes model systems which show low primary in vitro syngeneic cytotoxic responses to a Moloney-induced YAC tumor (syngeneic in A mice) and a Rauscher-induced RBL5 tumor (syngeneic in C57BL/6 mice) and examines different approaches to overcome these defects. Two major findings were obtained: (a) spleen cells from A mice, injected with tumor cells from an in vitro tumor line YAC-1, derived from YACL, could generate a significant syngeneic cytotoxic response. In contrast, spleen cells from A mice injected with tumor cells from the in vivo tumor line failed to generate a syngeneic cytotoxic response. Thus, tumor cells from the in vitro line were more immunogeneic that those from the in vivo line. (b) Spleen cells from A mice which were injected with the cross-reactive allogeneic tumor RBL5, could generate significant cytotoxic responses to the syngeneic tumors YAC and YAC-1. Similarly, spleen cells from C57BL/6 mice injected with the cross-reactive allogeneic tumor YAC-1, could generate a significant cytotoxic response to the syngeneic tumor RBL5. Thus, cross-reactive allogeneic tumors could stimulate syngeneic cytotoxicity. The theoretical and the practical implications of these studies are discussed.

Animals↗
PubMed1975

Tumor-secific immunity to chemically induced tumors. Evidence for immunologic specificity and shared antigenicity in lymphocyte responses to soluble tumor antigens.

Experiments were designed to explore the apparent paradox that methylcholanthrene-induced tumors of mice evoke tumor-unique transplantation immunity but reveal almost complete cross-reacting antigenicity in tests of lymphocyte behavior in vitro. The approach involved use of tumor membranes solubilized in 3 M KCl, employed both as the stimulating antigen source in a new in vitro proliferation assay of lymphocyte recognition, and as immunogens in vivo. The kinetics of the assay resembled those of in vitro tests of mitogen or specific antigen stimulation in other systems. Lymphoid cell proliferation was assessed in peripheral blood leukocytes, lymph nodes (LN), and spleen over the course of tumor bearing, and in animals immunized by tumor amputation or with the solubilized antigens. The pattern of spread of reactivity was from regional LN to spleen, peripheral blood, and nonregional nodes in each circumstance. An unexplained low antigen dose inhibitory phenomenon was encountered in spontaneously proliferating cell subpopulations taken from some tumor-bearing animals. In vitro responses to some but not all solubilized antigens made from multiple syngeneic tumors were detected in each circumstance. The soluble antigens also induced shared resistance to some tumors. The patterns of spread of responsiveness to syngeneic tumor antigens, the time-course, and relative intensity were most compatible with independent clonal responses to multiple tumor-borne antigens, some but not all of which are shared in any family of syngeneic tumors.

Animals↗
PubMed1977

Immune surveillance against virus-induced tumors and nonrejectability of spontaneous tumors: contrasting consequences of host versus tumor evolution.

Spontaneous tumours are defined as tumors that develop in the absence of all experimental interference. In contrast to the widely documented, strong rejection reactions against most virus-induced tumors, spontaneous tumors evoke little or no detectable rejection reaction in intact or preimmunized syngeneic hosts. The difference can be viewed in relation to the contrasting natural history of the two conditions. Spontaneous tumors evolve in several steps, as a fule. "Tumor progression" is a microevolutionary process at the level of the somatic tissue where successive clonal variants replace each other. Each new variant gains the upper hand due to its greater independence of some restricting host mechanism. Independence of immune restrictions must be part of this process. Host selection for immune resistance apparently plays no major role here, presumably because most of the naturally occurring tumors arise after the host has passed the peak of its reproductive period. Protection against the oncogenic effects of ubiquitous tumor viruses is, on the other hand, the result of host selection for immune mechanisms favoring prompt rejection of virus-transformed cells. This is neither synonymous with nor related to protection against the viral infection per se, which is frequently successful and usually quite harmless. A certain relationship can be perceived between the degree of viral ubiquity and the strength of immune protection against the corresponding tumor cells. Natural selection for host recognition of commonly occurring, virally induced changes in neoplastic cell membranes can be surmised to occur, at least in part, by the fixation of appropriate immune responsiveness (Ir) genes. The role of Ir genes for tumor recognition can be approached by the genetic analysis of the F1 hybrid resistance effect. Unresponsiveness to spontaneous tumors may be overcome by target-cell modification, e.g., by chemical coupling, somatic cell hybridization, or viral "xenogenization".

Animals↗
PubMed1979

Further observations on the inhibition of tumor growth by C. parvum with cyclophosphamide. VII. Effect of treatment prior to primary tumor removal on the growth of distant tumor.

The present investigations were directed toward determining whether primary tumor manipulation prior to its removal is advantageous for the control of metastases and survival. Studies were carried out to ascertain whether 1) there is justification for delaying surgical removal of a primary tumor to permit preoperative administration of cyclophosphamide (CY) and/or C. parvum (CP) and 2) there is an advantage to administering the immunotherapy directly into a primary tumor. After operation, in all investigations, systemic CP and CY was used. Despite the putative similarity of animals, tumors and treatment regimens there was marked variation in response of tumors to therapy. No benefit was derived from administering preoperative immunotherapy alone. When operation was delayed to employ systemic immuno-chemotherapy, a slight improvement in the control of distant tumor was noted. The employment of preoperative intratumor immunotherapy led to a greater prolongation of survival and more inhibition of distant tumor growth than did immediate primary tumor removal or the use of preoperative systemic immunotherapy. The results suggest that there may be an advantage to delaying removal of a primary tumor so that it may be employed in therapeutic strategies directed toward control of metastatic disease.

Animals↗
PubMed1979

Influence of factors derived from EMT6 tumors and from bone marrow of tumor-bearing mice on tumor and bone marrow stem cell kinetics.

Untreated EMT6 tumors in BALB/c mice were used to assess the regulatory mechanisms of tumor growth in these animals. This tumor can be quantitated for clonogenic cells by in vitro techniques, and the hydroxyurea suicide method makes it possible to determine the kinetic status of the clonogenic cells. The untreated EMT6 tumor does not seem to have internal humoral regulatory mechanisms explaining tumor growth kinetics. However, the exponentially growing EMT6 experimental tumor releases a factor capable of stimulating quiescent splenic colony-forming units into cycle. This is also true of bone marrow taken from tumor-bearing mice. This study was made possible using an in vivo-in vitro technique which separates the effector cells from the responder cells by a Millipore filter floating on the culture medium. The relationship between tumor growth and normal hematopoietic tissue of the tumor-bearing animal is discussed.

Animals↗
PubMed1978

Involvement of mouse mammary tumor virus in spontaneous and hormone-induced mammary tumors in low-mammary-tumor mouse strains.

The involvement of the mouse mammary tumor virus (MTV) in spontaneous and hormone-induced mammary tumors in low-mammary-tumor mouse strains was studied by comparing the amounts of MTV RNA and MTV DNA sequences in mammary tumors and other tissues of mice with an without hormonal treatments. The following results were obtained. (i) Mammary tumors which appeared in C3H mice as a result of an infection with MTV contained more MTV DNA compared with noninfected organs; these mammary tumors also contained more MTV RNA than was present in lactating mammary gland cells. (ii) Hormonal stimulation by administration of excessive amounts of prolactin via hypophyseal isografts in C3Hf and O20 mice resulted in an increased expression of MTV RNA in the mammary glands. This elevated level of MTV RNA expression was, however, not maintained in the hormone-induced mammary tumors. (iii) Spontaneous mammary tumors in BALB/c mice contained similar levels of MTV DNA and MTV RNA sequences as were found in other cells of these animals.

Animals↗
PubMed1976

Tumor bound immunoglobulins: the relationship between the in vivo coating of tumor cells by potentially cytotoxic anti-tumor antibodies, and the expression of immune complex receptors.

In this study we investigated the relationship between binding of anti-tumor antibodies by polyoma-virus-induced SEYF- a tumor cells and the expression of immune-complex receptors on these cells. It was shown that in vivo propagated cells became progressively coated with IgG. The increase in the IgG coating of SEYF-a cells, occurring during the second week of propagation, was directly correlated with an increase in the coating of cells with potentially cytotoxic anti-tumor antibodies. The activity of these antibodies was demonstrated by cell lysis following addition of exogenous complement. Cell populations propagated in vivo for longer periods (3 weeks or more) became less sensitive to exogenous complement although their IgG coating remained high, and although higher titers of anti-tumor antibodies could be eluted from them. This indicated that antibodies coating young tumor cell populations have the capacity to activate complement whereas those coating older tumor cell populations are incapable of complement activation. Previous findings that SEYF-a cell populations are able to bind unrelated immune complexes were confirmed in the present study. We also found that the capacity of these populations to bind such unrelated complexes decreased with propagation time in vivo. The involvement of anti-tumor antibodies in this phenomenon was indicated by the finding that such antibodies inhibited binding of unrelated immune complexes by young cells but not by old cells. Furthermore, treatments causing dissociation of Ig from the cell surface restored, to some extent, the capacity of anti-tumor antibodies to inhibit immune complex binding by old SEYF-a populations.

Animals↗
PubMed1979

In situ lymphoid cells of mouse mammary tumors. IV. Comparison of functional activity of lymphoid cells separated from mammary tumors to that of spleen and lymph node cells of tumor-sensitized mice.

Lymphoid cells isolated form several types of mouse mammary tumors are capable of stimulating tumor cell growth or survival in MCT assays. Lymph node and spleen cells of mice bearing such a tumor are specifically cytotoxic to the tumor cells. Surgical removal of the tumor is followed in 4 to 7 days by the appearance of stimulatory capacity in spleens and lymph nodes. By day 10, cytotoxic cells specific for the sensitizing tumor are again detected. These reach a peak on day 13. By day 17 no reactivity is detectable. The functional distribution of tumor-reactive lymphoid cells is different between tumor masses and peripheral lymphoid organs.

Animals↗
PubMed1979

Immunological characterization of mouse mammary tumor virus p10 and its presence in mammary tumors and sera of tumor-bearing mice.

Mouse mammary tumor virus (MMTV) p10 and gp52 were purified and used as radiolabeled antigens in sensitive radioimmunoassays. These radioimmunoassays were specific for MMTV proteins since detergent-disrupted MMTV from C3H/HeN, RIII, and GR/N mice gave complete competition, whereas C3H/HeNf liver extracts and other lysed retroviruses did not. Both gp52 and p10 are coded by the viral genome, since MMTV grown in a heterologous cell line (feline kidney cells) competed in these assays. Sera from mammary tumor-bearing mice and mammary tumors from C3H/HeN and C3H/HeNf mice competed in both the gp52 and the p10 assays. Although these radioimmunoassays detected predominantly group-specific antigenic determinants in C3H/HeN and C3H/HeNf tumor extracts, type specificity was also found with gp52. Absorption of the anti-MMTV serum with C3H/HeNf tumor extracts removed all antibodies directed against p10 and decreased the anti-gp52 titer approximately 30-fold. When this absorbed antiserum was used at limiting dilution in the gp52 radioimmunoassay, C3H/HeN tumor extracts gave complete competition, whereas no competition was found with C3H/HeNf tumor extracts.

Animals↗
PubMed1976

Discussion paper: dual effects of tumor antigens: induction of tumor resistance or tumor growth enhancement.

TA3-HA nonspecific tumors growing in ascites form shed their membrane components into the ascites fluid. This product can induce tumor growth enhancement if given together with or after i.p. tumor inoculation in relatively large quantities, but if given i.m. in small quantities, several days before tumor challenge, the mice show an elevated resistance to the tumor. The strictly strain-specific TA3-St line does not release such membrane components into the ascites fluid. It has also been found that the TA3-HA cells have a larger membrane fluidity than the TA3-St cells, as measured by membrane microviscosity, using the Shinitzki procedure. Isolation and gross chemical analysis of the TA3-Ha ascites fluid component was carried out. Results, so far, indicate that the active site of this product is probably carbohydrate in nature. The possible mode of action of such component in tumor growth enhancement is most probably by overwhelming and neutralizing immunocytes capable of recognition and eventually cytotoxic action.

Animals↗
PubMed1976

Nonspecific inhibition of tumor growth in vivo by admixed allogeneic tumor-sensitized lymphoid cells and identical inactivated allogeneic tumor cells.

With the in vivo tumor neutralization test (Winn test), growth of a transplanted (KMT-17) from Wistar-King-Aptekman rats was inhibited by allogeneic tumor (AH-66 from Donryu rats)-sensitized syngeneic lymphoid cells admixed with mitomycin C (MMC)-treated AH-66 cells. The observed tumor inhibition may be immunologically nonspecific, since no cross-antigens were detected by membrane immunofluorescence on the surfaces of KMT-17 and AH-66 cells. Close contact among KMT-17, AH-66-sensitized lymphoid cells and MMC-treated AH-66 cells was required for the inhibition of KMT-17 growth. AH-66 cells pretreated with formalin or ultrasonication lost tumor inhibitory activity when they were admixed with AH-66-sensitized lymphoid cells, and only MMC-treatment effectively preserved the tumor inhibitory activity of AH-66 cells. The sensitized spleen cells, draining lymph node, or peripheral blood cells inhibited tumor growth when they were admixed with MMC-treated AH-66 cells, whereas nucleated cells from bone marrow, thymus, or distal lymph node did not. Growths of KMT-17 were inhibited by admixed sensitized spleen cells and MMC-treated AH-66 even when pre-irradiated rats were used as recipients.

Animals↗