Search PubMed⌕ Search

Biomedical subjects

J H Coggin

Publications and source records attributed to J H Coggin.

18 recordsLinked to original sources
PubMed1992

Expression of 44-kilodalton oncofetal antigen as a premalignancy marker in X irradiation-induced murine T-cell lymphoma.

BACKGROUND: Oncofetal antigens (OFAs) are found on the surface of murine and human midgestation fetal cells, in human and rodent tumor tissues, and on human and rodent tumor and embryonic cell lines but not in normal neonatal or adult human and rodent tissue. PURPOSE: The usefulness of OFA as an early indicator of lymphoma development was evaluated. METHODS: With the use of monoclonal antibody directed against a 44-kd glycoprotein, cells from the thymus and spleen of RFM/UnCr mice receiving whole-body, split-dose x irradiation (1.75 Gy once a week for 4 weeks) or cells from these organs from control (nonirradiated) mice were analyzed for the presence of OFA in the flow cytometer and in limited intrathymic transplant. RESULTS: OFA was detected on thymocytes from 75% of irradiated mice by 2 months after treatment, reflecting eventual lymphoma development in the irradiated controls by flow cytometry and in intrathymic transplant. In general, the number of thymuses expressing OFA and the percentage of OFA+ cells increased with time after irradiation. By 4 months, OFA+ splenocytes were present, but only in mice possessing OFA+ thymocytes. Serially tested, irradiated RFM mice that never expressed OFA in the thymus reflected the percentage of irradiated RFM/UnCr mice that never developed lymphomas. This observation was also made in irradiated C57BL/6N mice, which attests to the tumor specificity of OFA expression. Spleen immunoglobulin-positive cells were decreased, while CD4+ and CD8+ cells were greatly increased. Indirect evidence of CD4/CD8 expression on OFA+ splenocytes suggests that the newly forming lymphomas were of immature T-cell origin. Major histocompatibility antigen expression did not vary significantly. Histopathologic examination revealed radiation-induced lymphomas in OFA-positive tissues characterized by a monomorphic population of large blastic immature lymphoid cells. CONCLUSION: The early expression of OFA in radiation-induced oncogenesis was established. IMPLICATIONS: OFA expression significantly preceded clear histologic evidence of malignant T cells or clinical lymphoma in irradiated RFM/UnCr mice that went on to develop T-cell lymphomas.

Animals↗
PubMed1991

Isolation and partial characterization of a soluble oncofetal antigen from murine and human amniotic fluids.

A soluble (cell-free) oncofetal antigen (OFA) was detected in murine and human amniotic fluids by immunostaining with the murine monoclonal antibody (MAb 115) produced by syngeneic immunization with mid-gestational mouse fetal cells. OFA was purified from the amniotic fluids by ammonium sulfate precipitation at 30-70% saturation, followed by successive gel chromatography of the OFA-containing fraction on Sephacryl-S300 HR, Q- and S-Sepharoses and lentil lectin agarose. The fraction eluted from the lentil lectin column gave a single band on SDS-PAGE of the same molecular weight as the membrane-bound OFA found on both fetal and tumor tissues of humans and several rodents. Both soluble and membrane-bound OFAs share several chemical characteristics, including binding to lentil lectin and wheat-germ agglutinin, molecular weight (44 kDa) and pI (6.8). Mild periodate oxidation of OFA did not affect its binding to MAb 115 in an enzyme-linked immunosorbent assay, indicating that the reactive epitope is a peptide.

Amniotic Fluid↗
PubMed1990

Differential expression of class I major histocompatibility complex determinants by lymphoblastic leukemia-lymphoma cell lines.

Two T-cell lines (XR11-4T and XR11-5T), established from radiation-induced, murine lymphoblastic lymphomas, were examined for the expression of class I major histocompatibility complex antigen and tumor induction. These cell lines expressed class I private determinants, H-2.9 and H-2.26, but not the monomorphic determinant defined by monoclonal antibody M1/42. Both cell lines produced tumors in syngeneic and allogeneic hosts. The monomorphic determinant could be demonstrated on both cell lines following growth in allogeneic (BALB/c mice) but not in syngeneic (RFM mice) hosts. The re-expressed determinant present on cells following growth in allogeneic mice was not of host origin. Thus, tumorigenic x irradiation may differentially affect the expression of class I major histocompatibility complex determinants.

Animals↗
PubMed1989

Immunogenicity of a soluble partially purified oncofetal antigen from murine fibrosarcoma in syngeneic mice.

A tumor/fetal associated antigen, termed oncofetal antigen (OFA), conserved in the tumor and fetal tissue of rodents and humans, was extracted from murine fibrosarcoma cells and tumors and was fractionated on an Ultrogel AcA34 gel filtration column. A monoclonal antibody 115 specific for the OFA identified three peaks of antigenic activity in the eluted fractions, designated fractions (Fr.) I, II, and III, in the molecular weight range of greater than 160, 90, and 44 kDa, respectively. Most of the activity resided in the high molecular weight fraction, Fr. I. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis and gel scanning of Fr. I showed multiple bands, one of which, constituting about 5.6% of the total protein bands in Fr. I, was the 44 kDa oncofetal antigen, apparently present in this fraction in a soluble complex form. Lectin binding studies and isoelectric focusing showed that the 44 kDa OFA is a glycoprotein, whose pI is 6.8. Spleen and peritoneal exudate cells of BALB/c mice immunized with Fr. I protected naive syngeneic mice, in adoptive transfer experiments, from developing tumors when challenged with syngeneic fibrosarcoma tumor cells, MCA-1315. Also, immune spleen cells were cytotoxic to the tumor target cells, MCA-1315, in a 51Cr release assay at several different effector to target cell ratios. This is the first description of a conserved, true, oncofetal antigen capable of inducing tumor transplantation resistance in syngeneic rodents in a semipurified form.

Animals↗
PubMed1989

Tumorigenic sublethal whole-body X-irradiation of RFM mice enhances cell-mediated cytotoxicity while transiently depressing T- and B-lymphocytes.

The immunocyte composition of spleens and peritoneal exudates (PEC) from RFM mice was examined following tumorigenic doses of whole-body, sublethal X-irradiation. T-cells, B-cells and macrophages were quantitated using mAb and flow cytometry. The cell mediated cytotoxicity (CMC) potential of PEC following immunization with allogeneic tumor cells was also assayed. Although the percentages of T- and B-cells were depressed in irradiated mice, the CMC activity of PEC from these same mice was increased. Thus irradiation resulted in an increased incidence of tumors coincident with an increased CMC potential against tumor targets.

Animals↗
PubMed1989

Cross-reacting tumor associated transplantation antigen on primary 3-methylcholanthrene-induced BALB/c sarcomas.

Immunization of adult, syngeneic BALB/c mice with irradiated, primary MCA-induced sarcomas conferred reproducible, nonisologous TATA-associated cross-protection against challenge with other primary MCA sarcomas or in vitro passaged MCA sarcoma cells. Isologous, individually specific TSTA-associated protection was also detected. Irradiated, normal BALB/c spleen or muscle tissues were not similarly protective. Pronounced cross-protection was best detected with secondary cultured, in vitro adapted sarcoma challenge inoculum, which could be accurately standardized. These findings paralleled the good cross-protection reported previously with long-term cultured MCA-induced sarcoma cell lines. OFA was expressed as a TATA on all syngeneic, primary MCA-induced sarcomas tested by syngeneic adoptive transfer experiments and on MuLv-free MCA-induced, syngeneic Meth A sarcoma cells.

Animals↗
PubMed1985

Mouse monoclonal antibody to embryonic antigen: development, cross-reactivity with rodent and human tumors, and preliminary polypeptide characterization.

Hybridomas producing IgM and IgG monoclonal antibodies (MoAb) to embryonic or fetal antigens (EA) were obtained in a completely syngeneic system. Lethally irradiated, 13-day-gestation, C57BL/6N mouse fetal cells or KCI extracts of these fetal cells obtained from primaparous donors were used as immunogens in several regimens to induce splenocytes in C57BL/6N mice that were utilized to form the hybridomas following fusion with a mouse myeloma line. Successful growth and cloning of the IgM-producing hybridomas required supplementation with factor(s) produced in the growth medium of the macrophage cell line RAW 264.7. An enzyme-linked immunosorbent assay (ELISA) was employed to screen the primary fusion hybridomas for antibody directed against fetal cell or adult cell determinants with the use of freshly explanted tissues. Glutaraldehyde-fixed fetal cells as well as crude fetal cell membranes were used as EA+ target cells (i.e., cell lines known to activate T-lymphocyte-mediated tumor resistance) in a solid-phase ELISA to perform quantitative ELISA adsorption tests of the MoAb. The anti-EA monoclonal IgM and the IgG detected common, embryo-specific antigen(s) on mouse, hamster, and human fetuses. Term fetal cells and adult normal tissues of the mouse, hamster, and human did not express cross-reactive determinants for the MoAb by absorption analysis and/or by direct binding in ELISA. EA expression as oncofetal antigens could also be detected with the monoclones on several rodent tumor cell lines tested as well as on a variety of human carcinomas but not on a spectrum of normal human tissues with the use of indirect ELISA absorption and affinity gel and sodium dodecyl sulfate-polyacrylamide gel electrophoresis analyses. Fluorescence analysis with the monoclones demonstrated specific reactivity with the surface of EA+ tumor cells in the FACS IV flow cytometer. The responsible antigen was carried on a 44- and a 200-kilodalton polypeptide.

Animals↗
PubMed1977

Characterization of immune responses to spontaneous hamster lymphomas.

Tumor resistance could be induced against the transplantation of cell lines derived from spontaneous lymphomas that occurred in the third of three lymphoma epizootics in a hamster colony. Immunization of normal hamsters with irradiated lymphoma cells promoted resistance to homologous lymphoma challenge and prevented the development of spontaneous lymphomas when immunized hamsters were exposed to the contaminated colony. This immunity could be transferred in an adoptive transfer assay. Resistance to direct challenge was not extended to simian virus 40(SV40)-induced sarcomas carrying SV40 tumor-specific transplantation antigen nor to herpesvirus-induced carcinoma cells, indicating specificity. The nature of the antigen(s) involved was discussed.

Animals↗
PubMed1976

The effect of exposure to dibutyryl cyclic adenylic acid on the membrane antigenicity of SV40 tumor cells.

When SV40 tumor cells (F5-1) in culture were treated with dibutyryl cyclic adenylic acid (DbcAMP),marked alterations occurred in their growth and morphology. Additionally, the incorporation or uptake of labeled thymidine, uridine, phenylalanine, and choline were reduced by this treatment. These modifications with DbcAMP exposure produced conditions simulating those of a contact-inhibited state. The immunization of hamsters with X-irradiated tumor cells previously cultured in the presence of DbcAMP indicated that the tumor-specific transplantation antigens and/or fetal antigens were altered during short-term expsoure to DbcAMP. Further examination of membrane antigens of SV40 tumor cells using the isotopic antiglobulin technique demonstrated a significant reduction in the tumor membrane antigen on cells cultured with DbcAMP.

Animals↗
PubMed1975

Forssman antigen and phase specific fetal antigens: an evaluation of their role in SV40 tumor immunity.

Forssman heterophile antigen was detected on hamster fetal cells which had been previously shown to be capable of eliciting transplantation resistance to syngeneic hamster SV40 tumors. The expression of Forssman antigen continued throughout fetal development and could be detected postpartum in the tissues of neonate hamsters. In contrast, fetal antigen(s) evoking immunity to SV40 tumors was also present on early fetal cells but, unlike Forssman antigen, was not expressed after the tenth day of gestation. Immunization of hamsters with guinea pig kidney cells or sheep erythrocytes which carry Forssman antigen failed to demonstrate significant protection against SV40 tumor development. Again by contrast, immunization with fetal cells was effective in evoking tumor immunity. Evaluation of serological responses to the FORSSMAN A ANTIGEN IN HAMSTERS INDICATED THAT THE HEMOLYTIC REACTIVITY PRODUCED BY IMMUNIZATION WITH GUINEA PIG KIDNEY CELLS OR SHEEP ERYTHROCYTES WAS ELICITED AGAINST ISOANTIGENS AND NOT THE Forssman antigen. A response to the Forssman determinant could only be detected in the serum from animals receiving exhaustive hyperimmunization with fetal cells or SV40 tumor cells. These data would eliminate a possible role of the Forssman heterophile antigen in the tumor protection evoked by immunization with fetal cells bearing embryonic antigens.

Animals↗