bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immunogenic variants obtained by mutagenesis of mouse mastocytoma P815. VI. Occasional escape from host rejection due to antigen‐loss secondary variants
Authors: Maryanski J. L. , Marchand M. , Uyttenhove C. , Boon T. 
Published: February 2007

AbstractAfter mutagenesis of mouse mastocytoma P815, it is possible to obtain variant (tum−) clones that are almost always rejected by syngeneic DBA/2 mice. Most tum− clones express new variant‐specific antigens that can be detected by cytolytic T cells (CTL). Occasionally, mice injected with tum− variants eventually develop progressive tumors. Cells from these tumors were analyzed for antigen expression with variant‐specific and P815‐specific CTL clones. Out of 13 tumors examined, 11 were composed of cells that had clearly lost a variant‐specific antigenic determinant. These results indicate that tum− variants induce a specific host rejection response which usually results in complete elimination of the variant cells, but that occasional antigen‐loss constitutes an important mechanism of escape. The loss of a variant‐specific antigenic determinant from one tum− clone that had escaped rejection allowed the detection of a residual variant‐specific determinant. This was demonstrated by isolating a new CTL clone that lysed both the original tum− clone and its antigen‐loss variant, but not other P815 targets. Thus, some complex transplantation antigens can be separated into independent determinants by using antigen‐loss variants.
Persistent in vitro infection by human T‐cell leukemia‐lymphoma virus (HTLV) of normal human T‐lymphocytes from blood relatives of patients with HTLV‐associated mature T‐cell neoplasms
Authors: Ruscetti Francis W. , Robert‐Guroff Marjorie , Ceccherini‐Nelli Luca , Minowada Jun , Popovic Mikulas , Gallo Robert C. 
Published: February 2007

AbstractHuman T‐cell lymphoma‐leukemia virus (HTLV), a novel type‐C retrovirus, has been identified in tumor cells of patients with mature T‐cell neoplasms. Attempts to transmit the first isolate of HTLV designated HTLV‐I(CR) to secondary cultures of animal cells and several attempts to transmit HTLV to normal human T cells, activated with PHA and grown with T‐cell growth factor (TCGF), obtained from randomly selected normal adult donors were unsuccessful. Peripheral blood leukocytes were obtained from blood relatives of patients with HTLV‐positive T‐cell neoplasms. These normal adult T cells were exposed to HTLV, and in 5 of 10 samples tested from three separate families, persistent infection of cultured T‐lymphocytes by HTLV occurred. HTLV infection was monitored by three methods: an indirect membrane immunofluorescence assay for HTLV p19; an in situ hybridization assay for intracellular viral RNA; and electron microscopic analysis for extracellular viral particles. Two of the five infected T‐cell lines have been continuously positive for HTLV for over 24 months in continuous culture. B‐cell lines from the same individuals could not be infected by HTLV‐I(CR). Despite the release of viral particles from the infected cultures detected by electron microscopy, no extracellular reverse transcriptase was found. HTLV infection stimulated increased long‐term growth of the T cells although all HTLV‐I(CR)‐infected cultured cells always remained dependent on the addition of TCGF for growth. Phenotypic characterization of the infected cells by monoclonal antibodies, HLA typing, cytochemical and cell surface markers showed that all the infected cells were mature T cells and were easily distinguished from the cells used as a source of HTLV for infection. The infected cells were either of a predominantly helper or of a suppressor phenotype showing that both mature T‐cell subsets can be infected. Whether these data indicate that there is a genetic basis for susceptibility of human T cells to HTLV infection or reflect an increased sensitivity of some cells to infection by low titers of HTLV remains to be determined. These results provide further evidence for a predominant T‐cell tropism of HTLV.
Monocytic origin of the human hematopoietic cell line U‐937 and its convertibility to macrophages evidenced by isoenzyme mapping
Authors: Radzun Heinz J. , Parwaresch Mohammad R. , Sundström Christer , Nilsson Kenneth , Eissner Michael 
Published: February 2007

AbstractU‐937 represents a well established permanent human hematopoietic cell line. Electron microscopical and enzyme cytochemical studies as well as the analysis of surface glycoproteins have provided ample evidence for the monocytic origin of U‐937. Upon stimulation with the tumour promotor 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA), U‐937 cells evolve into macrophage‐like cells with phagocytic capacities. Since human blood monocytes (BM) are characterized by five acid esterase (AcE; EC 3.1.1.6) isoenzymes which are cell‐specific in terms of isoelectric points (pi) and antigenicity, attempts were made in the present study to identify identical isoenzyme patterns in non‐ and TPA‐stimulated U‐937 cells. BM, cultured BM, non‐ and TPA‐stimulated U‐937 cells, as well as samples of resident human peritoneal macrophages (PM) as clearly‐defined functional derivatives of BM, were subjected to isoenzyme analysis using isoelectric focusing (IEF). The five monocyte specific isoenzymes of AcE were identified in both populations of U‐937. TPA‐stimulated samples showed two additional bands, identical to those appearing in cultured BM after 4 days of glass‐adherence and characteristic of resident human PM. Antisera raised against AcE of BM immunoprecipitated the two additional isoenzymes of TPA‐stimulated U‐937. It is concluded (1) the isoenzyme mapping of AcE documents the monocytic origin of U‐937. (2) TPA‐stimulation caricatures transformation of BM into resident tissue macrophages as far as pure morphology and AcE isoenzyme patterns are concerned. Thus, AcE isoenzyme mapping is apt for establishing reproducible and standardized criteria of different activation/differentiation states within the monocyte‐macrophage lineage.
Monoclonal antibody UJ 127:11 detects a 220,000‐240,000 kdal. Glycoprotein present on a sub‐set of neuroectodermally derived cells
Authors: Kemshead J. T. , Fritschy J. , Garson J. A. , Allan P. , Coakham H. , Brown S. , Asser U. 
Published: February 2007

AbstractThe monoclonal antibody UJ 127‐11 was raised following immunization of mice with human foetal brain and subsequent somatic cell hybridization of spleen cells with the mouse myeloma cell line P3‐X63‐Ag8‐653. Studies on normal foetal and adult tissues show that, by indirect immunofluorescence, the antigen recognized by UJ 127:11 is restricted in its expression to cells of neural rather than glial origin. Neural tumours such as neuroblastoma, medulloblastoma and ganglioglioma (neural component) bind the monoclonal antibody whereas malignancies originating from glial cells do not bind UJ 127:11. Biochemically the monoclonal antibody has been shown to bind to a glycoprotein of 220,000‐240,000 mol. wt. under reducing and non‐reducing conditions. Despite similarities in the molecular weight between human fibronectin and the antigen recognized by UJ 127:11, they have different serological and biochemical characteristics, suggesting that the monoclonal antibody is not binding to either cell or plasma fibronectin.
Clinical significance of circulating immune complexes in patients with metastatic breast cancer
Authors: Krieger G. , Kehl A. , Wander H.‐E. , Salo A.‐M. , Rauschecker H. F. , Nagel G. A. 
Published: February 2007

AbstractSerum circulating immune complexes (CIC) were repeatedly measured by means of the Cl binding assay (Cba) and the Raji cell assay (Rca) in 158 patients with metastatic breast cancer (mbc). Frequency of occurrence and levels of CIC were only slightly increased in mbc when compared to age‐matched healthy women. They were identical to those of patients with localized breast cancer prior to mastectomy and to those of post mastectomy patients without evidence of recurrent disease. In mbc the results of the Cba and the Rca showed a poor correlation, whereas in a control group of patients with rheumatoid arthritis both tests showed significantly elevated levels of CIC. Patients with mbc were followed up clinically and biochemically by serially measuring CIC for an average of 10 months. Patients with positive CIC did not prove to be an unfavorable group regarding progression of disease and response to chemotherapy. When CEA and CIC levels were compared, CIC, unlike CEA, was a poor tumor marker. In conclusion, CIC as measured by Cl binding assay and Raji cell assay are not clinically significant tumor markers or prognostic indicators in patients with metastatic breast cancer.
Production of colony‐stimulating factors by Hodgkin cell lines
Authors: Burrichter Heinz , Heit Wolfgang , Schaadt Michael , Kirchner Hartmut , Diehl Volker 
Published: February 2007

AbstractThis work was performed with L 428, a cell line established in 1978 from a patient with Hodgkin's disease. These in vitro cells represent counterparts of in vivo Hodgkin and Sternberg‐Reed cells. L 428 and its derived sublines produce a significant amount of colony‐stimulatling factor (CSF) compared to standard preparations of CSF (fetal liver conditioned medium). Hodgkin‐cell‐derived conditioned medium, tested in cord‐blood assays and in semi‐solid agar systems, induced myeloproliferation predominantly. Production of CSF is independent of fetal calf serum concentration in the cultures. L 428‐conditioined medium could provide an excellent source for characterization and purification of granulocyte CSF.
Evidence for involvement of the immunoglobulin heavy‐chain gene locus in the 8:14 translocation of human B lymphomas
Authors: McIntosh R. V. , Cohen B. B. , Steel C. M. , Read Helene , Moxley Marion , Evans H. J. 
Published: February 2007

AbstractAbnormalities of immunoglobulin (Ig) heavy chain synthesis occurring in human B lymphoid cell lines of malignant origin suggest that the Ig heavy‐chain gene complex is involved in the 8:14 chromosome translocation which these cells carry.
Changes in chromatin composition associated with hormone‐dependent mammary tumor regression
Authors: Goya Rodolfo G. , Sosa Yolanda E. 
Published: February 2007

AbstractThe chemical composition of chromatin from dimethylbenz(a)anthracene (DMBA)‐induced mammary tumors was compared in growing and regressing neoplasms. Tumor regression was induced by 2‐bromo‐α‐ergocryptine (CB‐154) administration to the tumor‐bearing rats. Seventy percent of the neoplasms showed a sharp fall in the levels of 3H‐thymidine incorporation into DNA after 7‐8 days of treatment (I mg CB‐154/day). These CB‐154‐responsive tumors showed a significant increase in non‐histone chromosomal proteins (NHCP) relative to DNA, while the histone fraction remained constant. Non‐responsive tumors showed no change in their chromatin composition. Low doses of ovine prolactin (18 IU) given together with CB‐154 (I mg) were able to prevent the effects of the latter on both DNA synthesis and chromatin composition of DMBA‐ induced mammary tumors. High doses of hormone (40 IU) produced a two‐fold increase in the tumors' DNA synthesis irrespective of the simultaneous administration of 1‐ or 2‐mg doses of CB‐154. This high dose of hormone was also able to prevent the effects of CB‐154 on chromatin composition of the tumors. We conclude that the above effects of CB‐154 are exerted mainly, if not exclusively, through the inhibition of prolactin secretion. On the other hand, the regression of these neoplasms after prolactin deprivation seems to be associated with an increase in the NHCP/DNA ratio. The possibility of an involvement of tumor cell membrane in the mechanism of regression of prolactin‐dependent mammary tumors is discussed.
Induction of epstein‐barr virus early antigens by corticosteroids: Inhibition by TPA and retinoic acid
Authors: Bauer G. 
Published: February 2007

AbstractCorticosteroids can induce the synthesis of EBV antigens in the Burkitt lymphoma line Daudi. As early as 12 h after application of the drug, an increase of EA‐positive cells can be seen, the maximum induction being reached after 2 days. Nanogram amounts per ml of hormone are sufficient for measurable effects. Early antigen induction by corticosteroids does not require replication of viral DNA. Induction by corticosteroid differs from induction by other systems in two major respects: (1) it does not cooperate with other inducers, and (2) it is specifically inhibited by 12‐O‐tetradecanoyl‐phorbol‐13‐acetate (TPA). Induction by corticosteroids, however, shares at least one retinoic acid‐sensitive step with induction by chemicals such as TPA, 5‐iodo‐2‐deoxyuridine (IdUrd), n‐butyric acid (n‐BA) or inducing serum factor. This study defines three qualitatively different effects of TPA in Daudi cells: an inhibitory effect on EBV induction by corticosteroids and two differential types of synergistic effects with serum factor or n‐BA, respectively. In this particular cell line, TPA exhibits no inducing capacity when applied alone.
Progression of rat mammary development with age and its relationship to carcinogenesis by a chemical carcinogen
Authors: Sinha D. K. , Pazik J. E. , Dao T. L. 
Published: February 2007

AbstractThe progression of mammary gland development in Sprague‐Dawley rats between 5 and 440 days of age was studied. Tumorigenesis of the mammary gland after administration of 7,12‐dimethylbenz(a)anthracene (DMBA) was also investigated during different prepubertal and postpubertal stages. The mammary gland starts as a single primary duct on day 5 and with age branches and grows into a complete gland. The growth of the gland was observed to start from the nipple area and progress into the empty fat pad. This growth was in the form of club‐shaped end‐buds which, after the onset of puberty, became gradually transformed into alveolar buds. [3H]‐thy‐midine labelling index (LI.) was high (19%) in prepubertal glands, but it eventually declined to 8% at 60‐65 days. The postpubertal gland at the age of 150 days was determined to be practically mitotically static, but at 440 days, there was another increase in LI. There was a direct relationship between mammary tumorigenesis by DMBA and LI. in the mammary gland at the time of treatment with the carcinogen. Up to 55 days of age, tumorigenesis was 90‐100%, and LI. was also high during this period. The carcinogen was practically ineffective at 150 days, when the mammary gland was non‐proliferative. Though the total tumor induction was high in the prepubertal rats, the majority of the tumors (up to 84%) were benign fibro‐adenomas, while almost all the tumors in postpubertal rats were adenocarcinomas. Thus, a relationship was observed between the presence of ovarian hormones and the induction of malignant tumors. It was concluded that cell proliferation index at the time of carcinogen treatment is important for tumor induction, but whether or not the tumor is malignant is determined by the presence or absence of ovarian hormones.
Cloned lines of SJL/J spleen cells with cytotoxic reactivity
Authors: Riccardi Carlo , Allavena Paola , Ortaldo John , Herberman Ronald B. 
Published: February 2007

AbstractCultures of spleen cells from normal SJL/J mice were initiated and maintained in the presence of lectin‐free interleukin‐2 (IL‐2). After about 8 weeks in culture, the frequency of progenitors of proliferative cells became quite high (1/8‐1/10) and it was possible to obtain many clones by the limiting dilution technique. Some of the clones had high levels of cytotoxic reactivity against tumor target cells, even at low effectontarget ratios, indicating that natural effector cells from this low‐NK‐reactive strain have the capability of expressing potent lytic effects. There was considerable heterogeneity among the clones in their patterns of cytotoxic activity, morphology and expression of T‐cell‐associated antigens. Although the overall pattern of reactivity resembled that of NK cells, some clones reacted against an anchorage‐dependent lung cancer cell line, M109, without detectable effects against the other target cells tested, including the highly NK‐susceptible lymphoma cell line, YAC‐I. The pattern of cytotoxic reactivity by the clones did not correlate with the morphological appearance of large granular lymphocytes (LGL), which has been highly associated with NK activity of fresh, uncultured lymphoid cells.
Infection and transformation of fresh human umbilical cord blood cells by multiple sources of human T‐cell leukemia‐lymphoma virus (HTLV)
Authors: Markham Phillip D. , Salahuddin Syed Z. , Kalyanaraman V. S. , Popovic Mikulas , Sarin Prem , Gallo Robert C. 
Published: February 2007

AbstractHuman T‐cell leukemia‐lymphoma virus (HTLV) was first isolated from sporadic patients with adult T‐cell malignancies in the United States and subsequently from T‐lymphocytes established in culture from additional T‐cell leukemia‐lymphoma patients living in different geographical areas of the world. Co‐cultivation of normal unbilical cord blood with lethally irradiated, HTLV‐positive lymphocytes established in culture from many of these patients resulted in the productive infection of the cord blood T‐lymphocytes which grew in suspension culture in the absence of exogenous TCGF. These transformed cord blood cells have morphological and cytochemical properties similar to HTLV‐positive fresh and cultured tumor T‐cells and are distinguishable from virus donor cells by HLA haplotype and chromosomal markers. These cells express HTLV proteins, release type‐C virus particles and contain surface receptors for TCGF. These results demonstrate that HTLV isolated from T‐cell leukemic donors from different parts of the world can productively infect and transform fresh human cord blood T‐lymphocytes, and that the transformed cells share many similarities with fresh or cultured leukemic cells.
Resistance of fibroblasts and hematopoietic cells to ecotropic murine leukemia virus infection; an Akvr‐1R gene effect
Authors: Rasheed Suraiya , Gardner Murray B. 
Published: February 2007

AbstractA gene named Akvr‐1segregates as a dominant allele in California wild mice (LC). Unlike Fv‐1 and Fv‐2 restriction alleles, the Akvr‐1confers resistance to replication of all ecotropic (N‐, B‐, and NB‐tropic) murine leukemia viruses (MuLV‐E) and prevents endogenous AKR virus‐induced lymphoma/leukemia in F1 hybrids of AKR × LC. We have tested fibroblasts and hematopoietic cells from mice of defined Akvr‐1 genotypes for in vitro susceptibility to various MuLV infections. Our results indicated a dominant in vitro resistance of exogenously MuLV‐E infected cells carrying Akvr‐1R allele although resistance was stronger in the homozygous cells than in the heterozygous cells. Moreover, resistance of cells to virus replication was not abrogated by high multiplicities of infection or by growth stimulation of hematopoietic cultures by various T‐ or B‐cell‐responsive mitogenic agents.
Expression of the bla antigen, defined by the monoclonal 38.13 antibody, on burkitt lymphoma lines, lymphoblastoid cell lines, their hybrids and other b‐cell lymphomas and leukemias
Authors: Klein George , Manneborg‐Sandlund Agneta , Ehlin‐Henriksson Barbro , Godal Tore , Wiels Joëlle , Tursz Thomas 
Published: February 2007

AbstractThe BLA expression of eight Burkitt lymphoma lines was high, whereas it was negative in four, including the two IgG producers tested. Most lymphoblastoid cell lines (LCL) of normal origin had only a low percentage of positive cells, not significantly above background, although a few had up to 30% positives. EBV conversion of the EBV‐negative Burkitt lymphoma line Ramos destabilized the high BLA expression, leading to a decrease in the average number of positive cells in the majority of the converted sublines in parallel with considerable fluctuation in antigen expression within each subline. Our group has previously shown that EBV‐conversion of Ramos cells can induce certain differentiation steps (Spira et al., 1981 a). EBV‐converted sublines of another EBV‐negative Burkitt lymphoma, BJAB, showed a much greater stability previously and remained unchanged with regard to BLA expression in our present experiments. Eight T‐cell leukemias, three myeloid leukemia lines and two diffuse histiocytic lymphomas were negative for BLA, whereas two myeloma lines were 30‐40% positive. A histiocytic tumor had marginal reactions. Hybrids derived from the fusion of high with low BLA‐reactive parental lines showed all three possible patterns (high, intermediate and low), provided that B‐cell lines were fused with each other. Fusion of two Burkitt lymphoma lines with the K562 erythroleukemia line led to the extinction of BLA expression, as well as to the eclipse of other B‐cell markers. B‐lymphoma and leukemia (CLL) cells harvested directly from the patient showed a heterogeneous reactivity pattern. Strong to intermediate BLA expression was found among CLL cells and in most histological groups of B‐CLL lymphomas except the centroblastic group (3/3 negatives). IgG‐expressing follicular lymphomas were less reactive than IgM ± IgD lymphomas of the same group. Immunocytomas were also low‐reactive. BLA can be thus expressed on a variety of B‐cell neoplasms; the degree of its expression appears to be related to the stage of differentiation.
Melanoma‐associated antigen p97 continues to be expressed after prolonged exposure of cells to specific antibody
Authors: Hellström Ingegerd , Brown Joseph P. , Hellström Karl Erik 
Published: February 2007

Abstractp97, a 97,000 molecular weight cell surface glycoprotein associated with human melanoma, has attracted attention as a possible target for tumor therapy. Melanoma cells were grown overnight in the presence of IgG2a or IgGI monoclonal antibodies specific for p97, and then exposed to complement and also tested for binding of monoclonal antibodies specific for other epitopes of p97. The results indicated that melanoma cells continued to express p97 after prolonged exposure to specific antibody, a prerequisite for many therapeutic applications.
Serological responses of melanoma patients to vaccines derived from allogeneic cultured melanoma cells
Authors: Livingston Philip O. , Takeyama Hideo , Pollack Marilyn S. , Houghton Alan N. , Albino Anthony , Pinsky Carl M. , Oettgen Herbert F. , Old Lloyd J. 
Published: February 2007

AbstractTwenty melanoma patients were immunized with a whole‐cell vaccine prepared from irradiated cells of the melanoma cell line SK‐MEL‐13. This line, derived from the melanoma of patient AH, expresses a differentiation antigen (initially defined by autologous antibody) which is restricted to melanomas and other cells of neural crest origin. The patients' sera were tested in resetting assays before and after vaccination for antibodies against cell surface antigens of autologous cultured melanoma cells and SK‐MEL‐13, and the specificity of observed reactions was defined by absorption tests. Nine patients developed antibodies against autologous cultured melanoma cells. In only one case, patient DM, were these antibodies directed against the AH antigen. In the remaining patients, the antibodies were related to fetal bovine serum in the vaccine growth medium. All patients developed antibodies against cell surface HLA alloantigens of the immunizing cell, SK‐MEL‐13, as demonstrated by absorption analysis with B cells from the donor of SK‐MEL‐13 and by serological typing with a panel of HLA typed peripheral blood T cells and B‐cell CLL cells. No specificity other than the AH antibody found in patient DM was detected after removal of alloantigens with B cells. We conclude that vaccines prepared from irradiated allogeneic melanoma cells expressing AH antigen, a demonstrably immunogenic differentiation antigen of the melanocyte lineage, are not effective in inducing AH antibody.