bluuebunny/crossref_metadata_2025_split huggingface dataset:
Corynebacterium parvum prevents immunization to admixed irradiated tumor cells by a local process
Authors: Titus Michael J. , Bartlett Gerald L. , Kreider John W. 
Published: February 2007

AbstractImmunization of mice with 106 irradiated LSTRA murine leukemia cells (LX) induced weak immunity to subsequent tumor‐cell challenge. Admixture of low doses (1.4‐14 μg) of C. parvum with the LX usually augmented the immunity. Higher doses (1,400‐7,000 μg) of admixed C. parvum not only failed to augment immunity, but prevented immunization by the contained LX. We investigated the mechanism by which 1,400 μg of C. parvum mixed with 106 LX prevents immunization by the LX. The inhibitory effect was a function of the ratio of C. parvum to tumor cells. Injection of 1,400 μg C. parvum, alone or mixed with the LX, did not prevent immunization by LX given simultaneously at a separate site. Injection of C. parvum, alone or mixed with the LX, did not prevent immunization by LX injected simultaneously at a separate site sharing a common lymph‐node drainage area. The high dose of C. parvum prolonged retention of radiolabelled LX at the injection site and decreased the rate of distribution of the LX to other organs, particularly the spleen. These results indicate that a high dose of C. parvum prevented immunization through a localized process at the injection site.
Effect of selenium on the induction of breast fibroadenomas by adenovirus type 9 and 1,2‐dimethylhydrazine‐induced bowel carcinogenesis in rats
Authors: Ankerst Jaro , Sjögren Hans O. 
Published: February 2007

AbstractSelenium in its organic and inorganic forms has been shown to inhibit the development of chemically induced, spontaneous and transplanted tumors. The present investigation was performed to study the effect of selenium (4 μg per ml of drinking water) on tumorigenesis of adenovirus‐type‐9‐induced breast fibroadenomas and on 1,2‐dimethylhydrazine‐induced bowel carcinogenesis in WF rats. It was found that identical treatment with Se under identical conditions and with no obvious toxic effects on the rats (I) resulted in inhibition of DMH‐induced large‐bowel carcinogenesis; (2) facilitated induction of small‐bowel cancer by the same carcinogen in the same animals, and (3) greatly facilitated induction of breast fibroadenoma by adenovirus type 9 in the same strain of rats. The effect of Se treatment on DMH‐induced largebowel carcinogenesis confirms previous findings and proves that the opposite effect on fibroadenoma development is not due to differences in e.g. effective dose, animal strains or condition of the animals. It is not yet clear through which mechanisms Se exerts these effects.
Cancers of the digestive tract, alcohol and tobacco
Authors: Turns A. J. , Péqljignot G. , Gignoux M. , Valla A 
Published: February 2007

AbstractIn a systematic search for risks associated with the consumption of alcohol and tobacco in relation to cancers of the digestive tract, oesophageal cancer was found to be significantly related to both factors. There was a slightly elevated risk for rectal cancer among alcohol consumers as well as a lower risk for gastric cancer. With the exception of oesophageal cancer, none of the other digestive tract cancers were found to be associated with tobacco consumption.
Abnormal sensitivity to UV‐radiation in cultured skin ibroblasts from patients with hereditary cutaneous malignant melanoma and dysplastic nevus syndrome
Authors: Smith Paul J. , Greene Mark H. , Devlin Deborah A. , McKeen Elisabeth A. , Paterson Malcolm C. 
Published: February 2007

AbstractThe dysplastic nevus syndrome (DNS) is a preneoplastic melanocyte abnormality which occurs in families affected by hereditary cutaneous malignant melanoma (HCMM). Although environmental exposures, especially solar UV‐irradiation, have been implicated as risk factors in sporadic melanoma, the role of such exposures in the pathogenesis of HCMM is unknown. We have studied the in vitro radiation responses of six non‐tumor skin fibroblast strains from HCMM/DNS patients representing five families. All six HCMM/DNS strains were found to show some degree of enhanced cell killing sensitivity, compared with normal controls, following 254 nm UV‐irradiation. The abnormal survival responses appeared to relate to specific characteristics of HCMM/DNS cells since the six strains had essentially normal sensitivity to γ‐radiation. The enhanced photosensitivity was not associated with abnormal patterns in either DNA repair synthesis or UV‐induced inhibition and recovery of de novo DNA synthesis. The survival results are consistent with the hypothesis that the genetically determined predisposition to malignant melanoma may directly or indirectly be the consequence of increased susceptibility to UV‐induced cellular damage.
Detection of polyoma‐virus‐induced tumor antigen(S) by macrophage migration inhibition
Authors: Szigeti Robert , Dalianis Tina , Klein George , Ito Yoshiaki , Magnusson Göran 
Published: February 2007

AbstractWe have applied the macrophage migration inhibition assay to study cell‐mediated immune responses to antigens of polyoma‐virus‐transformed cells. Macrophages from polyoma‐virus‐immunized mice, but not from control mice, showed significant migration inhibition when exposed to extracts of polyoma‐virus‐induced mouse and rat transformed cells. Extracts of non‐polyoma‐induced tumors had no such effect.
Role of NK cells in the control of metastatic spread and growth of tumor cells in mice
Authors: Gorelik E. , Wiltrout R. H. , Okumura K. , Habu S. , Herberman R. B. 
Published: February 2007

AbstractThe ability of BALB/c nude and C57BL/6 mice to eliminate tumor cells from the blood stream was severely impaired after a single inoculation of 0.2 ml of anti‐asialo BMI (asGMI) serum, diluted 1:40 to 1:320. The number of i.v.‐inoculated YAC‐I cells surviving in the lungs of BALB/c nude mice pretreated with anti‐asGMI serum was 28 times higher than in the control nude mice. In this respect, nude mice treated with anti‐asGMI behaved similarly to beige mice. The increase in the initial survival of tumor cells in the mice that was induced by pre‐treatment with anti‐asGMI resulted in a substantial increase in the number of artificial lung metastases that developed. In C57BL/6 +/+ mice treated with anti‐asGMI and in C57BL/6 beige mice, i.v. inoculation of B16 melanoma cells induced 10 times more metastatic foci in the lungs than in the control C57BL/6 +/+ mice. In contrast, in nude mice which possess higher levels of NK reactivity, metastatic growth was suppressed 7‐fold in comparison with intact C57BL/6 +/+ mice. In beige mice and in C57BL/6 +/+ mice treated with anti‐asGMI, multiple metastatic foci developed in the liver, whereas in control C57BL/6 +/+ and nude mice, no extrapulmonary metastases were found. These data indicate that B16 melanoma cells are able to grow in the liver, but their growth is ordinarily prevented by NK cells. The antimetastatic defense of C57BL/6 mice treated by anti‐asGMI could be restored by transplantation of 40 × 106 normal spleen cells. This antimetastatic effect of transplanted spleen cells was mediated by asGMI‐bearing cells, since after in vitro pre‐treatment of normal spleen cells with anti‐asGMI and complement, they lost their ability to inhibit the development of artifical metastases in the lungs of C57BL/6 mice. Suppression of NK reactivity by multiple injections of anti‐asGMI (every 4 to 5 days), in C57BL/6 mice inoculated intrafootpad (i.f.p.) with B16 melanoma or 3LL tumor cells, did not influence the growth of local tumors, but dramatically accelerated the development of spontaneous pulmonary metastases. These data demonstrate that NK cells may play an important role in resistance to the dissemination of tumor cells, and therefore contribute to the control of metastasis formation in mice.
Quantitation of proliferative and cytotoxic precursor cells directed against human tumours: Limiting dilution analysis in peripheral blood and at the tumour site
Authors: Vose Brent M. 
Published: February 2007

AbstractBlood and tumour‐infiltrating lymphocytes (TIL) from 16 cancer patients have been examined under limiting dilution conditions to determine the frequency of cells responding in mixed tumour‐lymphocyte cultures (MLTC) to autologous tumour and Interleukin‐2 (IL‐2). Tumour‐derived lymphocytes showed a high spontaneous response to IL‐2 alone 1/1,900 in TIL; 1/6,000 in PBL suggesting the presence of “activated” T cells in situ. Proliferative frequencies were increased in MLTC in both blood (1/3,779) and TIL (1/1,084). Phenotypic analyses showed that total T‐cell contents of the responder populations were comparable but TIL were enriched for the OKT8+ subset with a corresponding reduction in OKT4+. TIL showed increased numbers of OKMI+ and Tac+ lymphocytes. The major cytotoxic precursor expanding under these conditions was reactive against autologous tumour. K562 (NK) were present at a lesser frequency ‐particularly in TIL The data show a concentration and activation of reactive lymphocytes at the tumour site and establish conditions for the clonal expansion of specifically cytotoxck T cells.
Establishment and cytological characteristics of two in vitro T‐cell lines derived from a child with acute lymphatic leukemia and a man with adult T‐cell leukemia in Japan
Authors: Nagasaka Miharu , Maeda Sakan , Mabuchi Osamu , Takubo Takayuki , Nasu Kaori , Wano Yuji , Sugiyama Taketoshi 
Published: February 2007

AbstractTwo permanent T‐cell leukemia lines designated KH‐1 and KH‐2 were established from the peripheral blood of a 9‐year‐old boy with acute lymphoblastic leukemia and a 47‐year‐old man with adult T‐cell leukemia (ATL). No T‐cell growth factor was used. KH‐1 cells grew as single cells and KH‐2 cells formed clusters in suspension culture. E‐rosette formation, the absence of immunoglobulin determinants and Epstein‐Barr‐virus‐associated nuclear antigen, and the presence of T‐cell antigens revealed by monoclonal antibodies were characteristics of these cell lines as in other established T‐cell leukemia lines. Chromosome analysis at the beginning revealed mosaic presence of cells with 46, XY, t (8q+; 15q‐) and 46, XY which was later completely replaced by the latter karyotype in KH‐1, and abnormal karyotype, 47, XY, +3, t (8q‐; 10p+) was maintained throughout the period of in vitro passage in KH‐2. The donor patient of KH‐2 formerly lived in the south‐western part of Japan where ATL is considered endemic and numerous type‐C virus particles were detected electron microscopically, in KH‐2 cell pellets.
Effect of all‐trans retinoic acid on induction, lethality and immunogenicity of murine methylcholanthrene‐induced fibrosarcomas
Authors: Chauvenet P. H. , Paque Ronald E. 
Published: February 2007

AbstractThe effect of 200 μg doses of all‐trans retinoic acid, given over a long duration (daily for 8 weeks, suspended for 3 weeks, then resumed daily for 4 weeks) or short duration (daily for 30 days), on the induction of fibrosarcomas in C57BL/6J mice by MCA was evaluated. A reduced level of carcinogenesis was observed with both lengths of retinoic acid treatment, since respective incidences of MCA fibrosarcomas were 63 and 61% of those in saline‐treated controls. In other studies, the effect of all‐trans retinoic acid on syngeneic growth of two experimental fibrosarcomas (B6 25 and B6 27, induced previously in C57BL/6J mice by MCA) was assessed. Retinoic‐acid‐treated mice were more resistant to higher doses of viable B6 27 (LD50 = 2.85) and especially B6 25 (LD50 = 3.80) than were corresponding saline‐ or corn‐oil‐treated controls (LD50 <2.0). The strength of resistance conferred by retinoic acid treatment thus varied considerably between these tumors, despite their common strain derivation and histopathological origin. Additional studies explored the effect on B6 27 growth of giving all‐trans retinoic acid during either the sensitization or challenge stage of standard syngeneic immunogenicity tests. Mice given all‐trans retinoic acid during sensitization displayed a markedly increased resistance to challenge with the immunospecific B6 27 tumor (LD50 = 5.30), compared to challenged controls that received saline (LD50 = 2.60) or corn‐oil (LD50 = 2.55) during preimmunization. In contrast, when B6 27‐preimmunized mice were treated with all‐trans retinoic acid after challenge with homologous tumor, resistance to B6 27 (assessed by tumor growth rate and LD50 dose) was not increased but remained comparable to that of salineor corn‐oil‐treated controls. While the mechanism(s) by which all‐trans retinoic acid inhibits syngeneic growth of MCA tumors is unknown, our results support an immunostimulatory effect, evidenced by tumor resistance in both non‐immune and specifically preimmunized syngeneic hosts.
Abrogation of the in vitro generation of the cytotoxic T‐cell response to a murine tumor: The role of suppressor cells
Authors: Frost Philip , Prete Pamela , Kerbel Robert 
Published: February 2007

AbstractA reproducible in vitro assay for the effect of suppressor T cells on the generation of an in vitro cytotoxic response to a metastatic murine tumor is described. Suppression in this system is maximal. The model uses splenic T cells from DBA/2 mice bearing the MDAY‐D2 metastatic tumor as suppressors of the in vitro generation of a cell mediated cytotoxic response by syngeneic tumor‐bearer (i.e., primed) peripheral lymph node cells stimulated with mitomycin C‐treated MDAY‐D2 tumor cells. The effect of the cell mediated cytotoxic response is profound, specific and mediated by splenic T cells. The suppressor T cells appear to impair precursor rather than mature cytotoxic cells. A highly immunogenic variant of MDAY‐D2, namely MDWI, does not generate a suppressor response. Suppressor T cells from an MDAY‐D2 tumor‐bearer cannot suppress the in vitro response to MDWI. This model of potent suppressor T‐cell action is highly reproducible and offers an opportunity for the analysis of why some tumors generate an effective cell mediated cytotoxic response which others stimulate dramatic suppressor T‐cell response.
Leukemogenic activity of B‐ecotropic C‐type retroviruses isolated from tumors induced by radiation leukemia virus (RADLV‐RS) in C57BL/6 mice
Authors: Legrand E. , Guillemain B. , Daculsi R. , Laigret F. 
Published: February 2007

AbstractIn addition to the endogenous N‐tropic and xenotropic retroviruses in C57BL/6 mice, B‐tropic viruses which result from recombination between the endogenous parental viruses have frequently been isolated from old or leukemic animals. A thymotropic B‐tropic virus was also isolated after many serial in vivo passages from tumors induced by RadLV initially obtained by Kaplan from radiation‐induced thymic lymphosarcomas. Although this agent was shown to be responsible for the capacity of Kaplan RadLV to induce thymic lymphosarcomas (TLS), the oncogenic role of C57BL/6 B‐tropic viruses has never been demonstrated. Three B‐tropic viruses (T1223/B, T128/B and T98/B) were isolated from Duplan (RadLV‐Rs) extract which, like Kaplan isolate, originates from radiation‐induced TLS. Whereas thymotropism was retained by Kaplan extract, extra‐thymic lymphosarcomas were preferentially induced by RadLV‐Rs. Although the B‐tropic isolates emerged from recombinational events between the two endogenous parental viruses, their recombination pattern and their biological in vitro properties indicated that each of them was unique. The present experiments demonstrate, firstly, that in no case was an early disease ressembling that induced by RadLV‐Rs observed; secondly, that the three viruses induced a high percentage of extra‐thymic lymphomas whose latencies always exceeded 400 days; thirdly, that irrespective of the cloned virus a similar pattern of leukemogenesis was observed; fourthly, that B lymphomas predominated over thymic and extra‐thymic T or null lymphoma and erythromyeloid leukemias. The injected viruses shortened the latencies and increased the frequency of the spontaneous disease observed in old animals, which suggests that in both cases leukemogenesis may result from closely related mechanisms. Our observation that the leukemic process developed after a shorter latent period in animals injected at 400 days of age than in those injected at birth or at 30 days of age strongly suggests that the injected viruses need to undergo a second recombination with the endogenous viruses expressed in old mice before they are capable of inducing lymphomas. This hypothesis is supported by the result of the transplantation assay. It does not exclude the possibility of an impairment of the immune responsiveness contributed to the accelerated leukemogenesis in old animals. Thymic and extra‐thymic T lymphomas occurred preferentially in mice injected at birth, indicating that T‐populations present at this age might be necessary for the newly generated T‐tropic recombinants to emerge, replicate or find their target cells.
Cellular ingestion, toxic effects, and lesions observed in human bronchial epithelial tissue and cells cultured with asbestos and glass fibers
Authors: Haugen Aage , Schafer Paul W. , Lechner John F. , Stoner Gary D. , Trump Benjamin F. , Harris Curtis C. 
Published: February 2007

AbstractAlthough exposure to asbestos has been shown in previous epidemiological studies to synergistically increase the risk of bronchogenic carcinoma for cigarette smokers, the pathobiological mechanism(s) responsible for the cocarcinogenic action of asbestos is not known. Therefore, the effects of asbestos fibers on normal human tracheobronchial epithelium are of interest. Asbestos fibers, i.e., amosite, crocidolite and chrysotile (UICC samples) and glass fibers were initially assayed for their cytotoxcity. Bronchial epithelial cells exposed to either asbestos or glass fibers displayed inhibition of cell growth as a function of fiber concentration. When compared to glass fibers, asbestos fibers caused a statistically significant (p<0.05) decrease in cell population doubling rate. Chrysotile was approximately 10 times more cytotoxic than either amosite or crocidolite and more than 100 times more cytotoxic than the glass fibers. Epithelial cells were 10 to 15 times more sensitive to the cytotoxic effects of asbestos fibers than bronchial fibroblasts from the same donor. Using electron microscopy, asbestos fibers were seen to be ingested by epithelial cells. After exposure for 2 h short fibers (<12μm) were found both in the cytoplasm and within phagosomes. High‐voltage electron microscopy combined with stereo‐microscopy revealed asbestos fibers in the cytoplasmic matrix. A single exposure to amosite asbestos (100–1000 μg/ml) was found to induce focal hyperplasia and epidermoid metaplasia with cellular atypia in human tracheobronchial explants. Surface fine structure observations revealed asbestos fibers protruding from these lesions. Intra‐cytoplasmic and intranuclear fibers of amosite were identified in these focal lesions using X‐ray microanalysis in combination with transmission electron microscopy. With increasing time, fibers were also seen deposited within the submucosa of the explants. The preferential cytotoxicity of asbestos for epithelial cells and the metaplastic response of bronchial epithelium may be important in the cocarcinogenic action of asbestos.
Lymphoblastic lymphoma: Cytogenetic, pathologic, and immunologic studies
Authors: Kaneko Yasuhiko , Variakojis Daina , Kluskens Larry , Rowley Janet D. 
Published: February 2007

AbstractCytogenetic, pathologic, and immunologic studies were done on 10 patients with lymphoblastic lymphoma (LL). The median age was 21 years, and males predominated in a ratio of 9:1. At the time of diagnosis, 6 of the 10 patients had an anterior mediastinal mass, 3 had bone marrow involvement, and 2 had central nervous system involvement. All patients were treated with intensive combination chemotherapy. The median survival of the 8 patients who died (7 of whom were adults) was 10.5 months; all 8 achieved only a partial remission. Two other patients were children; they continue in complete remission. Immunologic marker studies were done on 9 of the patients; 5 had T‐cell LL, and the other 4 had non‐T, non‐B LL. In a study of T‐cell subpopulations with the use of monoclonal antibodies, the malignant T cells of the 2 patients tested appeared to be mature thymocytes. Clonal chromosome abnormalities were seen in involved tissues from 8 patients; the other 2 patients had a normal karyotype. A 9q+ chromosome, a 6q‐chromosome, and a 1q‐chromosome associated with 1q trisomy were each seen in 2 patients. No patient had a 14q+ chromosome, which is the most common abnormality in various lymphoproliferative disorders, including other T‐cell malignant diseases. The variable chromosome pattern in LL could be related to the heterogeneity of the immunologic phenotype of the malignant T cells. More data are needed before it can be established whether there are any correlations between a particular karyotype and the immunologic phenotype of LL cells.
Isolation and characterization of retrovirus‐like elements from normal human fetuses
Authors: Mondal Hrishikes , Hofschneider Peter Hans 
Published: February 2007

AbstractRetrovirus‐like particles have been isolated from normal fetal human plasma and from different embryonic organs collected from late first‐trimester fetuses. The majority of the virus‐like particles banded at a density region of 1.19–1.22 g/ml, although lighter particles having a density of 1.15–1.17 g/ml were observed in some fetal tissues. The particles appeared similar to retroviruses when viewed electron‐microscopically. They contained reverse transcriptase (RT) which accepted oligo (dG)‐poly(C) in Mn+2 over other synthetic template‐primers and transcribed heteropolymeric RNAs primed with oligo (dT). The enzyme was partially (40%) inhibited by the antiserum against RT of feline endogenous virus (RD114) and not at all by the antisera against RT of avian myeloblastosis virus (AMV), spleen necrosis virus (SNV) and gibbon ape leukemia virus (GALV). The simultaneous detection test in the presence of actinomycin D revealed that the particles contained high mol. wt. (70 S and 35 S) RNAs. The single‐stranded DNA complementary to RNA of the human fetal particle hybridized to DNA obtained from different tissues of human adults, showing that the nucleic acids of the virus‐like particles were endogenous. The particles could be isolated only from the embryonic organs during differentiation. This suggests that the retroviral gene expression is correlated with embryonic differentiation. These particles could not be induced and as yet infectivity has not been demonstrated, therefore, they are at present described as retroviral elements, not as retroviruses.