bluuebunny/crossref_metadata_2025_split huggingface dataset:
Spontaneous regression of friend‐virus‐induced erythroleukemia. VII. The genetic control of regression
Authors: Dietz Michael , Fouchey Susan , Furmanski Philip 
Published: February 2007

AbstractThe genetic control of spontaneous regression of erythroleukemia was studied in parental and hybrid mice in which leukemia was induced by the regressing strain of Friend virus (RFV). Because in previous studies parental regressor mouse strains tested (N/PLCR, SIM, NIH Swiss) all had the Fv‐I n/n genotype and the progressor mouse strains (SIM.R, 3ALB/c) had the Fv‐I b/b genotype, we determined the influence of Fv‐I alleles on regression. Genes which influence regression were dominant and had partial penetrance in (progressor X regressor) F1 mice. Regression occurred in hybrid mice which inherited the Fv‐I b/b genes of each of the progressor mouse strains. Regression and Fv‐I alleles also segregated independently in (N/PLCR X BALB/c) F2 mice, in random‐bred Swiss mice heterozygous for the Fv‐I gene, in partially inbred Swiss recombinant progressor and regressor mouse lines, and in hybrid mice carrying the Fv‐I b/b gene of SIM.R mice. Regressor SIM and progressor SIM.R mice, which were bred to be congeneic at the Fv‐I locus, also differ with respect to recovery from viremia, suggesting that their Rfv‐3 genes differ and influence regression. Crosses of SIM and SIM.R mice with the A.BY (Rfv‐3 s/s) mouse strain confirmed that SIM and SIM.R carry Rfv‐3 r/r and Rfv‐3 s/s, respectively. We conclude that Fv‐I b/b is not inhibitory to regression nor is the Fv‐I gene a genetic determinant in the process. The data suggest that regression is influenced by several genes, including those (Rfv‐1, Rfv‐2, Rfv‐3) shown to affect recovery from leukemia in other systems.
Canine transmissible venereal sarcoma: Leukocyte adherence inhibition (LAI) reactivity of various lymphoid tissues of dogs with tumors at different stages of growth
Authors: Harding Matthew W. , Yang Tsu‐Ju (Thomas) 
Published: February 2007

AbstractLeukocyte adherence inhibition (LAI) reactivity of various lymphoid tissues of dogs with canine transmissible venereal sarcoma (CTVS) at different stages of growth was determined by the tube LAI test. Tumors were classified at the time of excision into progressor, steady state, and regressor stages of growth. The LAI reactivity to CTVS antigen extract of spleen, draining and non‐draining lymph‐node cells, and peripheral blood leukocytes of regressors (non‐adherence index ‐ NAI of 172.8±46.8, 148.1±64.7, 138.7±47.3, and 172.2±60.7, respectively) was significantly greater than that of progressors (46.1±20.0, 38.5±21.5, 50.2±30.0, 24,6±37.2, respectively, p <0.001) and normal dogs (47.5±22.8, 54.6±24.6, 26.7±14.0, 50.9±22.4, respectively, p<0.001). In contrast, LAI reactivity of progressor lymphoid tissues to CTVS antigen extract did not differ significantly from that of normal dogs. LAI reactivity of lymphoid tissues from steady state tumor bearers (97.9±39.2, 80.7±47.3, 87.1±40.0, 85.1±53,9, respectively) was intermediate between and significantly different from LAI reactivities of regressor (p <0.05) and progressor (p <0.01) lymphoid tissues. Significant LAI reactivity observed in regressors suggests the presence of a functional effector cell mechanism associated with spontaneous regression of CTVS. The three distinct patterns of LAI reactivity observed in tumor‐bearing dogs appear to correlate with the clinical course of tumor growth.
In vivo formation of benzo (a) pyrene diol epoxide‐deoxyadenosine adducts in the skin of mice susceptible to benzo (a) pyrene‐induced carcinogenesis
Authors: Ashurst Stephen W. , Cohen Gerald M. 
Published: February 2007

AbstractThe hydrocarbon‐deoxyribonucleoside adducts formed in mouse skin DNA have been determined following topical application of an initiating dose of benzo(a)pyrene to Swiss mice, a strain shown to be susceptible to benzo(a)pyrene‐induced skin carcinogenesis. Several DNA‐bound products were formed, of which the major one (60 % of total adducts), in agreement with other workers' findings, was derived from reaction of (±) 7β, 8α‐dihydroxy‐9α, 10α‐epoxy‐7,8,9,10‐tetrahy‐drobenzo(a)pyrene (BPDE) with the exocyclic amino group of deoxyguanosine. A further product (9–10% of total adducts), previously observed only after microsomal activation of benzo(a)pyrene, was observed and co‐chromatographed with a further metabolite of 9‐hydroxybenzo(a)pyrene bound to an uncharacterized base in the DNA. Two other products (2–3 % of total adducts) were also found in the in vivo studies which co‐chromatographed with BPDE‐deoxyadenosine adducts and arose from cis and trans addition of the exocyclic amino group of deoxyadenosine to the 7R form, but not the 7S form, of BPDE. In contrast to this, the major in vitrodeoxyadenosine‐bound products, formed following reaction of BPDE with calf‐thymus DNA, were derived from the 7S form of BPDE, suggesting either stereo‐selective formation or reaction of the 7R form of BPDE in mouse skin in vivo. Similar amounts of BPDE‐deoxy‐guanosine and BPDE‐deoxyadenosine adducts, as well as those derived from further metabolism of 9‐hydroxy‐benzo(a)pyrene, were formed in three strains of mice reported to have widely differing susceptibilities to polycyclic hydrocarbon‐induced skin carcinogenesis. The relevance of these different hydrocarbon‐DNA adducts to carcinogenesis requires further investigation.
Metastasis and the reticuloendothelial system. II. Effect of triamcinolone acetonide on organ retention of malignant cells in endotoxin‐treated mice
Authors: Glaves Dorothy , Weiss Leonard 
Published: February 2007

AbstractThe lung retention patterns of B16 melanoma cells were determined after intravenous injection of [125I]dUrd‐labelled tumor cells into B16 melanoma‐bearing mice. Experiments were performed to assess the effects of a synthetic glucocorticoid, triamcinolone acetonide, on the retention of B16 melanoma cells arrested in the lungs of mice with endotoxin‐induced reticuloendothelial system hyperfunction. Lung clearance of malignant cells was greatly accelerated in mice treated with endotoxin alone but was markedly inhibited in mice with only triamcinolone acetonide. In mice treated with both endotoxin and subsequently triamcinolone acetonide after tumor‐cell arrest processes had occurred, the endotoxin‐induced increase in clearance was nullified. These results are discussed in terms of the mutually antagonistic activity of both pharmacologic agents upon the reticuloendothelial system and the role of the latter in regulating organ retention of disseminated malignant cells.
The effect of high doses of poly (i>poly (c) induced mouse l cell interferon on rauscher leukemia virus induced erythroleukemia in balb/c mice
Authors: Herman R. A. C. P. , Prins M. E. F. , Bosveld I. J. , Trapman J. 
Published: February 2007

AbstractThe effect of high doses of poly (l)‐poly (C)‐induced mouse L‐cell interfered on the development of Rauscher murine leukemia virus (R‐MuLV)‐induced erythro‐leukemia in BALB/c mice was determined. Female mice, 4 to 5 weeks old, were infected with R‐MuLV and treated with interferon every 24 h starting 6 h after virus inoculation. Under these conditions injection of 3–5 × 104 units of interferon caused a partial inhibition of the leukemic process. Daily application of 3 × 105 units completely or almost completely inhibited the eryth‐roleukemia. After 14 days of treatment with these high doses of interferon, spleen weights of interferon‐treated infected mice were comparable to those of uninfected animals which received only interferon. Also, no Rauscher cells in spleens and livers of R‐MuLV‐infected interferon‐treated animals could be demonstrated and the spleen structure was well preserved in these mice. In interferon‐treated infected animals no virus could be detected in the serum as judged from the absence of reverse transcriptase activity in the serum. Moreover, no virus‐infected cells could be demonstrated in spleen or liver as deduced from negative immunofluorescence data using anti‐p30 and anti‐gp70 sera. No virions budding from spleen cell membranes were seen by electron microscopic studies. However, when interferon treatment was stopped the leukemic process was reactivated and all the mice died. In control experiments interferon caused an inhibition of red blood cell formation and a 50 to 100% enlargement of the spleen. Pharmacokinetic data showed that, after intraperitoneal inoculation, maximum amounts of interferon were present in the peripheral blood after 1–2 h. After 12–24 h almost all interferon activity had disappeared from the blood.
Isolation of two novel envelope recombinant leukemogenic viruses from moloney leukemia virus stocks
Authors: Gisselbrecht Sylvie , Fischinger Peter J. , Elder John H. , Levy Jean Paul 
Published: February 2007

AbstractTwo dual tropic recombinant murine leukemia viruses were isolated from Moloney leukemia virus passed in France for 17 years. These new isolates share most of the biological properties of previously described HIX virus isolated from a line of Moloney virus maintained in the United States. However, they differ from the HIX virus and from other recombinant viruses by the absence of a xenotropic oligopeptide thought to have been characteristic of all xenotropic and recombinant virus envelope glycoprotein.
Solubilization and partial characterization of a tumor‐rejection antigen from an ultraviolet light‐induced murine tumor
Authors: Ransom Janet H. , Schengrund Cara‐Lynne , Bartlett Gerald L. 
Published: February 2007

AbstractTumor rejection antigen (TRA) of an ultraviolet‐light‐induced murine skin tumor was solubilized, fractionated and partially characterized. Subcellular fractions were prepared by differential centrifugation of tumor cells that had been ruptured via nitrogen cavitation. Only the 110,000‐g membrane fraction induced significant tumor protection, as determined by in vivo immunization and challenge assays. Extraction of the membrane fraction with 3 M KCI resulted in solubilization of material that could induce in vivo tumor‐rejection immunity. Both the membrane fraction and soluble extract had a limited effective dose range. The KCI extract was separated on a Sepharose, CL‐6B column in the presence of 6 M guanidine‐HCI. Only one of five fraction pools (molecular weight range of 76,000–127,000 daltons) was immunogenic. It contained at least eight protein bands by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS‐PAGE), but no lipid components. This immunogenic Sepharose fraction was chromatographed on a Sephadex G‐150 column. Each of the four Sephadex fraction pools was immunogenic. One protein component was common to each of those fractions. It migrated as a single 76,000‐dalton band on SDS‐PAGE and contained [14C]‐leucine and [3H]‐glucosamine that had been incorporated during cell growth. These results suggest that the TRA of this tumor is a 76,000‐dalton glycoprotein.
Detection of a histone‐2a related polypeptide in differentiated human myeloid cells (hl‐60) and its distribution in human acute leukemia
Authors: Pantazis P. , Sarin P. S. , Gallo R. C. 
Published: February 2007

AbstractA human myeloid cell line, HL‐60, has been shown to terminally differentiate to mature granulocytes in the presence of dimethylsulfoxide (DMSO) and other compounds. A histone polypeptide (HP) with an apparent molecular weight of 12,500 has been identified among the acid‐extractable chromosomal proteins of DMSO‐treated HL‐60 cells. The detection of HP in total chromatin, total cell proteins or acid extracts of intact HL‐60 cells treated with DMSO indicates that HP is present in intact cells and is not generated during the isolation procedures used for preparation of chromatin or histones. No radiolabelled HP was detected when chromatin was isolated from a mixture of radiolabelled mouse cells and HL‐60 cells treated with DMSO. The relative increase in the amount of HP in DMSO‐treated HL‐60 cells correlates with a concomitant decrease of histone H2A. Fingerprint analysis of tryptic digests shows HP to be related to histone H2A. Generation of HP from endogenous and exogenous H2A is probably due to a proteolytic enzyme associated with the chromatin of the differentiated HL‐60 cells. HP was not observed in chromatin from a number of human or mouse hematopoietic tissues and cell lines but low levels of HP were detected in human lymphocytes and granulocytes prepared from peripheral blood of normal donors. HP was also detected in leukocytes from patients with acute leukemia. Our results suggest that: (1) HP is a proteolytic product of histone H2A and not a product of an independent gene; (2) the observed level of HP in HL‐60 cells is related to the stage of differentiation; and (3) HP is a potential biological marker for human acute leukemia.
The effect of hysterectomies and screening on mortality from cancer of the uterus in canada
Authors: Miller A. B. , Visentin T. , Howe G. R. 
Published: February 2007

AbstractThe trends in mortality from cancer of the uterine cervix, cancer of the endometrium and all uterus in Canada and the ten Canadian Provinces from 1951‐53 to 1974‐76 at ages 30‐64 have been re‐evaluated in relation to screening for cancer of the cervix in 1966 and 1971 and hysterectomies for non‐malignant conditions from 1969 to 1976. By means of a series of mathematical models, the effect of different prior extrapolations of the numbers of hysterectomies performed by age and province has enabled the potential impact of hysterectomies on the trends of mortality from uterine cancer to be evaluated by relating deaths to ‚uteri at risk’︁ rather than ‚women at risk’︁ irrespective of the presence of an intact uterus. It has been found that the numbers of hysterectomies performed have little impact on the fall in mortality certified to cancer of the cervix or to all uterine cancer, but in the decade 1964‐66 to 1974‐66 they convert an apparent fall in mortality from cancer of the endometrium to stability. Re‐evaluation of the fall in mortality from 1960‐62 to 1970‐72 in relation to the intensity of screening shows little impact of the hysterectomies performed on the significant correlation reported previously. However, after extension of the analysis to 1974‐76 the correlation disappears. This finding may indicate a more limited potential for the application of screening, as practised in Canada, to reduce mortality from cancer of the cervix, than has been anticipated previously.
Cytomegalovirus: Detection in human colonic and circulating mononuclear cells in association with gastrointestinal disease
Authors: Roche J. K. , Cheung K ‐S , Huang I. Boldogh , Lang D. J. 
Published: February 2007

AbstractThe specificity and strength of the reported association between cytomegalovirus (CMV) and colonic adenocarcinoma were tested by analysis of a consecutive series of surgically resected colons for: CMV‐DNA by a DNA‐DNA reassociation kinetics (hybridization) procedure; latent virus by co‐cultivation of fresh tissue with indicator fibroblasts; and CMV viral antigens by immunofluorescence. Ten of 13 cancer patients whose colonic tissue was able to be examined by all techniques showed some evidence of active or prior CMV infection. Four cancer specimens were CMV‐DNA (hybridization)‐positive; an additional specimen from a cancerous colon was culture‐positive. In six instances, CMV DNA was detected in mucosal cells adjacent to colon adenocarcinoma. In tissue from one of three patients with ulcerative colitis and two of seven patients with other non‐neoplastic colonic disease, CMV DNA was also detected. No fresh colonic tissues were demonstrated to have CMV surface or nuclear antigens when examined by immunofluorescence. Culture of peripheral lymphocytes was positive for CMV in three of 14 cancer patients. A CMV‐specific defect in humoral immunity could not be documented in that most cancer patients, as well as cancer‐free patients, exhibited circulating specific antibody to CMV and had a normal capacity for CMV‐specific antibody‐dependent cellular cytotoxicity. We conclude that CMV, probably in a latent form, is readily detectable in colonic cells of man, including those derived from malignant, pre‐malignant and non‐malignant tissues. Neither preferential replication in damaged tissue nor carriage of CMV by peripheral lymphocytes homing to gut appear to explain the presence of CMV in colon cells.
Class‐specific antibodies (Igg and Iga) to membrane antigens of herpes simplex type‐2 infected cells in patients with cervical dysplasia and neoplasia
Authors: Mendis Lalitha N. , Best Jennifer M. , Banatvala J. E. 
Published: February 2007

AbstractIndirect immunofluorescence (IF) techniques were used to measure IgG and IgA antibodies to membrane antigens (anti‐MA) and IgA antibodies to virus capsid antigens (anti‐VCA) of herpes simplex type 2 (HSV‐2)‐infected cells in sera from patients with cervical dysplasia and neoplasia, controls who had been matched for ethnic origin, age and social class, patients with other malignancies and patients with genital herpes. IgA anti‐MA were detected significantly more frequently and at higher titres in patients with cervical dysplasia and neoplasia than among matched controls. A high proportion of patients whose cervical cancer had previously been treated by radiotherapy, patients with other squamous carcinomas and patients with genital herpes also had IgA anti‐MA and at higher titres than matched controls and patients with non‐squamous cancers. In contrast, IgG anti‐MA and IgA anti‐VCA did not distinguish patients from controls. The IgA anti‐MA response was more type‐specific than the IgG anti‐MA response. IgA anti‐MA appeared to persist in sera from patients with genital herpes for at least 17 months after clinical attack, while IgA anti‐VCA were usually detected for only 2‐3 months. The persistence of IgA anti‐MA may suggest a persisting antigenic stimulus among patients with genital herpes as well as patients with cervical dysplasia and neoplasia. HSV‐2‐specific antibodies measured by ELISA were also detected in a significantly higher proportion of patients with cervical neoplasia than in matched controls, although 32–48% of patients did not possess these antibodies. Furthermore, there was no consistent difference in the prevalence of HSV‐2‐specific antibodies when cohorts of patients with cervical neoplasia and controls born at the same time were compared. The possibility is discussed that IgA anti‐MA, which were detected in a high proportion of patients with other squamous carcinomas as well as in patients with squamous carcinoma of the cervix, are reacting with cross‐reacting antigens found both in human squamous carcinoma cells and in HSV‐infected cells.
Detection and characterization of viral genomes and search for tumoral antigens in two hamster cell lines derived from tumors induced by bovine papillomavirus type 1
Authors: Breitburd FrançOise , Favre Michel , Zoorob Rima , Fortin Dominique , Orth Gérard 
Published: February 2007

AbstractTwo cell lines, designated HT2 and HT3, were isolated from two transplanted hamster sarcomas induced by bovine papillomavirus type I (BPV‐I) and studied after 50 to 60 subcultures. Cells are tumorigenic for hamsters and showed no detectable viral capsid protein synthesis by immunofluorescence technique. Cells contained multiple copies of the entire BPV‐I genome, 100 to 500 and 10 to 100 per diploid amount of HT2 and HT3 cell DNA, respectively, as determined by blot hybridization experiments. In unrestricted cell DNA, viral genomes migrated as free single viral DNA molecules and slow migrating species. HT2 cell DNA restricted by single cut enzymes for BPV‐I DNA (Eco RI and Bam HI endonucleases) yielded only one viral genome unit length DNA molecule, indicating that the slow migrating species could correspond to free oligomeric or catenated molecules. Patterns of HT3 cell DNA restricted by Eco RI or Bam HI enzymes showed the presence of additional bands, suggesting that the slow migrating species could correspond to viral DNA sequences integrated in cell DNA. Up to five polypeptides (190 K, 125 K, 59 K, 33 K, 30 K) were reproducibly precipitated from [35S]‐methionine‐ or 32P ‐ labelled HT2 or HT3 cell extracts by sera from hamsters bearing HT2 or HT3 cell‐induced tumors and by sera from pikas bearing BPV‐I induced fibrosarcomas. Polypeptides with similar molecular weights were detected by HT2 sera in a SV40 tumor hamster cell line (TSV5 CI.2) and in a rat cell line transformed in vitro by SV40 DNA form I (VII FI CI. I). The 190 K polypeptide was also detected in a normal hamster embryo cell strain (EH). Conversely, a pool of SV40 tumor hamster sera precipitated the 59 K and the 33 K polypeptides from HT2 cells. The polypeptides thus identified are most probably transformation‐related cell proteins. Whether or not their synthesis is related to the expression of some BPV‐I transforming genes remains to be established.
Control of a human tumour (ewing sarcoma) in mice by a single lethal dose of dimethyl‐myleran and bone marrow
Authors: Floersheim G. L. , Torhorst J. 
Published: February 2007

AbstractA Ewing sarcoma grown in immunosuppressed mice was eradicated with a single lethal dose of dimethylmy‐leran (DMM) followed by autologous or syngeneic bone marrow. Sarcomas treated 2 weeks after grafting in a phase of rapid proliferation disappeared and large sarcomas treated after 6 or 10 weeks were reduced to necrotic tissue. A human osteosarcoma also regressed distinctly after this therapy while a human colon carcinoma responded poorly. Sub‐lethal DMM treatment induced complete remissions in only 62% of the mice. Tumours which display sensitivity in this model may be treated clinically with lethal doses of DMM and autologous marrow transplantions.
Adoptive transfer of immunity induced by semi‐allogeneic hybrid cells, against a murine fibrosarcoma
Authors: Payelle Béatrice , Poupon Marie‐France , Lespinats Geneviè 
Published: February 2007

AbstractSemi‐allogeneic somatic hybrid cells derived from the fusion of a C57BL/6 fibrosarcoma (MCB6–1) and A9 cells (C3H origin) were used to immunize C57BL/6 mice against the parental tumor cells. These hybrid cells expressed H‐2 histocompatibility antigens of both parental cells (H‐2b and H‐2k), and failed to produce tumors in normal C57BL/6 mice. A single i.p. injection of hybrid cells induced anti‐tumor immunity which could be transferred to normal C57BL/6 recipient mice by immune spleen or peritoneal cells; the efficient cells were T cells, as this activity was completely abrogated by treatment with anti‐Thy‐1–2 antiserum and complement. Among immune splenic T cells, only the light‐density T cells, obtained after fractionation on Percoll gradient, were effective in the transfer of immunity. Immunity induced by the hybrid cells was specific for MCB6‐1 parental tumor cells. This immunity could be transferred during two brief periods, 7 to 12 days, and 40 to 50 days, after hybrid cell injection; there appeared to be an intermediate period, 12 to 40 days after immunization, during which no immunity could be transferred. These results suggest a suppressive mechanism implicated during hybrid cell immunization and interacting with the anti‐tumor immune response.