bluuebunny/crossref_metadata_2025_split huggingface dataset:
EL‐4 metastases in spleen and bone marrow suppress the nk activity generated in these organs
Authors: Sarzotti Marcella , Baron Samuel , Klimpel Gary R. 
Published: February 2007

AbstractThe relationship between metastatic cells in the spleen and bone marrow of tumor‐bearing mice and the NK activity generated in vitro by cells obtained from these organs was investigated. EL‐4 lymphoma and B16 melanoma cells injected intraperitoneally into syngeneic mice (106 cells/animal) killed the recipients in 16 days. These tumors had a different metastatic profile: EL‐4 metastasized to the spleen and bone marrow while B16 did not. The number of metastatic cells was evaluated by plating spleen or bone‐marrow cells of tumorbearing mice in agarose cultures; in parallel, the ability of spleen and bone‐marrow cells to generate NK activity in vitro was assessed. The presence of 105 EL‐4 cells/106 spleen or bone‐marrow cells correlated with a total lack of NK activity in these organs; in contrast, no decrease in NK activity was evident in the spleen or bone marrow of B16‐bearing mice. The removal of metastatic EL‐4 cells (by antibody and complement) from the spleen or bone marrow did not rescue the NK activity. The lack of NK activity in spleen and bone marrow colonized by metastatic cells was not due to induction of a suppressor cell in the host. Metastatic EL‐4 cells appeared to have a direct and irreversible suppressive effect on the generation of NK activity by spleen or bone marrow. A possible cause‐effect relationship between metastatic colonization of lymphoid organs and suppression of local NK activity is considered.
Patterns of nasopharyngeal cancer mortality in the united states
Authors: Levine Paul H. , McKay Frank W. , Connelly Roger R. 
Published: February 2007

AbstractWe examined the geographic pattern of nasopharyngeal cancer (NP cancer) mortality in the United States using economic sub‐regions (ESRs) as the basis for analysis. The distribution of 15,145 deaths from NP cancer over the years 1950‐1979 revealed clustering in the 119 ESRs that was not detected in analyses of distribution by the 48 states, 506 state economic areas or 3,056 counties or combinations of counties of the coterminous United States. NP cancer mortality among white males was concentrated on the south‐east Atlantic and Gulf coasts. This newly described pattern is not due to any recent changes in mortality rates and should provide leads to further epidemiologic study.
Pretreatment prognostic factors and scoring system in 407 small‐cell lung cancer patients
Authors: Cerny T. , Anderson H. , Bramwell V. , Thatcher N. , Blair V. 
Published: February 2007

AbstractIn 407 patients with small‐cell lung cancer (SCLC), 61 pretreatment variables were evaluated in a Cox multiple regression analysis to assess their prognostic value. All patients received short‐term intensive regimens (cyclophosphamide, etoposide and methotrexate or ifosfamide and etoposide, both followed by thoracic irradiation if complete response was noted). Lactate dehydrogenase (p = 0.0001), tumour stage (p = 0.0001), serum sodium (p = 0.0009), pretreatment Karnofsky performance score (p = 0.0121), alkaline phosphatase (p = 0.0186) and serum bicarbonate (p = 0.0321) were the important prognostic factors. Once these variables were taken into account no other variable provided additional prognostic information. A simple scoring system (“Manchester Score”) using these variables was established and shows little loss of information compared to the Cox analysis. The score distinguishes 3 prognostic groups, the best of which contains all long‐term survivors, whereas the bad prognostic group contains no patient surviving longer than one year. The scoring system may help to design new treatment strategies and may also facilitate the comparison of different studies.
Progenitor and pre‐B lymphocytes transformed by epstein‐barr virus
Authors: Ernberg Ingemar , Falk Kerstin , Hansson Mona 
Published: February 2007

AbstractBy rosetting with SRBC coupled to rabbit‐anti‐human IgM, the surface IgM‐negative cells of human fetal bone marrow were enriched, and subsequently infected and transformed by Epstein‐Barr virus (EBV). Single clones of the transformed cells were obtained. Ninety percent of the resulting cell clones were surface‐immunoglobulin‐negative, and of 8 clones which were further studied, 5 lacked intracellular, cytoplasmic Ig as measured by immunofluorescence. Control cell clones derived from the same material without pre‐selection expressed surface Ig and also secreted Ig. Utilization of a panel of B‐cell‐specific monoclonal antibodies (MAbs) showed no difference between the cell clones expressing surface Ig and those that did not. The progenitor B‐cell lines did not show a phenotype resembling that of cell lines derived from B‐cell malignancies, such as high agarose clonability. In spite of their immature Ig‐phenotype, these clones showed rearrangement of at least one heavy chain Ig‐allele. Efforts to induce differentiation in these clones were unsuccessful. These clones may represent progenitor B cells, or B cells with faulty heavy‐chain rearrangement. EBV can apparently be used as a tool to derive cell lines representing different levels of B‐cell differentiation, and can also transform immature B cells, which may be useful in the analysis of B‐cell differentiation.
HTLV‐III infection of EBV‐genome‐positive B‐lymphoid cells with or without detectable T4 antigens
Authors: Salahuddin S. Z. , Hunter E. A. , Sturzenegger S. , Markham P. D. , Gallo R. C. , Ablashi D. V. , Gonda M. A. 
Published: February 2007

AbstractThe infection of a number of new and established B‐cell lines by human T‐cell lymphotropic virus III (HTLV‐III) was investigated. The B lymphocytes differed in their expression of T4 antigens detected by specific monoclonal antibodies (MAbs) and the presence of Epstein Barr virus (EBV)‐DNA or antigens. The presence of the EBV genome was the only requirement for infection of B‐lymphocytes by HTLV‐III, although its presence did not ensure infection. Two EBV genome and T4 antigen‐positive B‐cell lines, lacking EBV early antigens (EA) and viral capsid antigens (VCA), could be productively infected with no induction of known EBV antigens. Two other EBV genome‐positive cell lines, lacking T4, EA, and VCA could also be infected. Another genome‐positive cell line (P3HR‐I) that was EBV‐EA, VCA‐positive and produced non‐transforming EBV, could also be infected by HTLV‐III. However, 3 EBV genome‐ and T4 antigen‐negative B‐cell lines could only be infected with HTLV‐III after successful conversion to an EBV‐genome‐positive state by pre‐infection with EBV. Five other EBV‐genome‐positive B‐cell lines lacking T4 antigens were not infectible with HTLV‐III even after superinfection with EBV. Incomplete inhibition of the HTLV‐III infection of a T4‐positive (LDV‐7) and a T4‐negative (Craig) was obtained by preadsorption with specific MAb to T4 (OKT4A and Leu 3A). From these observations, it is not clear whether the presence of T4 antigen on the cell surface is needed for the infection of B lymphoblastoid cells; however, successful infection does depend upon the presence of the EBV genome. The mechanism of interaction of HTLV‐III and EBV‐infected B‐cell lines permitting this infection is not fully understood. Although the clinical implications of these observations remain to be determined, it is possible that infection of EBV‐positive B‐cells may contribute to aberrant humoral responses and/or increased frequency of B‐cell malignancies observed in HTLV‐III‐infected individuals.
Establishment and characterisation of three new human ovarian carcinoma cell lines and initial evaluation of their potential in experimental chemotherapy studies
Authors: Hill Bridget T. , Whelan Richard D. H. , Gibby Elizabeth M. , Hosking Louise K. , Thomas Rupniak H. , Sheer Denise , Shellard Sharon A. 
Published: February 2007

AbstractThree new human cell lines have been established from biopsy specimens of ovarian cystadenocarcinomas: line JA‐I was derived from a primary “solid” tumour from an untreated patient, whilst the other lines were derived from ascites from patients previously treated with chlorambucil plus either cyclophosphamide (TR175) or cisplatin (TR170). Their in vitro characteristics are compared with those of the established SK‐OV‐3 line of similar origin. Each line has a distinct morphology and expresses a unique isozyme profile and karyotype. All 4 lines have comparable population doubling times of 28–38 hr. Only 3 lines reproducibly form colonies in soft agar, but the JA‐I line, which failed to clone, readily produces xenografts in nude mice. Drug sensitivity testing, using clonogenic or growth‐inhibition assays, shows that these lines express a wide range of sensitivities to cisplatin (> 20‐fold), with the TR175 cells proving particularly sensitive, but a narrower range of sensitivity (≤ 10‐fold) to adriamycin. Following 6 24‐hr pulsed exposures in vitro to drug concentrations between IC50 and IC90 values, significant resistance develops to adriamycin in each line tested. In contrast, with cisplatin treatment, all lines retain their original sensitivities, except for TR170 cells exposed to the highest concentration, which express cisplatin resistance.
The immune basis of dosage‐induced reversal of the rank‐order of strain susceptibility to MCA
Authors: Prehn Liisa M. , Lawler Ellen M. 
Published: February 2007

AbstractEven AHH‐inducible mouse strains vary in their susceptibilities to MCA sarcomagenesis. Previous work showed that the rank‐order of strain susceptibility depended upon the dosage of MCA; the strain most susceptible to a high dose became the least susceptible to a low one and vice versa. We now confirm our previous findings and test the hypothesis that the reversal, with dosage, of the rank‐order of relative strain‐susceptibility has an immunological basis. This was tested in two ways: by examining the effect of immunosuppression on strain‐susceptibility to sarcomagenesis and by transplanting parental bone marrow into irradiated F1 hybrid to see if the relative MCA‐susceptibility characteristics of the parental donors could be transferred. The results of both studies suggest that the rank‐order‐reversal phenomenon is caused, at least in part, by differences in the immunological reactivities of the strains. Inasmuch as immunosuppression inhibited the response of the C3 mice to a high dose of carcinogen, but facilitated carcinogenesis among the B6, the level of innate immune capacity most conducive to high‐dose carcinogenesis is apparently intermediate between the levels of these two strains.
Effects of DL‐α‐difluoromethylornithine on the growth and metastasis of b16 melanoma in vivo
Authors: Kubota Shunichiro , Ohsawa Nakaaki , Takaku Fumimaro 
Published: February 2007

AbstractThe effects of DL‐α‐difluoromethylornithine (DFMO), a specific irreversible inhibitor of ornithine decarboxylase, on the growth of experimental mouse B16‐F10 melanoma cells were investigated. DFMO (3%) in drinking water was administered to B16‐F10 melanoma‐bearing mice. At 24 days, B16‐F10 melanomas in DFMO‐fed mice weighed 75% less than those in control mice (p < 0.001). DFMO reduced putrescine and spermidine levels in B16‐F10 melanoma by 98% and 84%, respectively, and prolonged the mean survival time from 25.9 ± 1.2 to 35.7 ± 2.2 days (p < 0.001). The effects of DFMO on experimental metastasis were also investigated. DFMO treatment resulted in a significant decrease in pulmonary metastasis induced by i.v. injection of B16‐F10 melanoma cells.
Anti‐tumor effects of tumor necrosis factor in combination with chemotherapeutic agents
Authors: Regenass Urs , Müller Marcel , Curschellas Enrico , Matter Alex 
Published: February 2007

AbstractThe anti‐tumor activity of partially purified tumor necrosis factor (TNF) was analysed in combination with chemotherapeutic drugs against intradermally transplanted Meth A sarcoma. Tumors were allowed to grow until they reached an average diameter of about 8 mm. TNF was given once i.v. (16,000 units as determined on L‐M cells) and the chemotherapeutic agents adriamycin (1‐10 mg/kg), 5‐FU (3‐100 mg/kg), cyclophosphamide (50–200 mg/kg) were applied once i.p. 4 hr after TNF injection. The strongest anti‐tumor effects in normal BALB/c mice were observed when TNF was combined with the following doses of chemotherapeutic agents: cyclophosphamide 100 mg/kg, adriamycin 5 mg/kg, 5‐FU 30‐100 mg/kg. The most effective combinations induced complete regressions. When TNF was combined with varying doses of adriamycin and cyclophosphamide, bell‐shaped dose‐response curves were obtained. Experiments were repeated in Meth A sarcoma‐bearing BALB/c nu/nu mice. In this case TNF combinations with cyclophosphamide and 5‐FU did not induce tumor regressions. The highest dose of the chemotherapeutic agent was the most effective in drug combinations. Histological analysis revealed a potentiation of the TNF‐induced necrosis by cyclophosphamide. Increased hyperemia and extravasation of erythrocytes could be found in tumors of animals treated with the drug combination.
Tobacco and occupation as risk factors in bladder cancer: A case‐control study in southern belgium
Authors: Schifflers Eugéne , Jamart Jacques , Renard Véronique 
Published: February 2007

AbstractA pilot case‐control study on bladder cancer, with population‐based controls matched for each of 74 cases, has been conducted in two industrial areas of Southern Belgium in order to analyze the influence of tobacco use and occupation. Observed bladder cancer risk for smokers is more than 5 times higher than that for non‐smokers, and the risk for people having an a priori hazardous occupation is about 3.5 times higher than that of other subjects. A dose‐response relationship was found for tobacco exposure and duration of employment. It seems that the risk is increased in a log‐linear way by these variables. Population attributable risks show that in 20 cases of bladder cancer, 17 could be explained by the two factors combined. This study also reveals an increased risk for metal workers, truck and engine drivers, coal‐miners, and rubber and coal‐tar workers. The risk for metal workers is specially high in the case of turners, metal fitters, blacksmiths, stokers and workers exposed to hot metal.
Characterization of human ovarian carcinoma‐associated antigens defined by novel monoclonal antibodies with tumor‐restricted specificity
Authors: Miotti S. , Canevari S. , Ménard S. , Mezzanzanica D. , Porro G. , Pupa S. M. , Regazzoni M. , Tagliabue E. , Colnaghi M. I. 
Published: February 2007

AbstractThree new monoclonal antibodies (MAbs) (MOv16, MOv18 and MOv19) were raised against human ovarian carcinoma. To obtain more specific reagents than those produced so far, we adopted the following experimental approach which consisted of: (1) the selection of a poorly differentiated ovarian carcinoma which was unreactive with all the MAb previously selected in our laboratory; and (2) the application of a particular immunization protocol. The reactivity of the selected MAbs was studied by solid‐phase RIA on live and fixed cells from tumor cell lines and by immunofluorescence on frozen sections from surgical specimens. The MAb MOv16 reacted with 60% of ovarian carcinomas as well as with a high percentage of other carcinomas and with some normal tissues. In contrast, MOv18 and MOv19 appeared to have restricted specificities for ovarian carcinomas and cystadenomas. Reactivity on other carcinomas was only observed in a few cases and no reactivity was found on non‐epithelial tumors or normal tissues. Immunoprecipitation experiments indicated that MOv16 recognizes a 48‐50‐kDA protein, whereas MOv18 and MOv19 both identify a 38‐40 kDA glycoprotein band. Cross‐competition experiments, together with a double‐determinant immunoradiometric assay which uses MOv18 as catcher and MOv19 as tracer, suggested that they recognize different epitopes carried by the same molecule. The affinity constants of MOv18 and MOv19 were estimated to be in the range of 108 ‐ 109 M‐1. Taken together, the properties of these antibodies, their restricted ovarian tumor specificities and relative high affinity constants, suggest that they could represent promising tools for in vivo applications.
Tissue‐specific markers in flow cytometry of urological cancers. III. Comparing chromosomal and flow cytometric dna analysis of bladder tumors
Authors: Smeets A. W. G. B. , Laarakkers L. , Pauwels R. P. E. , Beck J. L. M. , Vooijs G. P. , Ramaekers F. C. S. , Geraedts J. P. M. , Debruyne F. M. J. , Feitz W. F. J. 
Published: February 2007

AbstractThirty‐seven transitional‐cell carcinomas (TCC) of the urinary bladder were analyzed by DNA flow cytometry (FCM). After labelling of the cell suspensions with antibodies to cytokeratin, the cytokeratin‐positive cells and the non‐epithelial cytokeratin‐negative cells could be analyzed separately. After estimation of S‐ and G2M phase, 3/17 cases (18%) with a normal DNA index showed elevated proliferative levels, among cytokeratin‐labelled suspensions only. Of these 17 cases, 14 showed chromosomal abnormalities. The remaining 20 cases were abnormal, irrespective of the technique used. Although immuno‐labelling of tumor cells for cytokeratin in FCM increases the sensitivity of this method in detecting aneuploid tumors or tumors with high proliferation fractions, the discriminating power of chromosomal analysis of TCC is greater than FCM.
Mass screening for cervical cancer in øtfold county of norway 1959‐77
Authors: Magnus Knut , Langmark Frøydis , Andersen Aage 
Published: February 2007

AbstractIn 1959, the Norwegian Cancer Society started a research project in Østfold county to assess the effect of a mass screening program for cervical cancer. The program comprised 5 screening rounds during the period 1959‐77. At each screening a clinical gynecological examination was performed in addition to the cytological test. A total of 45,960 women aged 25‐59 years at the first screening were invited to participate. The follow‐up, which was based on the data base of the Cancer Registry of Norway, lasted until December 31, 1982. For the follow‐up period as a whole, the observed incidence and mortality were reduced to 78% and 83% of the expected values, respectively. Through the initial phase of the program there was a cumulation of patients with early‐stage disease, while the incidence of advanced disease and mortality were reduced. In the later part of the follow‐up period, a decrease in incidence of early and advanced disease as well as in mortality was observed. Women not participating in the screening program had a significantly higher risk of cervical carcinoma than the reference population, and a less favorable stage distribution as well. Among participants in the screening program, the reduction of risk was dependent upon the number of previous negative smears. Women with 5 previous negative smears had a risk of disease which was only 18% of that expected. Problems concerning choice of reference population, migration, attendance rates, sensitivity and specificity of the cytological tests and intervals between screenings are discussed. Also, the probable conversion rates of pre‐cancerous lesions to cancer and the health hazards involved in possible over‐treatment of pre‐cancerous cases which otherwise would have regressed, are considered. A dynamic model is suggested. In order to achieve a reduction of mortality in the short term, the efforts of the program should initially be concentrated on older women. To achieve a reduction of incidence in the long run, younger women should gradually be included. Finally, special efforts should be made to increase attendance rates among high‐risk women.
Characterization of 3ll‐tumor variants generated by in vitro macrophage‐mediated selection
Authors: Remels Linda M. , de Baetselier Patrick C. 
Published: February 2007

AbstractFollowing sequential interactions between activated syngeneic Mϕs and 3LL tumor cells, stable Mϕ‐resistant 3LL variants were isolated. Unlike the unselected 3LL cells, these Mϕ‐selected variants were relatively resistant to the cytostatic and cytolytic activity of activated effector Mϕs. Such Mϕ‐resistant 3LL variants evade the Mϕ tumoricidal activity by at least two mechanisms. Firstly, they manifest a reduced susceptibility towards Mϕ‐related cytotoxins such as TNF. Secondly, they actively suppress the cytotoxic potential of Mϕs through secretion of Mϕ‐inhibitory factors. The resistance of the 3LL variants to Mϕ effector cells in vitro was reflected in vivo by a higher tumorigenic and metastatic potential. No strict correlation was found between the NK sensitivity of Mϕ‐resistant and Mϕ‐sensitive 3LL cells and their metastatic ability. Hence, activated tumoricidal Mϕs may play a central role in either the elimination or selection of neoplastic cells.
Epstein‐barr virus‐specific t‐cell recognition of B‐cell transformants expressing different ebna 2 antigens
Authors: Wallace L. E. , Young L. S. , Rowe M. , Rickinson A. B. , Rowe D. 
Published: February 2007

AbstractEpstein‐Barr (EB) virus isolates can be classified as type A or type B depending upon the identity of the virus‐encoded nuclear antigen EBNA 2; the EBNA 2A and 2B proteins show limited amino‐acid homology and induce largely non‐cross‐reactive antibody responses in humans. To examine whether EBNA 2 might also be a target for virus‐specific cytotoxic T‐cell responses (like “intracellular” antigens in other viral systems), normal B cells from non‐immune donors of known HLA type were transformed in vitro with virus isolates either of type A (from the B95‐8 and IARC‐BL74 cell lines) or of type B (from the AG876 and IARC‐BL16 cell lines) to provide a suitable panel of target cells. DNA hybridization with type‐specific probes and immunoblotting with type‐specific antisera confirmed the EBNA 2 type of the resident virus in the various in vitro transformants. These cells were then tested as targets for virus‐specific cytotoxic T cells, the latter being prepared from type‐A virus‐infected donors by in vitro reactivation of memory cells from peripheral blood using autologous type‐A virus‐transformed cells as stimulators. Such effector cells lysed type‐A virus‐transformed and type‐B virus‐transformed target cells equally well, indicating that EBNA 2 (in particular that part of the protein which varies between virus types) seems not to be a dominant antigen for the induction of EB virus‐specific cytotoxic responses.
Production of stable cytolytic T‐cell clones directed against autologous human melanoma
Authors: Hérin M. , Lemoine C. , Weynants P. , Vessière F. , Van Pel A. , Boon T. , Knuth A. , Devos R. 
Published: February 2007

AbstractWe have attempted to optimize the production of stable human cytolytic T lymphocyte clones directed against autologous melanoma cell lines. MLTC were restimulated every week with irradiated melanoma cells in medium containing human serum and IL‐2. After 21 to 35 days, in 5 out of 6 patients, these cultures expressed a preferential cytolytic activity against the autologous melanoma cells, as compared to autologous EBV‐B cells or NK target K562. Limiting dilution of MLTC responder cells was performed at times varying from days 7 to 28, in medium containing IL‐2 and allogeneic EBV‐B cells as feeders. Approximately 1% of these responder cells gave rise to CTL clones that lysed the autologous melanoma cells, but did not lyse K562 or autologous B cells. It was possible to maintain in culture for several months a large number of CTL clones that retained this specificity with high activity, and multiplied more than 5‐fold every week. Some of these CTL clones were dependent on the presence of the autologous melanoma cells for their growth. With one melanoma, the use of autologous CTL clones made it possible to identify 3 different antigens on the tumor cells.