bluuebunny/crossref_metadata_2025_split huggingface dataset:
Light‐induced chromatid damage in human skin fibroblasts in culture in relation to their neoplastic potential
Authors: Parshad Ram , Gantt Raymond , Sanford Katherine K. , Jones Gary M. , Camalier Richard F. 
Published: February 2007

AbstractSkin fibroblasts from ataxia telangiectasia and xeroderma pigmentosum (XP) donors and from the XP sib (possible heterozygote), all genetically predisposed to a high risk of cancer, show an increased susceptibility to light‐induced chromatid breaks after culture in vitro. Light‐induced chromatid breaks were shown previously to result from generation of hydrogen peroxide (H2O2) during light exposure. The level of susceptibility attained is significantly higher than that observed in 13 lines of fibroblasts from normal skin of donors ranging in age from 3 days to 92 years or from fetal skin tested at various population doubling levels. Two lines of normal skin fibroblasts transformed by chemical carcinogens to neoplastic cells also show a significant increase in susceptibility as compared with their untransformed controls. These data indicate for human cells, as reported earlier for mouse cells, an association between enhanced susceptibility to light‐induced chromatid damage and neoplastic potential; this association is further supported by the high susceptibility of cells derived from a human adenocarcinoma. Two observations are consistent with the concept that the increased susceptibility does not result from greater initial damage to the DNA of the neoplastic cells. First, activities of the ubiquitous H2O2 scavenging enzyme, glutathione peroxidase, are similar in the paired normal and neoplastic cell populations. Second, cells of the paired lines are equally sensitive to DNA breakage by exogenous H2O2. The enhanced susceptibility associated with neoplastic potential may result from an impaired capacity to repair DNA rather than a greater initial sensitivity of the neoplastic cells to the damaging agent.
Establishment of attached and non‐attached cell lines from an uncommon human glioma
Authors: Westermark B. , Larsson E. , Brunk U. , Lubitz W. , Mark J. 
Published: February 2007

AbstractA New cell line, U‐706, established from an uncommon human glioma (possibly giant‐cell glioblastoma) is reported in this communication. The tumor gave rise to two permanent sublines, one attached (U‐706M) and one non‐attached (U‐706S) cell line. The growth characteristics, chromosome banding pattern, electronmicroscopic picture and cell surface characteristics of the two sublines are described.
Suppressor pathways in tumor immunity: A requirement for Qa‐1 positive tumor‐bearer spleen t cells in suppression of the afferent immune response to tumor antigens
Authors: Mulé James J. , Stanton Thomas H. , Hellström Ingegerd , Hellström Karl Erik 
Published: February 2007

AbstractSpleen cells from mice bearing large methylcholanthrene (MCA)‐induced sarcomas were injected intravenously into mice challenged in the hind footpads with heavily‐irradiated cells from the same or a different sarcoma. As measured by [3H]‐thymidine incorporation on day 5 or 6, cellular proliferation in the draining popliteal lymph nodes of these mice was significantly depressed as compared to control animals receiving normal spleen cells or medium intravenously. The suppression was found to be mediated by a Qa‐1‐positive, Thy‐1‐positive cell. It was relatively resistant to cyclophosphamide treatment (100 mg/kg). Furthermore, it had both antigen‐specific and non‐specific components. The findings are discussed in relation to a suppressor activator cellsuppressor acceptor cell pathway in the immunoregulation of tumor immunity.
Impairment of in vitro generation of cytotoxic or T suppressor lymphocytes by friend leukemia virus infection in mice
Authors: Garaci E. , Migliorati G. , Jezzi T. , Bartocci A. , Gioia L. , Rinaldi C. , Bonmassar E. 
Published: February 2007

AbstractSpleen cells collected from DBA/2 (H‐2d) mice inoculated with the polycythemic variant of Friend‐Leukemia Virus Complex (FLV‐P) were tested for T‐dependent immune functions, such as the in vitro generation of cytotoxic T lymphocytes (CTL) and of non‐specific T suppressor lymphocytes (STL). CTL were generated against H‐2b splenocytes, and STL were obtained following a 5‐day lymphocyte culture without stimulator cells. A progressive and severe impairment of the generation of both CLT and STL was found from 2 weeks onward after infection, being almost totally abolished 3–4 weeks after virus challenge. Suppressor cells (SC) capable of inhibiting CTL generation was detected in FLV‐P bearing mice. Suppressor activity was unaffected by anti‐Thy 1.2 serum and complement but was removed following iron‐magnet depletion or passage through nylon‐wool column. Moreover complete recovery of the competence of CTL generation was attained when FLV‐P infected splenocytes were passed through nylon‐wool column. It is concluded that FLV‐P infection depresses T‐dependent cytotoxic and suppressor responses in mice, by the appearance of non‐T adherent phagocytic cells, capable of impairing CTL generation in vitro.
The usefulness of human tumor cell lines in the study of chemosensitivity. A study of malignant melanomas
Authors: Tveit Kjell Magne , Fodstad Øystein , Pihl Alexander 
Published: February 2007

AbstractThe chemosensitivity of human melanoma cells has been studied before and after continuous in vitro culture. Altogether, nine cell lines were studied, two derived from patients' biopsies, and seven from xenografts in athymic mice. The sensitivity to the agents DTIC (Dacarbazine), CCNU (Lomustine), procarbazine, vinblastine, abrin and ricin was assayed. Furthermore, in five cases the chemosensitivity of the cell lines was compared to that of tumors obtained by injecting the cell lines into athymic mice. In all cases the sensitivity was measured in an in vitro soft agar assay. Upon cultivation in vitro, two of the cell lines, one derived from a patient's metastasis and one from a xenograft in athymic mice, showed marked increases in sensitivity to some of the drugs, whereas sensitivity to other drugs showed little or no change. For the other cell lines small, but definite increases or decreases in chemosensitivity were observed. Permanent cultures showed the same chemosensitivity as early subcultures. The tumors formed by injecting the cell lines into athymic mice showed moderate changes in chemosensitivity, as compared to the cell lines in vitro. The data indicate that considerable changes in chemosensitivity may occur when cells are brought from in vivo to in vitro conditions and vice versa and that such changes may be highly specific. Therefore, although cell lines may be useful in some respects, they should be used with caution in attempts to evaluate quantitatively the sensitivity of human tumors to cancerostatic drugs.
Sister chromatid exchange in lymphoma lines and lymphoblastoid cell lines before and after heterotransplantation into nude mice
Authors: Fonatsch Christa , Kirchner Hartmut H. , Schaadt Michael , Günzel Manfred , Diehl Volker 
Published: February 2007

AbstractThe sister chromatid exchange (SCE) rates of cell lines derived from patients with different malignant and premalignant diseases were studied before and after intracerebral inoculation into nude mice and were compared to the SCE frequencies of cell lines from healthy controls. Lymphoma lines characterized by chromosomal markers as well as chromosomally normal lymphoblastoid cell lines were used. The SCE frequencies of nude mouse tumor‐derived cell lines did not show a homogeneous pattern. They were either as high as, or higher or lower than, the SCE levels of the original cell line. But all cell lines, karyotypically abnormal as well as normal, originating from patients with malignant and premalignant diseases, showed significantly higher SCE rates than the control lines from healthy donors.
Effects of human lymphoblastoid interferon on cultured breast cancer cells
Authors: Shibata Hideo , Taylor‐Papadimitriou Joyce 
Published: February 2007

AbstractThe effect of human interferon on growth and fibronectin production in a range of cultured breast cancer cell lines has been investigated. The cell lines differ in their sensitivity to interferon's growth‐inhibitory effect as determined from growth curves, but the degree of sensitivity varies according to the method of assay. When growth was measured in cultures seeded with fairly large numbers of cells, five out of seven lines examined showed a reduction of 50% or more in the number of attached cells after treatment for 8 days with 1,000 units/ml of interferon. Growth of the two cell lines least affected by interferon treatment in dense culture could, however, be markedly inhibited under conditions of clonal growth in agar or when sparsely seeded on plastic and this was due to inhibition of initiation of growth. In some breast epithelial lines, where the number of attached cells was regulated in part by cell shedding, it was found that interferon not only inhibited cell proliferation, but also increased cell shedding. To determine if interferon increased cell shedding by affecting fibronectin production, the total and cell associated fibronectin was estimated in control and interferon‐treated cultures. Four of 10 cell lines examined produced detectable amounts of fibronectin, and in only one of these lines, Hs578T derived from a carcino‐sarcoma, was the production and retention of fibronectin inhibited by interferon treatment. In those breast carcinoma lines which produced detectable amounts of fibronectin, the level of production and retention of the protein, expressed as a proportion of the total protein, did not change after interferon treatment, but showed an increase if expressed on a per cell basis. This is explained by the fact that the interferon‐treated cells showed an increase in cell volume.
Diploid human lymphoblastoid and burkitt lymphoma cell lines: Susceptibility to murine NK cells and heterotransplantation to nude mice
Authors: McCormick Kenneth J. , Giovanella Beppino C. , Klein George , Nilsson Kenneth , Stehlin John S. 
Published: February 2007

AbstractHuman lymphoid cell lines which had been classified on the basis of studies on clonality and morphological, chromosomal and functional parameters as lymphoblastoid cell lines (LCL) of presumed non‐neoplastic origin and Burkitt lymphoma (BL) lines of proven malignant origin, were tested for susceptibility to natural killer (NK) cells obtained from the spleens of athymic nude mice. The 20 lines included normal diploid LCL and aneuploid BL lines. All cells carried the Epstein‐Barr virus (EBV) genome. In addition, two EBV‐negative BL lines were tested. The pronase‐induced release of 14C‐DNA from 14C‐thymidine‐labelled target cells was used to assess the sensitivity of the cell lines to NK activity. When attempts were made to correlate the growth of the EBV‐positive LCL and the EBV‐positive BL cell lines in the subcutaneous space of adult nude mice with their susceptibility to NK cells, no significant correlation was observed. The EBV‐negative BL cell line, Ramos, however, could be transplanted subcutaneously in nude mice and was more resistant to NK activity than was the EBV‐negative BL cell line, BJAB, which cannot be transplanted subcutaneously. Growth of heterotransplanted EBV‐converted cell lines in the subcutaneous space of adult nude mice may be influenced by immune effectors other than NK cells.
Lysis of human B‐lymphocyte‐derived lymphoma/leukemia cells of established cell lines by interferon‐activated natural killer (NK) cells
Authors: Pattengale Paul K. , Gidlund Magnus , Nilsson Kenneth , Sundström Christer , Örn Anders , Wigzell Hans 
Published: February 2007

AbstractCultured cell lines derived from malignant Epstein‐Barr virus (EBV)‐negative B cells, and representative of the more common types of naturally occurring non‐Hodgkin lymphomas and related leukemias, were found to be sensitive to lysis by human natural killer (NK) cells. The observed lysis of such cell lines was mediated by a population of interferon‐augmentable, FcR‐positive, non‐adherent lymphoid cells, which were also able to kill the “standard” NK targets K562 and Molt‐4. When the NK susceptibility of the neoplastic, EBV‐negative B cells was compared to that of diploid, EBV‐carrying, non‐neoplastic B lymphoblastoid cell lines (BLCLs) and of the “standard” NK target K562, several distinct patterns were observed. The killing of the neoplastic B cell lines was significantly less than that of K562, but significantly greater than that of the EBV‐derived BLCLs of non‐neoplastic origin. An additional finding was a similar NK susceptibility profile for the neoplastic, true histiocytic cell line U‐937 (i.e., K562>U937>BLCLs). Furthermore, all cell lines, with the exception of the BLCLs, could effectively compete for the observed killing in cold target inhibition assays. The implications of these findings are discussed in relation to both neoplastic and non‐neoplastic targets of NK lysis.
Expression of SV40 T antigen polypeptides in cells biochemically transformed by plasmids containing the herpes simplex virus thymidine kinase gene and the genome of an SV40tsA mutant
Authors: Kit Saul , Otsuka Haruki , Qavi Hamida , Trkula David , Dubbs Del Rose 
Published: February 2007

AbstractTo study the expression of SV40 tsA genomes that had been non‐selectively introduced into mouse cells, SV40 tsA207 DNA was cleaved with BamH 1 and ligated to BamH 1‐cleaved plasmid pAGO DNA, which contains a functional HSV‐1 thymidine kinase (TK) gene in the form of a 2 kbp Pvu II fragment inserted at the Pvu II site of pBR322. Recombinant plasmids (11–12 kbp) were isolated and amplified in E. coli K12 strain RR1. Restriction nuclease analyses demonstrated that recombinant plasmids pSB15 and pSB10 contained intact SV40 genomes with the polarity of transcription oriented in the same direction (clockwise) or the opposite direction (counterclockwise), respectively, in relation to that of the HSV‐1 TK gene. C1a 1‐cleaved pSB10 and pSB15 DNAs were used to transform LM(TK−) cells to TK+. Serological and disc PAGE analyses showed that clonal lines transformed by these plasmids all expressed the selected marker, HSV‐1 TK. Molecular hybridization experiments showed that transformed clonal lines TF pSB10 C7 and TF pSB15 C10 had integrated intact SV40 genomes at one integration site, TF pSB10 C3 had integrated an SV40 genome with a small deletion near the BamH 1 site, but TF pSB15 C1 had integrated a plasmid from which most of the SV40 nucleotide sequences had been deleted. IF assays with hamster anti‐SV40 tumor sera showed that TF pSB10 C7 and TF pSB15 C10 strongly expressed SV40 T antigens in over 90% of the cells, TF pSB10 C3 expressed SV40 T antigens in a minority of the cells, and TF pSB15 C1 did not express SV40 T antigens at all. [35S]‐methionine labelling and immunoprecipitation experiments showed that, at 36.5°C: (1) TF pSB10 C7 and TF pSB15 C10 expressed 92K and 20K mol. wt. species of SV40 T antigens and 50–55K cellular protein; (2) expression of all three was reduced in TF pSB10 C3 cells; and (3) TF pSB15 C1 expressed none of the SV40 T antigens, nor did parental LM(TK−) or TF 8‐2 transformed cells (which contained the HSV‐1 TK gene but not SV40 DNA). At 40°C, labelling of the 50–55K cellular protein was markedly reduced in TF pSB10 C7 and pSB15 C10 cells. The results suggest that SV40 large T antigen (92K) induces and/ or stabilizes the 50–55K cellular protein in these mouse cells.
Rat mammary carcinoma cells secrete active collagenase and activate latent enzyme in the stroma via plasminogen activator
Authors: O'Grady Robert L. , Upfold Linda I. , Stephens Ross W. 
Published: February 2007

AbstractA spontaneous mammary adenocarcinoma (AC) from an inbred female rat was investigated with regard to secretion of neutral proteases. Cultures of neoplastic epithelial cells derived from the tumour secreted an enzyme that fulfilled the criteria for a specific collagenase. In contrast to cultures of non‐neoplastic cells, tumour collagenase was present as an active enzyme, since treatment with trypsin or p‐aminophenylmercuric acetate (APMA) did not increase activity. The neoplastic cells were also prolific producers of plasminogen activator (PA). Dexamethasone (Dex) (10−6M) markedly reduced the levels of both enzymes. Addition of tranexamic acid (TA), an inhibitor of plasmin and of plasminogen activation, did not affect collagenase activity, even at 10−1M TA, nor did latent collagenase accumulate. Latent collagenase was secreted in culture by normal fibroblasts from neonatal rat lungs. This latent enzyme was activated by the addition of tumour cell medium plus plasminogen, but this effect was inhibited by the addition of TA. These results demonstrate that the neoplastic cells themselves secrete collagenase as an active enzyme. PA is also secreted, is not involved with tumour collagenase, but is capable, in the presence of plasminogen, of activating latent collagenase produced by the non‐neoplastic cells within the tumour or in the surrounding tissue. This tumour possesses potent collagenolytic ability in vitro which may be partly responsible for its rapid invasion in vivo.
Adjuvant reactivity predicts survival in patients with “high‐risk” primary malignant melanoma treated with systemic BCG
Authors: Cochran Alistair J. , Buyse Marc E. , Lejeune Ferdy J. , Macher Egon , Revuz Jacques , Rümke Philip 
Published: February 2007

AbstractWe report the prognostic importance of strength of reaction to BCG, tumor histology and clinical factors in patients with previously untreated high‐risk (Clark, III, IV and V) primary malignant melanoma. One hundred and one such patients received high‐dose BCG (1 × 108viable units) by Heaf gun as an adjuvant to standardized primary surgery according to EORTC Protocol 18741. Univariate analysis of disease‐free interval (DFI) indicates that the degree of maximum reaction to BCG (p= 0.0003), Breslow thickness (p= 0.0003) and Clark level (p= 0.002) are highly significant prognostic factors. When a multivariate model using Cox's proportional hazard regression was used for DFI, the degree of maximum reaction to BCG and Breslow thickness were by far the most significant criteria. A prognostic equation was obtained to predict DFI from maximum BCG reaction and Breslow thickness. From analysis of the “scores” calculated in this way it appears that the two variables act independently. This technique permits the determination of values that are predictive of DFI and discriminate between subgroups of patients with different DFI characteristics (5 groups,p< 0.0001). This exercise was repeated for survival and similar results were obtained. The degree of a patient's immune reaction to BCG administered therapeutically is of paramount importance in determining the likelihood of survival. This factor and the Breslow thickness can be integrated to produce a mathematical equation which accurately predicts survival for appropriately treated melanoma patients.
Natural killer cell activity in reticulum‐cell sarcomas of SJL/J MICE. III. Characterization of the effector cells within RCS that mediate NK lysis
Authors: Fitzgerald Karen L. , McMaster John S. , Ponzio Nicholas M. 
Published: February 2007

AbstractVarious cell depletion techniques were employed to identify the cells responsible for the natural killer (NK) activity against YAC‐1 targets that is present in lymphoid tissues of SJL/J mice bearing transplantable reticulum‐cell sarcomas (RCS). The NK‐activating potential of irradiated RCS cells (X‐RCS) allowed a comparison of three NK‐cell activities in this model system: conventional, induced and RCS‐cell‐mediated cytotoxicity, represented by effector cells derived from lymphoid tissues of normal, X‐RCS‐injected and RCS‐bearing donors, respectively. Both the conventional and induced NK cells were resistant to pretreatment with anti‐la serum and C, whereas RCS‐mediated NK activity was significantly reduced by similar antiserum treatment. The cytotoxicity expressed by both conventional and induced NK cells was moderately radiosensitive, however, 5‐ to 10‐fold higher doses of irradiation were required to effect an equivalent reduction of RCS‐mediated NK activity. To further characterize the effector cells that mediated RCS‐associated NK activity, viable RCS tumor cells were injected into SJL F1 hybrids that either supported (SJL × C57EL/6 and SJL × A.TH) or did not support [SJL × B10.S(7R)] RCS growth. After pretreatment of RCS cell preparations taken from these F1 mice with alloantisera directed against the non‐SJL parental H‐2 haplotype, to remove F1 host cells (F1‐purified RCS), >75% of NK activity was recovered in the RCS‐injected SJL × C57BL/6 and SJL × A.TH F1 hybrids; however, <15% of NK activity was apparent in RCS‐injected SJL × B10.S(7R) F1 recipients. 89Sr treatment of SJL mice abrogated their ability to show increased (induced) NK activity following injection of X‐RCS. In contrast, viable, F1‐purified RCS cells demonstrated both growth and NK activity in 89Sr‐treated SJL mice that was comparable to that seen in normal controls. Treatment of effector cells with three different NK‐reactive antisera (αLy‐11.2, αNK‐1.2 and αasialo‐GM1) effectively depleted conventional and induced NK activities, but had a minimal effect on RCS‐cell‐mediated NK cytotoxicity. These data support the conclusion that RCS tumor cells of SJL/J origin possess NK cytotoxic function and that, by virtue of their pre‐B‐cell characteristics, they may represent a unique class of NK effectors.
Induction of target antigens and conversion to susceptible phenotype of NK‐cell‐resistant lymphoid cell line
Authors: Clark Edward A. , Sturge Jerrilyn C. , Falk Laurence A. 
Published: February 2007

AbstractTwo autologous Herpesvirus papio producer lymphoid cell lines and one autologous non‐producer line were compared for susceptibility to natural killer (NK) cell‐mediated lysis. The non‐producer cell line, 26CB‐1, was more resistant to NK cell killing compared to one viral producer counterpart 13CB‐1, but equally resistant when compared to another, 8CB‐1. Treatment with chemical agents that affect differentiation or activate the viral cycle, including n‐butyrate, luDR, 5‐azacytidine and tunicamycin, increased the susceptibility to killing of the non‐producer line but had less effect on the 13CB‐1 producer line. The increase in susceptibility was due to induction of new target antigens: activated 26CB‐1 cells were more effective at inhibiting NK‐cell‐mediated lysis and were bound by more NK cells than untreated control cells. The expression of NK target structures may be related to the differentiated state rather than to the viral production status of target cells.
Transformation of rat thyroid epithelial cells by kirsten murine sarcoma virus
Authors: Fusco Alfredo , Pinto Antonio , Ambesi‐Impiombato Francesco Saverio , Vecchio Giancarlo , Tsuchida Nobuo 
Published: February 2007

AbstractFischer rat thyroid epithelial cells (FRT) growing continuously in culture were infected with the Kirsten murine sarcoma virus KiMSV(KiMuLV) and found to produce this virus constitutively. Although the morphology of the FRT cells did not change appreciably, the cells became malignant after infection with KiMSV(KiMuLV) as shown by the growth of infected cells in semi‐solid media (uninfected FRT cells did not grow) and by the tumorigenicity of infected cells when injected into syngeneic animals (uninfected FRT cells or FRT cells infected with non‐transforming retro‐viruses were not tumorigenic). The induced tumors morphologically resembled moderately differentiated carcinomas. Two markers of thyroid epithelial differentiation were absent in the original FRT clone and remained unexpressed after transformation. Fully differentiated rat thyroid epithelial cells (FRT‐L cells) infected with another strain of the Kirsten murine sarcoma virus, the KiMSV(MolMuLV), were also transformed as demonstrated by the ability also of these cells to grow as carcinomas (after in vitro transformation) in syngeneic animals. Our results clearly demonstrate that the Kirsten murine sarcoma virus can transform in vitro cells of epithelial as well as of fibroblastic origin.