bluuebunny/crossref_metadata_2025_split huggingface dataset:
Malignant melanoma: Cross‐reacting (common) tumor rejection antigens
Authors: Hearing Vincent J. , Vieira Wilfred D. , Law Lloyd W. 
Published: February 2007

AbstractThe expression of tumor‐associated transplantation antigens (TATA) by 3 different murine melanomas was examined. A comparison was made between different modes of inducing tumor‐rejection activity, including immunization with irradiated cells from tissue culture lines, with irradiated cells from solid tumor lines, and with viable cells growing in footpads (followed by amputation). Melanoma cell lines examined included the spontaneous B 16 melanoma, the ultra violet‐light‐induced K 1735 melanoma, and the dimethyl benzanthracene‐induced JB/RH melanoma. The data presented demonstrate that not only do all 3 melanoma lines studied express cell surface antigens sufficient to elicit immune response which result in tumor rejection activity, but that these antigens show cross reactivity among the 3 melanoma lines studied. The specificity of the TATA appears to be restricted to the melanomas, since crossreactivity was not observed with 2 different fibrosarcoma cell lines, or with 2 sarcoma cell lines. In addition, it was found that both the JB/RH and K 1735 melanoma cells release (or shed) cell surface antigens which can elicit tumor rejection activity, and that these antigens can be extracted with aqueous butanol, as has been demonstrated with B 16 melanoma.
Procoagulant activity of mouse and human cultured cells following various types of transformation
Authors: Curatolo Laura , Alessio Grazia , Passerini Carlo Gambacorti , Casali Bruno , Morasca Luciano , Semeraro Nicola , Donati Maria Benedetta 
Published: February 2007

AbstractThe presence of fibrin deposits in the micro environment of tumor cells has been reported repeatedly and considered to play an important role in tumor biology. Among the mechanisms by which fibrin may be deposited in tumors, procoagulant activities (PCA) of different types have been described in cancer cells. The present study was aimed at establishing whether the nature of cellular PCA was a characteristic associated with malignant transformation. PCA of normal and transformed cells was investigated on pairs of murine and human origin. The transformed counterparts were obtained after treatment with low‐dose radiation, chemical carcinogen, viral infection or after in vitro spontaneous immortalization. Both before and after any type of transformation cell PCA was of the tissue thromboplastin type, identified on the basis of biological criteria: requirement of factor VII for its expression and lack of inhibition by the serine protease inhibitor diisopropylfluorophosphate (DFP). Transformed cells of murine origin showed significantly lower activity than their normal counterparts, whereas all the transformed human cell lines expressed significantly higher activity than normal. An inverse correlation between the levels of PCA and the cell density in culture was observed in all but one of the lines tested. These findings suggest that the factor X activating property described in some tumors or in transformed cells cannot be considered as a general marker of transformation.
A dual expression of cytokeratin and neurofilaments in bronchial carcinoid cells
Authors: Lehto Veli‐Pekka , Miettinen Markku , Virtanen Ismo 
Published: February 2007

AbstractIntermediate filaments (IF) are ubiquitous cytoplasmic structures which, by virtue of their cell‐ and tissue‐type‐specific characteristics, are widely used as markers of tissue derivation and as differential diagnostic aids in surgical pathology. In contradistinction to other IFs, vimentin filaments, characteristic of mesenchymal cells, may be coexpressed with other cell‐type specific IFs—cytokeratin filaments, desmin filaments, glial filaments and neurofilaments—in some tumor cells, embryonic cells, and cells in vitro. In this study we describe a novel type of IF coexpression which does not involve vimentin‐filaments, viz. the presence of both cytokeratin filaments and neurofilaments in human bronchial carcinoid tumor cells.
Distinctions between endemic and sporadic forms of epstein‐barr virus‐positive burkitt's lymphoma
Authors: Rowe M. , Rooney C. M. , Rickinson A. B. , Lenoir G. M. , Rupani H. , Moss D. J. , Stein H. , Epstein M. A. 
Published: February 2007

AbstractTumour cell lines were established in vitro from 16 cases of Epstein‐Barr (EB) virus genome‐positive Burkitt's lymphoma (BL), 7 of “endemic” origin (i.e. from holoendemic malarial areas of Africa and of New Guinea) and 9 of “sporadic” origin (i.e. from outside such high‐incidence areas). All the BL cell lines thus established were monoclonal by immunoglobulin iso‐type expression and displayed a characteristic chromosomal translocation, t(8:14) or t(8:22), confirming their malignant origin. Clear differences observed between the individual BL cell lines appeared to be related to their endemic or sporadic status. All 7 endemic cell lines began growth as a carpet of single cells, often with small, loose cumps appearing in later passage. Whilst 3 lines of sporadic origin displayed a similar pattern to the above, the majority of sporadic lines grew as large, tight clumps of cells from the first passage onwards. These differences in growth pattern were reflected by differences in cell surface phenotype, as defined in indirect immunofluorescence tests using a panel of monoclonal antibodies (MAbs) specific for B‐lineage‐associated antigens. BL cell lines could be classified into 3 separate groups on the basis of their reactivity with 6 particular antibodies (MHM6, AC2, Ki‐1, Ki‐24, J5 and 38.13). All 7 endemic BL cell lines and 2 of the 3 sporadic BL cell lines which began growth as single cells showed a group‐I cell‐surface phenotype (MHM6, AC2, Ki‐1, Ki‐24 negative; J5, 38.13 positive) in early passage. In contrast, all 6 sporadic BL cell lines which began growth in large clumps displayed a distinct group‐11 phenotype (MHM6, AC2, Ki‐1 positive/negative; Ki‐24, J5, 38.13 positive); in later passage most of these sporadic lines progressed to a group‐III phenotype (MHM6, AC2, Ki‐1, Ki‐24 positive; J5, 38.13 negative) without loss of those immunoglobulin and chromosomal markers identifying the cells' malignant origin. These clear differences between endemic BL cell lines on the one hand and the majority of sporadic BL cell lines on the other suggest that endemic BL arises from a more restricted range of progenitor B cells than does the sporadic form of the disease.
Papillomavirus infection of the lower genital tract: Detection of viral DNA in gynecological swabs
Authors: Schneider Achim , Kraus Herbert , Schuhmann Roland , Gissmann Lutz 
Published: February 2007

AbstractA total of 311 smears from the lower genital tract were examined by the filter in situ hybridization method to identify human papillomavirus (HPV) DNA.Of these 311 smears, 229 came from clinically and cytologically negative patients and served as a control group. In this group HPV‐DNA was detected in 5 cases (2.2%).Of 82 cytologically positive cases (25 confirmed by histology) 56 (68%) contained HPV‐DNA. A high prevalence of HPV 6/11 and absence of HPV 16/18 was found in cases with cytological signs of permissive HPV infection. In mild and moderate dysplasia all viruses occurred at almost the same frequency. In severe dysplasia/carcinoma in situ HPV 16/18 was found 5 times more frequently than HPV 6/11. HPV 16/18 was identified in all 4 invasive cancer cases.Cervical irrigation of colposcopically suspect areas was performed in 15 cytologically and HPV‐DNA positive cases using the hydrodynamic filtration method. In 12 cases only the cells obtained from the colposcopically positive areas contained HPV‐DNA.The sensitivity and reproducibility of the filter in situ hybridization was shown by: (1) comparing the results obtained by HPV‐DNA hybridization using Southern blot analysis of tumor biopsies; (2) analysing the correlation of cytologic diagnosis and presence of HPV‐DNA in follow‐up examinations, and (3) diagnosing presence or absence of HPV‐DNA in parallel filters from the same patients.
Detection of nk activity and antibody‐dependent cellular cytotoxicity of lymphocytes by human tumor clonogenic assay‐its correlation with the 51cr‐release assay
Authors: Nomori Hiroaki , Saljo Nagahiro , Fujita Jiro , Hyoi Megumi , Sasaki Yasutsuna , Shimizu Eiji , Kanzawa Fumihiko , Inomata Motoko , Hoshi Akio 
Published: February 2007

AbstractNK activity of human peripheral blood lymphocytes (PBL) for cells of the human myeloid line K562, and antibody‐dependent cellular cytotoxicity (ADCC) of PBL for cells of human lung adenocarcinoma line PC‐9 were determined by the human tumor clonogenic assay (HTCA). Incubation of K562 cells or anti‐PC‐9 serum treated PC‐9 cells with PBL before plating inhibited the formation of colonies of these tumor cells. The percent inhibition of tumor cell colony formation was dependent on the effector/target ratio, the incubation time before plating and, in the case of PC‐9 cells, on the dilution of anti‐PC‐9 serum. PBL activated with human T‐cell growth factor (TCGF), lympho‐kine‐activated killer (LAK) cells, significantly augmented the inhibition of colony formation of K562 cells, compared to the control lymphocytes. The increase in colony inhibition was dependent on the concentration of TCGF and the time of incubation of PBL with TCGF. The HTCA determining the colony inhibition of K562 cells incubated with LAK or PBL correlated with the 51Cr‐release assay (p < 0.001). The HTCA determining the colony inhibition of anti‐PC‐9 serum‐treated PC‐9 cells incubated with PBL also correlated with the 51Cr‐release assay (p < 0.001). We found that the NK activity and ADCC of lymphocytes on K562 and PC9 tumor lines could be detected with HTCA.
Distribution of laminin and collagen type‐IV in benign and malignant lesions of melanocytic origin
Authors: Natali P. G. , Nicotra M. R. , Bellocci M. , Cavaliere R. , Bigotti A. 
Published: February 2007

AbstractUsing antisera for two specific basement membrane (b.m.) antigens such as laminin and collagen type‐IV, together with efectron microscopy, we have shown that fully antigenic b.m. and morphologically typical basal lamina (b.l.) are associated with normal and transformed cells of the melanocyte lineage in different ways. Thus, while b.m. and b.l. surround individual choroidal melanocytes, intradermal nevic cells and cells of blue nevi are not detectable at the periphery of resting and proliferating epidermal melanocytes. They have a low degree of expression with a heterogeneous pattern of distribution in primary and meta‐static melanoma. This heterogeneity is present within single metastases and among autologous metastases. These findings indicate that the presence of b.m. can be an additional marker for cells of the melanocyte lineage and should be considered when applying ser‐ological means for the detection and control of neoplasms of melanocytic origin.
Inhibition of growth of certain human tumour cell lines by a factor derived from human fibroblast‐like cell lines. I. Demonstration by mixed culture and by use of cell washings
Authors: Wu Ke‐Fu , Pope John H. , Ellem Kay A. O. 
Published: February 2007

AbstractThe growth of 7/9 Burkitt's lymphoma (BL) cell lines and 5/6 human melanoma cell lines was inhibited by certain human fibroblast‐like cell lines, especially human myofibroblast cell lines. In contrast to BL lines, 3/5 lymphoblastoid cell lines were less susceptible and 3/4 human leukaemic lines were resistant. The effect was time‐ and concentration‐dependent. Co‐cultivation led to inhibition of tumour‐cell growth within 3 days, but after removal from the fibroblasts, washing, and resuspending in fresh medium some tumour cells recovered and growth improved. The inhibitory activity was also demonstrated with washings of fibroblast‐like cell lines, and was sensitive to pronase. The biological significance of this factor remains to be defined.
Sequential degradation of heparan sulfate in the subendothelial extracellular matrix by highly metastatic lymphoma cells
Authors: Bar‐Ner M. , Kramer M. D. , Schirrmacher V. , Ishai‐Michaeli R. , Fuks Z. , Vlodavsky I. 
Published: February 2007

AbstractA highly metastatic variant (ESb) of a methylchol‐anthrene‐induced T lymphoma elaborates a heparan sulfate (HS) degrading endoglycosidase (heparanase) to a much higher extent than its non‐metastatic parental subline (Eb). Whereas a serum‐free medium conditioned by either subline contained a trypsin‐like serine protease, heparanase activity was detected only in the ESb‐conditioned medium (CM). ESb CM was incubated with a naturally produced, sulfate‐labelled subendothelial extracellular matrix (ECM) or with a soluble, high‐MW labelled proteoglycan first released from the ECM by incubation with Eb CM or with the partially purified ESb protease. Sulfate labelled degradation products were analyzed by gel filtration on Sephrose 6B. The optimal pH for degradation of ECM‐bound HS was 6.2 as compared to pH 5.2 for degradation of the soluble proteoglycan. Heparanase‐me‐diated degradation of both ECM‐bound and soluble HS was inhibited by heparin. Addition of either tryp‐sin, plasmin or to a lower extent, the purified ESb protease, stimulated between 5‐ and 20‐fold the ESb CM‐mediated degradation of ECM‐bound HS but had no effect on heparanase‐mediated degradation of the soluble proteoglycan. This stimulation was inhibited in the presence of heparin or protease inhibitors. These results indicate that both a protease and heparanase are involved in the ESb‐mediated degradation of ECM‐bound HS and that one enzyme produces a more accessible substrate for the next enzyme. This sequential cleavage is characteristic of degradation of a multimolecular structure such as the subendothelial ECM and hence cannot be detected in studies with its isolated constituents.
Muscarinic cholinergic receptors in pancreatic acinar carcinoma of rat
Authors: Taton Gérard , Delhaye Myriam , Swillens StéPhane , Morisset Jean , Larose Louise , Longnecker Daniel S. , Poirier Guy G. 
Published: February 2007

AbstractThe active enantiomer of tritiated quinuclidinyl benzilate (3H(‐)QNB) was used as a ligand to evaluate the muscarinic receptors. The 3H(‐)QNB binding characteristics of muscarinic cholinergic receptors obtained from normal and neoplastic tissues were studied to determine changes in receptor properties during neoplastic transformation. Saturable and stereospecific binding sites for 3H(‐)QNB are present in homogenates of rat pancreatic adenocarcinoma. The proportions of high‐ and low‐affinity agonist binding sites are similar for neoplastic and normal tissues. The density of muscarinic receptors is higher in neoplastic (200 femtomoles/mg protein) than in normal pancreatic homogenates (80 femtomoles/mg protein). The muscarinic binding sites of the neoplastic and fetal pancreas show similar KD values which are higher than those observed for normal pancreas.
Transforming potential of a retrovirus isolated from lung carcinoma of sheep
Authors: Safran N. , Zimber A. , Irving S. G. , Perk K. 
Published: February 2007

AbstractA retrovirus isolated from experimentally induced sheep lung carcinoma (SPCTV) was propagated in chronically infected Himalayan tahr ovarian cells and in normal sheep lung cells. Follow‐up of infection of the cells with SPCTV showed the appearance of syncytium, plaque formation, partial recovery and the establishment of a chronic infection. Virus‐associated reverse transcriptase activity in the medium fluctuated but remained at a constantly high level at the stage of chronic infection. Stages of type‐C virus morphogenesis were demonstrated by electron microscopy. The viral genome was detected in both the nucleus and cytoplasm by in situ hybridization. Chronically infected cells formed colonies when plated in soft agar. Following subcutaneous inoculation of chronically infected cells (of fibroblast origin) into nude mice, lymphoid tumors developed at the site of inoculation and in vital organs.
Spontaneous and induced primary oncogenesis in natural killer (nk)‐cell‐deficient beige mutant mice
Authors: Haliotis Tina , Ball Judith K. , Dexter David , Roder John C. 
Published: February 2007

AbstractSpontaneous tumor development and primary oncogenesis were compared in a large number of NKAbbreviations: NK, Natural killer; s.c, subcutaneously; i.u., infectious units; d.f., degree(s) of freedom; DMBA‐LV, dime‐thylbenzanthracene‐induced murine leukemia virus; PVM, pneumonia virus of mice; Reo‐3, Reo virus 3; MHV, murine hepatitis virus; LCM, lymphocytic choriomeningitis virus; MEV, murine encephalomyelitis virus; MVM, minute virus of mice; BP, benzo[alpha]pyrene.
‐deficient, homozygous C57B1/6‐bg/bg mice and their NK normal, heterozygous + /bg littermate controls. In a group of 167 retired breeders followed for spontaneous tumors, the probability of survival for mice eventually dying with a tumor was greater for the NK‐competent, +/bg than for the NK‐deficient, homozygous C57BL/6‐bg/bg mice (p = 0.0019), although the higher overall incidence of tumors in the bg/bg group (48%) was not significantly different from that in the +/bg group (37%). In the bg/bg group the incidence of tumor death appeared to increase relatively sharply in the 25‐ to 29‐month age bracket compared to the fairly regular increase in incidence observed in the +/bg group. All the spontaneous tumors except 2 (discovered in +/bg mice) were classified histologically as widely disseminated malignant lymphomas. The other two were one squamous‐cell carcinoma and one sarcoma. A total of 73 bg/bg mice injected s.c. with benzo[alpha]pyrene (BP) had a higher overall incidence of tumors (81%) (rhabdomyosarcomas) than 138 +/bg mice (64%) and in the largest group (0.3 mg, n = 85) the bg/bg group developed tumors, at a higher incidence (p = 0.01) and with a shorter latency (p = 0.025) than the +/bg group. On the other hand, mice injected with dimethylbenzanthracene or given 4 weekly doses of 160 rads of gamma irradiation showed no difference in overall tumor incidence. In addition, mice injected with various doses of DMBA‐induced murine leukemia virus (DMBA‐LV) also showed no significant difference in tumor incidence. Others have reported that some of these treatments (DMBA, split‐dose irradiation) cause profound NK suppression, thereby reducing NK differences between the two groups of mice. These results suggest that a partial NK impairment in beige mutant mice early in life may lead to significantly greater rates of death with spontaneous malignant tumors late in life. Some primary oncogenesis treatments (BP) but not others (DMBA, split‐dose irradiation, leukemia viruses) cause tumors with a greater incidence and shorter latency in beige mice. The results suggest, but do not prove, that NK cells play a role in surveillance against spontaneously arising, and possibly some types of carcinogen‐induced, tumors.
The effect of murine interferon‐alpha/beta on an established rauscher murine leukemia virus‐induced erythroleukemia in balb/c mice
Authors: Herman R. A. C. P. , Trapman J. 
Published: February 2007

AbstractRauscher murine leukemia virus (R‐MuLV) induces a rapidly developing erythroleukemia in BALB/c mice. Previously, we have shown that mouse interferon‐α/β (Mu IFN‐α/β) applied shortly after virus inoculation efficiently inhibits the leukemic process (Hekman et al., 1981). Here we describe the effect of Mu IFN‐α/β on an established leukemia. Varying doses of Mu IFN‐α/β were injected over 3 days, starting 8 to 12 days after virus inoculation. The effect of Mu IFN‐α/β on the leukemic process was monitored by measuring the spleen weight, reverse transcriptase activity in the serum and, in selected experiments, by microscopic examination of sections of the spleen using standard histological and immunological staining techniques. Depending on the spleen weight at the start of its application (maximal about 450 mg), Mu IFN‐α/β caused a dramatic reduction in the number of virus‐infected erythroleukemic cells in the spleen. Also, R‐MuLV disappeared from the serum within 3 days. If Mu IFN‐α/β was injected into R‐MuLV‐infected mice with an already 10‐fold enlarged spleen, it could only stop further development of leukemia. Results obtained with crude Mu IFN‐α/β preparations were confirmed with absolutely pure Mu IFN‐β.
Hsv‐ and chemical carcinogen‐induced amplification of sv40 dna sequences in transformed cells is cell‐line‐dependent
Authors: Matz Bertfried , Schlehofer Jörg R. , Zur Hausen Harald , Huber Bernd , Fanning Ellen 
Published: February 2007

AbstractEleven simian virus 40‐transformed cell lines from 5 different species were tested for their ability to amplify integrated simian virus 40 DNA upon infection with herpes simplex virus type I or treatment with various chemical carcinogens. Four cell lines were positive only for virus‐induced gene amplification and two lines were positive for both carcinogen‐ and virus‐induced gene amplification. Individual cell lines were assayed for (1) the presence of an intact SV40 origin of replication, (2) the expression of a functional SV40 T‐antigen, and (3) permissivity to herpes simplex virus replication. These parameters were found to be positive in all 6 amplification‐competent cell lines. The ability of herpes simplex virus to amplify SV40 DNA sequences in transformed cells is greater than that of chemical carcinogens and can be suppressed by specific inhibitors of the herpes virus‐encoded DNA polymerase.
Tumor‐associated desmoplasia in the rabbit mesentery characterized by morphological, biochemical and cytophotometric methods
Authors: Haemmerli G. , Müller‐Glauser W. , Bruckner P. , Hauser‐Urfer I. , Sträuli P. 
Published: February 2007

AbstractIntraperitoneal implantation of V2 carcinoma cells in the rabbit leads to invasion of the mesentery and to structural tissue alterations which are concomitantly of a destructive and a desmoplastic type. In this report, we describe the desmoplastic changes which are characterized by the increased formation of collagen and of proteoglycans resulting in an increased thickness of the membrane. Biochemical data indicate that the total amount of collagen increases with time after implantation, whereas the relative amount per unit of dry weight, as well as the contributions of type I (15–25%) and type III (6–8%), stay within the same range. The increased synthesis of extracellular matrix is accompanied by a change in the appearance of the fibroblasts which now show the morphologic features of synthesizing cells. Also, an appreciable number have entered the S‐phase. We propose that the desmoplastic changes are tumor‐associated, since implantation of epithelial cells from normal rabbit liver does not result in similar alteration. Our findings are discussed in view of the role played by tumor and/or host cells in the increased production of extracellular matrix, of possible factor(s) elaborated by the tumor cells, and of the general significance of desmoplastia for tumor spread.
Monoclonal antibody production to a B16 melanoma associated antigen
Authors: Tomita Yasushi , Montague Paul M. , Hearing Vincent J. 
Published: February 2007

AbstractEight different rat hybridoma cell lines have been produced which secrete MAbsAbbreviations: BSA, bovine serum albumin; ELISA, enzymelinked immunosorbent assay; MSA, murine serum albumin; PBS, phosphate‐buffered saline; MAb, monoclonal antibody; s.c., subcutaneous.
identifying the melanoma‐specific B700 antigen. This antigen has been previously shown to have significant sequence homology to the mammalian serum albumins, but antibodies specifically raised against B700 cross‐react only with murine albumin. Each of these MAbs has been shown by Western immunoblotting to recognize an independent epitope on the B700 protein; it is concluded not only that the B700 protein is a highly immunogenic antigen, but also that the sequence homologies between the B700 antigen and murine albumin must occur extensively throughout the molecule.