bluuebunny/crossref_metadata_2025_split huggingface dataset:
Simultaneous presence of herpes simplex and human papilloma virus sequences in human genital tumors
Authors: Di Luca D. , Rorola A. , Pilotti S. , Monini P. , Caselli E. , Rilke F. , Cassai E. 
Published: February 2007

AbstractHerpes simplex virus (HSV) and human papillomavirus (HPV) sequences were analyzed in tumors of the female lower genital tract, by probing DNA from 13 intraepithelial and 30 invasive neoplastic lesions with radiolabelled HPV‐16 and HPV‐18 DNA as well as cloned fragments of HSV‐2 DNA. Careful removal of stromal tissue from the pathological specimens allowed authentic tumor DNA to be processed. Normal genital tissue obtained from the patients and genital condylomata were included as internal controls. The presence of HPV‐16 or 18 DNA was detected in 12/13 (92.3%) intraepithelial neoplasms and in 16/30 (53.3%) invasive carcinomas. No significant difference was detected in titer or frequency of antibodies to HPV group‐specific antigen in sera from patients and controls. Hybridization to BgIII N fragment of HSV‐2 DNA was detected in 4/13 (30.8%) intraepithelial neoplasms and 4/30 (13.3%) invasive carcinomas but in none of the control tissues. All the 8 samples harboring HSV‐2 homologous sequences were also positive for HPV, supporting the hypothesis of a synergistic association between the 2 viruses. The hybridization analyses performed to study c‐myc involvement in genital oncogenesis did not reveal c‐myc amplification in either invasive or pre‐invasive lesions.
Space‐time clustering and bone tumours: Application of Knox's method to data from a population‐based cancer registry
Authors: Silcocks P. B. S. , Murrells T. 
Published: February 2007

AbstractThe possibility of space‐time clustering in osteosarcoma and Ewing's tumour was studied in a sample of 182 patients aged under 25 years, drawn from a population‐based cancer registry. No evidence of space‐time clustering was found for either disease and this finding supports previous work in this field.
Plasminogen activator production by human tumor cells: Effect on tumor cell‐extracellular matrix interactions
Authors: Varani James , McKeever Paul E. , Fligiel Susanne E. G. , Sttrin Robert G. 
Published: February 2007

AbstractCell lines derived from 3 different types of human tumor (e.g., squamous carcinomas, melanomas and gliomas) were examined for production of plasminogen activator activity and for attachment and spreading on various extracellular matrix components in the presence or absence of plasminogen. All of the squamous carcinoma and melanoma lines produced high levels of plasminogen activator activity. In contrast, 4 of 6 glioma lines had undetectable activity. Cells from all 3 tumor types attached and spread on fibrinogen‐coated or fibrin‐coated plastic dishes in the absence of plasminogen. In the presence of exogenous plasminogen, the attachment and spreading of the cells which produced high levels of plasminogen activator activity was inhibited. The plasminogen activator‐deficient cells were much less sensitive to exogenous plasminogen. In the presence of plasminogen, attachment and spreading on fibronectin‐coated dishes was also partially inhibited. In contrast, plasminogen had no effect on the attachment and spreading of the cells on type‐1 or ‐IV collagen, laminin or thrombospondin. Previous studies have shown that tumor‐cell adhesion to the extracellular matrix depends on the synthesis of receptors for extracellular matrix components or on the synthesis of extracellular matrix components themselves. The present study shows that, in addition, the production of enzymes which are capable of degrading these components also influences tumor‐cell adhesion to extracellular matrix moieties.
Contact‐inhibitory factor induces alterations in the distribution and content of specific cytoskeletal elements in an established line of rat hepatic tumor cells
Authors: Higgins Paul J. , Lipkin George , Rosenberg Martin , Ryan Michael P. 
Published: February 2007

AbstractEstablished 72/22 rat hepatic epithelial tumor cells, which possess intracellular aggregates of intermediate‐sized filaments resembling Mallory‐body‐like inclusions, were used to assess changes in tumor cell growth and morphology associated with exposure to contact‐inhibitory factor (CIF). CIF reduced 72/22 proliferative rate, increased mean population doubling time by 42%, lowered culture saturation densities to 34–50% of control values and inhibited formation of dense foci. These proliferative changes were due to an apparent prolongation of the G1 phase of the cell cycle during the period of CIF exposure. CIF concomitantly induced a marked increase (by 70%) in cell spreading and loss of both the usual tight (epithelioid) cell juxtaposition and typical ordered colony structure characteristic of untreated populations. However, CIF exposure failed to achieve complete cytoarchitectural “normalization” in 72/22 cells (i.e., dispersal of the Mallory‐body‐like aggregate of intermediate filaments and restoration of a more typical hepatocytic phenotype). Most obvious was a reduction In the integrity of the peripheral band of mlcrofilaments (a structure involved in the maintenance of epithelial cell shape) and a decrease in the content of desmoplakin (a protein component of desmosomal plaques). Changes in these major structural elements appear to be critical events in development of the pleomorphic phenotype and reduced sub‐stratum adhesiveness observed during treatment. CIF‐related fragmentation of peripheral band structures was not reflected in changes in either the total cellular or cytoskeletal‐associated actin contents. The morphologic changes observed under conditions of CIF exposure closely paralleled induced decreases in the cellular content of the actin‐associated membrane skeleton protein p35. These data collectively suggest that CIF may act to alter the composition of the cortical skeleton in cultured liver tumor cells.
The anti‐tumor effect of recombinant interferon alpha or gamma is influenced by tumor location
Authors: Brunda Michael J. , Sulich Viveca , Bellantoni Donna 
Published: February 2007

AbstractThe in vivo anti‐tumor effects of a recombinant human hybrid interferon alpha, rHulFN‐αA/D, and recombinant murine interferon gamma (rMulFN‐γ) were evaluated against experimental hepatic metastases and s.c. tumor growth of the murine reticulum cell sarcoma M5076. The 2 interferons were equally active in preventing experimental hepatic metastases. However, the interferons differed in their relative ability to influence the growth of the same tumor when treatment was initiated following injection of tumor cells. Greater efficacy was obtained in the treatment of metastatic foci in the liver with rHulFN‐αA/D, while rMulFN‐γ was more active in the therapy of an s.c. growing M5076 tumor. These results demonstrate that the same tumor growing at different sites can have different relative sensitivities to IFN‐α and IFN‐γ.
Measurement of plasminogen activator activity from human fibrosarcoma cells by a new microassay
Authors: Rezaee M. , Chen L. , Kramer R. H. 
Published: February 2007

AbstractElevated levels of plasminogen activator (PA) activity have been correlated with neoplasia and may have an important role in tumor‐cell invasion and metastasis. We have developed a new caseinolytlc assay that uses an immunochemical approach to measure the activity of PA elaborated by malignant tumor cells. The highly sensitive assay consists in incubating a source of PA (viable tumor cells, cell extracts, or conditioned medium) with purified plasminogen in micro titer plates pre‐coated with a suitable protein substrate such as casein. Clearance of the immobilized protein substrate by PA‐generated plasmin is then measured by a technique based on the enzyme‐linked immunosorbent assay. In experiments using uro‐kinase as a source of PA, the assay displayed near linearity over several log units of urokinase activity and could detect is little as 10−2 Ploug units of PA activity. Besides successfully measuring PA activity produced by the human HT1080 fibro‐sarcoma cell line, the assay permitted detection of significant plasminogen‐independent proteolytic activity generated by intact tumor cells cultured in direct contact with immobilized protein substrates.
The absence of γ‐glutamyltransferase activity in transport‐dependent methotrexate‐resistant hepatoma cells
Authors: Kruger‐McDermott C. , Johnson T. B. , Rej R. , Vanderhoeven T. , Nair M. G. , Galivan J. 
Published: February 2007

AbstractA cell line derived from H35 hepatoma cells resistant to methotrexate (MTX) as a result of a defective transport system for MTX has been examined to determine how closely the variant resembles the parent cells with regard to other biochemical properties. The capacity of extracts of resistant cells to catalyze the poly‐γ‐glutamylation of MTX was approximately twice as great as that of wild‐type cell extracts. Evidence of similarity between wild‐type and H35 R0.3 cells was derived from the equitoxic activity to both cell lines of non‐classical antifolates and other miscellaneous antineoplastics which act by a variety of mechanisms. Two phenotypic markers of hepatic cell function, α‐aminoisobutyric acid (AIB) transport and tyrosine aminotransferase (TAT) activity inducibility, were present in both cell types, demonstrating the maintenance of these phenotypic properties in the H35 R0.3 cells. γ‐Glutamyltransferase (GGT, EC 2.3.2.2) activity differed in that it was present in wild‐type cells and barely detectable in H35 R0.3 cells. The GGT activity reappeared in the H35 cells when they regained MTX sensitivity after incubation for 14–20 weeks in MTX‐free media. Although defective MTX transport appeared to be correlated with the disappearance of GGT activity in an H35 variant cell line, no functional relationship between them is apparent at this time. It is possible that a lack of GGT activity may be evidence of a more differentiated phenotype in the transport‐resistant cell line.
Effects of retinoids and interferon‐gamma on cultured breast cancer cells in comparison with tumor necrosis factor alpha
Authors: Marth Ch. , Zech J. , Böck G. , Mayer I. , Daxenbichler G. 
Published: February 2007

AbstractThe combination of retinoic acid or tumor necrosis factor alpha (TNF‐alpha) with interferon gamma (IFN‐gamma) resulted in a synergistic amplification of the anti‐proliferative effect of IFN‐gamma on cultured breast cancer cells. Retinoic acid could be replaced by other biologically active retinoids. This synergism was also observed for the induction of 2′‐5′‐oligoac enylate‐synthetase, an enzyme which is not expressed constltutively on BT‐20 human breast cancer cells and not inductile by retinoic acid or TNF‐alpha alone. However, both substances augmented the IFN‐gamma‐mediated expression. On the other hand, only TNF‐alpha and not retinoic acid was able to increase the IFN‐gamma induced expression of HLA‐DR on the cell surface. Both cytokines antagonized the IFN‐gamma effect on detachability of cultured BT‐20 cells. The combinations of retinoic acid with IFN‐gamma increased the down‐regulation of specific binding sites for 125 l‐IFN‐gamma. On the other hand, IFN‐gamma exerted no effect on the cancer traction of the cytoplasmic binding protein for retinoic acid. Data obtained in this study demonstrate a different patten of action between retinoic acid and TNF‐alpha regarding their synergism in combination with IFN‐gamma.
Influence of docosahexaenoic acid in vitro on intracellular adriamycin concentration in lymphocytes and human adriamycin‐sensitive and ‐resistant small‐cell lung cancer cell lines, and on cytotoxicity in the tumor cell lines
Authors: Zulstra J. G. , De Vries E. G. E. , Muskiet F. A. J. , Martini L. A. , Timmer‐Bosscha H. , Mulder N. H. 
Published: February 2007

AbstractAn increase in the therapeutic effects of cancer chemother‐apeutic agents and circumvention of drug resistance in cancer cells might result from an increase in the intracellular drug lave. Alteration of the lipid domain of the cell membrane can result in a higher intracellular drug level. This alteration was achieved in human lymphocytes and in human adriamycin (ADR)‐sensitive and ‐resistant small‐cell lung carcinoma cells in vitro by incubation with docosahexaenoic acid (22:6). Incorporation of the fatty acid in cellular phospholipids was measured by gas chromatographic analysis. A significant increase of 22:6 could be reached without loss of viability in all 3 cell types. Incorporation was demonstrated notably in the phos‐phalidyl choline, phosphatidyl ethanolamine and phosphati‐dylserine, and was most pronounced in the phosphatidyl cholne of the ADR‐resistant line. After a 1‐hr incubation with ADR, a 10–30% increase in intracellular adriamycin concentration was found in all 3 cell types previously incubated for 4 days with 22:6. After 1 hr incubation with ADR there was no increase in cytotoxicity in the sensitive cell line when measured by soft agar clonogenic assay and a partial reversal (52 to 14) of resistance factor (ratio of drug doses to produce 50% growth inhibition) in the resistant cell line. Increasing the time of ADR exposure from 1 to 4 hr further reduced the resistance factc r to 8.6.
Characterization of a new human papillomavirus (HPV 41) from disseminated warts and detection of its DNA in some skin carcinomas
Authors: Grimmel M. , De Villiers E.‐M. , Neumann Ch. , Pawlita M. , zur Hausen H. 
Published: February 2007

AbstractA new human papilla ma virus type (HPV 41), distantly related to known HPV prototypes, was isolated from a patient with disseminated facial, peri‐anal and foot warts (epidermodysplasia verruciformis was not diagnosed). The viral DNA was molecularly cloned in 2 BamHI restriction fragments with sizes of 6.5 kb and 0.98 kb, respectively. The classification of this cloned DNA as a new type is based on the degree of cross‐hybridization with 40 HPV types under conditions of varying stringency. A total of 106 benign and malignant skin lesions, as well as 71 malignant tumours of different origins, were screened for the presence of HPV‐related sequences. In 2 out of 10 squamous‐cell carcinomas and in I of 3 arsenic keratoses HPV 41 DNA sequences could be detected.
The significance of new abnormal isoenzymes of 5′‐nucleotide phosphodiesterase in the diagnosis of human liver cancer
Authors: Lin Ke‐Min , Ye Si‐Yuan , Liu Qi‐Fu 
Published: February 2007

AbstractIn 1986, we reported that abnormal 5′‐nudeotide phosphodiesterase (5′‐NP) (oligonucleate: 5′‐nucleotidohydrolase, EC 3.1.4.1) isoenzymes (5′‐NP 1 and 5′‐NP V + VI) were observed in the serum of patients with liver cancer. The results of the present study show that the 5′‐NP 1 positivity rate is 99.2% (234/236), specificity 74.9%; and the 5′‐NP V + VI posittvity rate is 77.5% (183/236), specificity 95.3% in liver cancer. 5′‐NP 1 positivity rate is 86.7% (13/15) and 5′‐NP V + VI positivity rate is 46.7% (7/15) in metastatic liver cancer. These 3 abnormal isoenzyme bands were all present in the serum of 6 patients with liver cancer before radical resection and disappeared after successful resection, but they were all present in the serum of 6 other liver cancer patients before and after palliative operation. In 2 cases of small liver cancer (diameter less than 4cm), 5′‐NP I and 5‐NP V + VI were strongly positive. It may be considered that the new 5′‐NP abnormal isoenzyme bands are specific markers and will be useful for diagnosis of human liver cancer.
An immunohistochemical study of laminin, type‐IV collagen and type‐III pN‐collagen with relation to reticular fibres in Hodgkin's disease
Authors: Karttunen Tuomo , Alavaikko Martti , Apaja‐Sarkkinen Meeri , Autio‐Harmainen Helena 
Published: February 2007

AbstractThe distribution of aminoterminal propeptide of type‐III procollagen (indicating the presence of type‐III pN‐collagen, i.e., type‐III collagen molecule with a non‐cleaved aminoterminal propeptide}, laminin and type‐IV collagen was studied by immunohistochemical methods. The results were compared with the distribution of reticular fibres using Gomori's reticulin stain. Lymph nodes from 20 cases of Hodgkin's disease (HD) and 3 spleens affected by nodular sclerosis HD were studied. The reticular fibres stained for all the antigens investigated, the strongest reaction being for pN type‐III collagen. Thick fibres stained mainly for type‐III pN‐collagen, the BM proteins being located in a fragmented rim on the surface. The distribution and composition of fibres was similar in both, nodal and extranodal infiltrations. The morphological alterations noted in the fibres comprised (1) compression between nodules in the nodular type of lymphocyte‐predominant HD, and (2) fragmentation, present in collections of histiocytes in lymphocyte‐predominant HD. BM proteins and type‐III pN‐collagen were present in the walls of the sinuses and vessels. The marginal sinuses were often partially spared in spite of extracapsular invasion. Our results suggest that laminin, type‐IV collagen and type‐III pN‐collagen are important components of reticular fibres in HD and that the composition of the, fibres is similar to that seen in the normal lymph node.
Mouse tumor‐associated macrophages do not generate procoagulant activity in response to different stimuli
Authors: Erroi A. , Casali B. , Donati M. B. , Mantovani A. , Semeraro N. 
Published: February 2007

AbstractMononuclear phagocytes, an integral part of the lymphoreticular infiltrate of human and experimental tumors, might contribute to fibrin deposition within malignant tissues through the production of procoagulant activity (PCA). We have studied the PCA of tumor‐associated macrophages (TAM) in 2 poorly immunogenic, metastatic murine sarcomas (mFS6 and MN/MCAI); peritoneal macrophages (PM) from tumor‐bearing and control animals were also studied, as reference cell populations. PCA was evaluated by a one‐stage clotting assay immediately after isolation (basal PCA) and following in vitro stimulation. Basal PCA was very low (< 1 U/104 macrophages) in all cell preparations. Exposure of PM from both normal and tumor‐bearing animals to bacterial endotoxin (lipopolysaccharide, LPS), phorbol myristate acetate (PMA) or the chemotactic peptide formyl‐methionyl‐leucyl‐phenylalanine (FMLP) resulted in 10‐, 7‐ and 3‐fold increases in PCA, respectively. In contrast, TAM from mFS6 and MN/MCAI consistently fatted to generate PCA in response to different concentrations of the same stimuli. Treatment of TAM with aspirin did not affect cell unresponsiveness. Fluorescence microscopy showed that almost all PM were stained with fluorescein isothiocyanate (FITC)‐LPS, while < 10% of the TAM were stained. These data, coupled with previous evidence that TAM have a lower number of specific binding sites for phorbol esters than PM, suggest that the defective responsiveness of TAM to endotoxin, PMA and, possibly, FMLP, is due to the lack, or very tow expression, of binding sites for these agents on the cell surface. The tumor environment may orient the functional status of in situ macrophages in a direction less favorable to the host.
Reducing effects of rodent malaria on hepatic carcinogenesis induced by dietary aflatoxin B1
Authors: Angsubhakorn Subhkij , Bhamarapravati Natth , Sahaphong Somphong , Sathiropas Permsin 
Published: February 2007

AbstractThe present study was undertaken to evaluate the effects of Plasmodium berghei infection on the development of liver tumors induced in male Buffalo rats by aflatoxin B1 (AFBF). Intraperitoneal (i‐p.) injection of 106 parasitized red blood cells (pRBC) into the rat 12 days prior to administration of 2 ppm dietary AFB1 for 10 weeks diminished hepatocellular carcinoma (HCC) induction compared to that observed in rats given AFB1 alone at weeks 60–82. No animals in a control group developed HCC lesions, while only 1 of 22 rats treated With P. berghei alone developed a neoplastic nodule at week 82. These data suggest a reducing effect of P. berghei on the development of liver tumors induced by AFB1 in male Buffalo rats.
Metastasis of a human melanoma cell line in the nude mouse
Authors: Wilson E. Lynette , Gartner Maria F. R. M. , Campbell J. A. H. , Dowdle Eugene B. 
Published: February 2007

AbstractA human melanoma cell tine has been established which when inoculated subcutaneously into nude mice, is consistently metastatic. In order to document blood‐borne spread, it was necessary to excise the primary tumour so prolonging the life of the animal and allowing metastases to become apparent. Macroscopicatly detectable metastatic spread at autopsy was reliably indicated by weight loss of the animals. Metastases were widespread and involved the lungs, abdominal cavity and organs and the gonads. The size of the primary tumour at the time of its removal, and nat the period of s.c. growth, determined the incidence of metastatic disease. Removal of tumours weighing less than 0.6 g prevented metastasis, whereas all of the animals showed widely disseminated disease if the tumour was allowed to attain a size of 1.6 g before excision.
Role of different normal hematopoietic regulatory proteins in the differentiation of myeloid leukemic cells
Authors: Lotem Joseph , Shabo Yosef , Sachs Leo 
Published: February 2007

AbstractThere are 4 different normal myeloid hematopoietic cell growth‐inducing proteins MGI‐I (CSF or IL‐3) that induce normal precursor cells to multiply and form clones containing only macrophages (MGI‐IM = M‐CSF = CSF‐I), only granu‐locytes (MGI‐IG = G‐CSF), both granulocytes and macrophages (MGI‐IGM = GM‐CSF), or granulocytes, macrophages, eosinophils, mast cells, megakaryocytes and erythroid cells (interleukin‐3) (IL‐3). There is another type of normal myeloid regulatory protein (MGI‐2) with no MGI‐I (CSF or IL‐3) activity which can induce differentiation of normal myeloid precursors and certain clones of myeloid leukemic cells. The present results with MGI‐2 and pure recombinant MGI‐IG, MGI‐IGM and IL‐3 have shown that different clones of myeloid leukemic cells can be induced to differentiate by different hematopoietic regulatory proteins. One type of leukemic clone is induced to differentiate to mature cells only by MGI‐2 and is partially differentiated by MGI‐IG, a second type is differentiated only by MGI‐IGM or IL‐3, and other workers have found a third type that is differentiated only by MGI‐IG. The presence of surface receptors does nat necessarily make leukemic cells differentiation competent for these hematopoietic regulatory proteins. All 4 types of MGI‐I (CSF or IL‐3) induce endogenous synthesis of MGI‐2 in normal myeloid precursor ceils. It is suggested that, in addition to their potential therapeutic effect on the development of normal hematopoietic cells, MGI‐2, MGI‐IG, MGI‐IGM and IL‐3 all have the potential for differentiation‐directed therapy of leukemia in leukemic cells that can be differentiated by one of these normal hematopoietic regulatory proteins.