bluuebunny/crossref_metadata_2025_split huggingface dataset:
Murine monoclonal antibody recognizing a 90‐kDa cell‐surface determinant selectively lost by multi‐drug‐resistant variants of cem cells
Authors: Cianfriglia M. , Cenciarelli C. , Tombesi M. , Barca S. , Mariani M. , Morrone S. , Santoni A. , Samoggia P. , Alessio M. , Malavasi F. 
Published: February 2007

AbstractWe describe a murine IgG, monoclonal antibody (MAb56), specific for a cell‐surface protein structure (MC56 determinant) expressed by the human CEM cell line. A large band of approximately 90 kDa was identified as the main specific component of the MC56 determinant. Such a 90‐kDa protein is significantly associated with the drug‐sensitive phenotype, its expression being progressively reduced quantitatively in multi‐drug‐resistant (MDR) variants of CEM cells, according to the extent of drug resistance. In addition, the MC56 determinant is expressed de novo in drug‐sensitive revertant cell lines derived from MDR cells and unreactive with the MAb56. The MAb56 shows a high affinity towards the immunizing drug‐sensitive CEM cell line (Ka =1.86 × 109 L/mole) while not binding to MDR cell variants. The expression of the MC56 molecule on a variety of human cells and tissues makes such a cellular determinant a candidate as a marker for studying the MDR phenomenon both in vivo and in vitro.
B700, a melanoma‐specific antigen, catalyzes metabolism of prostaglandin E2
Authors: Farzaneh Nushin K. , Walden Thomas L. , Hearing Vincent J. , Gersten Douglas M. 
Published: February 2007

AbstractB700 is an albumin‐like mouse‐melanoma‐specific antigen of unknown primary structure and biochemical function. The ability of mouse serum albumin to catalyze weak degradation of prostaglandin E2 has been utilized to compare functional similarities between B700 and mouse serum albumin. Both proteins catalyze the degradation of prostaglandin E2 to prostaglandin A2 and prostaglandin B2. This catalytic ability is related to the amino acid composition of the two proteins within the functional region rather than the 3‐dimensional configuration, since the activity is not altered upon boiling. The primary prostaglandin E2 metabolite in the presence of mouse serum albumin is prostaglandin B2, while prostaglandin A2 predominates in B700 catalyzed degradations. An additional product, presently unidentified, is produced during B700 catalyzed degradation of prostaglandin E2. Our studies indicate that the B700 protein has weak enzymatic activity for prostaglandin E2 similar to that of albumin. To our knowledge, B700 is the only melanoma antigen for which enzymatic activity has been demonstrated.
Til from renal‐cell carcinoma: Restimulation with tumor influences proliferation and cytolytic activity
Authors: Alexander Jeannine , Rayman Patricia , Edinger Mark , Connelly Robert , Tubbs Raymond , Bukowski Ronald , Pontes Edson , Finke James 
Published: February 2007

AbstractTIL were cultured from human renal‐cell carcinoma (RCC) in 1,000 U/ml rIL2 and restimulated with autologous tumor in efforts to establish which conditions would best expand the number of lymphocytes cytotoxic for autologous tumor. Greater cell yields resulted from multiple restimulations of TIL with autologous tumor. In most instances, these TIL lysed autologous tumor better than TIL grown in rIL2 alone. Enhanced proliferation was seen also after restimulation of TIL with allogeneic RCC as well as with tumor cells of non‐renal origin. Although in some instances lysis of autologous tumor appeared to be specific, restimulation with autologous tumor did not consistently result in the generation of specific cytolytic T cells. Attempts to culture more specific cytolytic T cells by using 50 U/ml rIL2 were successful in expanding TIL with enhanced lytic activity; however, this activity was not specific for autologous tumor. The phenotype of the tumorrestimulated TIL generally did not change. In most of the TIL cultures, CD3+ CD4+ cells were predominant with low numbers of CD3+ Leu19+ cells and minimal numbers of CD3‐Leu 19+ cells. Thus, the cytotoxic response to tumor was mediated by T cells and not NK cells. Overall, our data indicate that restimulation of TIL with autologous tumor may be beneficial for growing larger numbers of cells which have increased lytic activity and for prolonging the presence of lytic activity among the expanded TIL.
Cancer procoagulant in serum of rats during development of experimental epithelioma
Authors: Mielicki W. , Wierzbicki R. 
Published: February 2007

AbstractThe activity of cancer procoagulant (CP) during the development of Guérin epithelioma was studied in the blood of Wistar rats. Blood was collected from the carotid artery and, after clotting, proteins adsorbing on aluminum hydroxide were removed from the serum. Then procoagulant activity was determined in the test system without factor VII by means of substrate S‐2222 specific for factor Xa. A statistically significant increase in the activity of CP in serum was detected, coinciding with the period of intensive tumor growth (15th–25th day of disease).
Persistent infection of rabbits with HTLV‐I: Patterns of anti‐viral antibody reactivity and detection of virus by gene amplification
Authors: Cockerell Gary L. , Lairmore Michael , De Barun , Rovnak Joel , Hartley Trudie M. , Miyoshi Isao 
Published: February 2007

AbstractTwo groups of rabbits were inoculated on the day of birth or at 4 weeks of age with a human T‐cell leukemia virus type‐I (HTLV‐I)‐infected and transformed rabbit cell line (Ra‐I). Rabbits seroconverted to HTLV‐I, as determined by indirect immunofluorescence, by 3 weeks after inoculation and remained persistently seropositive during a 22‐month period of observation. Seroconversion did not occur in salineinoculated controls. Using Western immunoblotting and radio‐immunoprecipitation, persistent seroconversion occurred against viral antigens p24, p55 and gp68, while reactivity to p19 was variable between rabbits. Using the polymerase chain reaction (PCR) with HTLV‐I gag and pol primer pairs, HTLV‐I sequences were demonstrable in peripheral blood mononuclear cells and other tissues collected at 70 and 90 weeks after inoculation. DNA extracts from normal rabbit tissue remained negative under the same conditions. No qualitative or quantitative changes in leukocytes or erythrocytes were detected in the infected rabbits and no clinical signs could be directly attributed to infection with HTLV‐I.
Multidirectional differentiation in a newly established human epithelioid sarcoma cell line (GRU‐1) with co‐expression of vimentin, cytokeratins and neurofilament proteins
Authors: Gerharz C. D. , Moll R. , Ramp U. , Mellin W. , Gabbert H. E. 
Published: February 2007

AbstractA new permanent cell line (GRU‐1) derived from the lymph‐node metastasis of a human epithelioid sarcoma was established in tissue culture. Immunohistochemically, the original tumor had exhibited an intriguing potential for multidirectional differentiation with features of mesenchymal, epithelial and neural differentiation, evidenced by the co‐expression of vimentin, cytokeratins and neurofilament proteins, respectively. This capability for multidirectional differentiation was fully preserved in the cultured cells. GRU‐1 tumor cells proved to be uniformly positive for vimentin and a considerable proportion of the tumor cells exhibited a positive reaction for cytokeratins and neurofilament proteins. The neural markers neuron‐specific enolase (NSE) and synaptophysin were observed in a small proportion of GRU‐1 cells. Ultrastructurally, GRU‐1 cells showed desmoplastic activity in vitro, being enmeshed by collagen fibrils. DNA distribution, as studied by flow cytophotometry, revealed DNA‐diploidy (DNA index =1) and a G0/G1‐proportion of 70.5%. After heterotransplantation in nude mice, GRU‐1 tumor cells expressed vimentin and cytokeratin only, whereas the neural markers could not be further demonstrated.
Yolk‐sac carcinoma develops spontaneously as a late occurrence in slow‐growing teratoid tumors produced from transplanted 7‐day mouse embryos
Authors: Van Berlo R. J. , Oosterhuis J. W. , Schrijnemakers E. , Schoots C. J. F. , De Jong B. , Damjanov I. 
Published: February 2007

AbstractSeven‐day embryos of BALB/c mice transplanted underneath the kidney capsule of adult syngeneic recipients form either benign teratomas or teratocarcinomas, which can be distinguished from one another histologically at 8 weeks postembryonic transplantation. Embryo‐derived (ED) teratomas were allowed to remain in the host for an additional period up to 1 year after embryo transplantation, to test their malignant potential. It was found that a considerable number of slow‐growing small tumors derived from embryonic transplant give rise to parietal yolk‐sac carcinomas. A proportion of these tumors contained foci of visceral yolk‐sac and trophoblastic differentiation, which gradually disappeared in successive transplantations. We conclude that parietal yolk‐sac carcinoma develops as a late event in some ED teratomas. These malignant tumors originate either from small foci of yolk sac originally included in the grafted embryo or, more likely, from the yolk sac formed from the differentiating embryonic stem cells.
Increase in topoisomerase‐II‐mediated dna breaks and cytotoxicity of VP16 in human U937 lymphoma cells pretreated with low doses of methotrexate
Authors: Lorico Aurelio , Boiocchi Mauro , Rappa Germana , Sen Soumitra , Erba Eugenio , D'Incalci Maurizio 
Published: February 2007

AbstractPre‐treatment with low, non‐toxic concentrations (0.04μM) of methotrexate (MTX) for 16 hr increased etoposide (VP16)‐induced growth inhibition and cytotoxicity in the U937 human histiocytic lymphoma cell line. VP16 cytotoxicity was significantly potentiated when the drug was given for 2 hr immediately after MTX pre‐treatment or between 2 and 4 hr or 4 and 6 hr after recovery from MTX pre‐treatment. By 24 hr after recovery from MTX, no potentiation was evident. The increased cytotoxicity of VP16 was associated with an increase in drug‐induced DNA breaks as assessed by the alka‐line elution method after proteinase K digestion. The amount of DNA single‐strand breaks (DNA SSB) increased when the drug was given 0, 2, and 4 hr after MTX pre‐treatment. DNA SSBs induced by the drug between 6 and 24 hr after MTX pre‐treatment were similar to those seen in cells without pre‐treatment. The amount of DNA double‐strand breaks (DNA DSB) caused by VP16 increased significantly when the drug was given 4 hr after recovery from MTX pre‐treatment. VP16‐induced DNA DSBs were still higher 6 hr after MTX pre‐treatment, but by 24 hr they were similar to those observed in MTX‐untreated cells. Flow cytometric analysis showed that MTX pre‐treatment was causing an accumulation of U937 cells at the G1‐S boundary of the cell cycle. When MTX was removed, a wave of synchronization followed. Using Western blot electrophoresis and polyclonal antibodies to antitopoisomerase II, we found that MTX pre‐treatment raised the cellular topoisomerase II content. Our findings suggest that the potentiation of VP16 cytotoxicity on U937 cells by low, non‐toxic MTX pre‐treatment is due to a larger fraction of S‐phase cells containing a higher concentration of topoisomerase II, which is the putative target of VP16 action.
Effect of vip on the glycogen metabolism of human colon adenocarcinoma cells studied by 13C nuclear magnetic resonance spectroscopy
Authors: Galons Jean‐Philippe , Fantini Jacques , Vion‐Dury Jean , Cozzone Patrick J. , Canioni Paul 
Published: February 2007

AbstractMetabolic pathways of glucose utilization have been investigated in a human colon adenocarcinoma cell line (HT29) using carbon‐13 Nuclear Magnetic Resonance spectroscopy. HT29 cells were adapted to grow on a polystyrene beaded microcarrier and were perfused when attached to the beads in a specially designed NMR cell. Abnormalities in carbohydrate metabolism already observed in several cancer cells were studied in HT29 cells fed with (I‐13C)‐enriched glucose. The cells were first perfused with a glucose‐free medium for 2 hr in order to deplete the intracellular store of glycogen, and they were subsequently perfused with a medium containing enriched glucose at an initial concentration of 5.5 mM. Sequential 13C‐NMR spectra, recorded at 100.5 MHz (5 min accumulation), show that HT29 cells were able to utilize glucose through the glycolytic pathway while storing glucose as glycogen (glucose was utilized at a rate of 3.9 μmol/mg protein/hr). The glycolytic activity determined by the amount of lactic acid produced was 4.6 μM/mg protein/hr, corresponding to the formation of 1.2 lactic acid per glucose molecule. Glycogen accumulation corresponded to 16 μg/mg of protein. Treatment of HT29 with 10 nM vasoactive intestinal peptide (VIP) induced a transient decrease in the level of labelled glycogen to 50% of the initial value. Control level was recovered 12 min after VIP loading.
Inhibition of growth and squamous‐cell differentiation markers in cultured human head and neck squamous carcinoma cells by β‐all‐trans retinoic acid
Authors: Jetten Anton M. , Kim Jun S. , Sacks Peter G. , Rearick James I. , Lotan Dafna , Hong Waun K. , Lotan Reuben 
Published: February 2007

AbstractVitamin A and some of its metabolites such as β‐all‐trans retinoic acid (RA) have been implicated in the regulation of differentiation of normal and malignant epithelial cells in vivo and in vitro. In the present study effects of RA on the growth and differentiation of 7 cell lines derived from human head and neck squamous‐cell carcinomas (HNSCCs) were examined. RA (>0.01 μm) inhibited the proliferation in monolayer culture of 6 of 7 HNSCC cell lines. One cell line (UMSCC‐35) was very sensitive, 5 (UMSCC‐10A, ‐19, ‐30, ‐22B and HNSCC 1483) were moderately sensitive, and I (HNSCC 183) was insensitive. Three of the cell lines (UMSCC‐22B, ‐30, and HNSCC 1483) were capable of forming colonies in semisolid medium—a capability that was suppressed by RA. The HNSCC cell lines expressed various levels of the squamouscell differentiation markers type 1 (particulate, epidermal) transglutaminase (TGase) and cholesterol sulfate (CS). RA treatment (1 μ, 6 days) decreased TGase activity by more than 50% in 3 (UMSCC‐10A, ‐228 and 1483) of the 7 cell lines, and the effect on UMSCC‐22B was dose‐dependent. Type II TGase (soluble, tissue type) activity was detected in 3 cell lines, and after RA treatment its activity increased in HNSCC 1483 and 183 cells and decreased in UMSCC‐19. Following RA treatment, CS levels decreased by 20, 25, 70, 76, 89 and 91% in cell lines UMSCC‐30, ‐10A, 183, UMSCC‐35, ‐22B, and HNSCC 1483, respectively. The suppression by RA of CS accumulation in the 1483 cells was dose‐dependent. Cholesterol sulfotransferase activity, which is responsible for CS synthesis, was suppressed by 40–97% after RA treatment of UMSCC‐19, ‐22B, and HNSCC 1483. Our results demonstrate that RA inhibits the growth and decreases the level of 2 squamous differentiation markers in HNSCC cells.
Tumour cells which develop resistance to cytolysis by tumour necrosis factor have a different glycoform of a 105‐kda glycoprotein and lose the capacity to invade and metastasize
Authors: Lynne Neale M. , Fiera Rosemary A. , Matthews Nicholas 
Published: February 2007

AbstractA plastic‐adherent variant of human myelomonocytic leukaemia cells (U937) is highly susceptible to direct TNF cytolysis in vitro. Previously, we found that a subline selected for resistance to TNF cytolysis (U937/R) was much less motile and more plastic‐adherent than the parental line. In the present study we show that U937 and U937/R cells have different glycoforms of a 105‐kDa cell‐surface glycoprotein. This protein is predominantly N‐glycosylated and has the physicochemical properties of the LAMP‐1 glycoprotein. In nude mice, U937 cells are highly malignant whereas U937/R cells form a benign, encapsulated tumour. Therefore, possession of a different glycoform of the 105‐kDa glycoprotein by U937/R cells correlates not only with loss of TNF susceptibility but also with reduced invasiveness and metastasis.
DNA‐ploidy as prognostic factor in prostatic carcinoma
Authors: Haugen O. A. , Mjølnerød O. 
Published: February 2007

AbstractDNA‐ploidy in 143 cases of prostatic carcinoma was assessed by flow cytometric analysis of paraffin‐embedded biopsy material. The majority of the tumours (64.3%) were diploid, but in advanced stages the DNA‐aneuploidy rate increased from 15 to over 60%. No hypoploid tumour was observed and most of the hyperploid tumours were neartetraploid. DNA‐aneuploidy was also strongly related to histological grade. Survival analysis using Cox multivariate regression model revealed that low histological grade (high Gleason score), advanced stage and increased level of prostatic acid phosphatase were the most important prognostic factors. DNA‐ploidy per se did not contribute independently as a predictor of survival.
A case‐control study of hepatocellular carcinoma in osaka, Japan
Authors: Tsukuma Hideaki , Hiyama Tomohiko , Oshima Akira , Sobue Tomotaka , Fujimoto Isaburo , Kasugai Hiroshi , Kojima Junnosuke , Sasaki Yo , Imaoka Shingi , Horiuchi Naruto , Okuda Shigeru 
Published: February 2007

AbstractA case‐control study was undertaken to evaluate the roles of hepatitis B virus (HBV), blood transfusion, alcohol drinking and cigarette smoking in the etiology of hepatocellular carcinoma (HCC) in Osaka, Japan. A total of 229 cases and 266 hospital controls were included in our study. The relative risks of HCC obtained after adjustment for age, sex and other important variables were 14.3 (95% confidence interval (CI): 5.7–36.3) for HBsAg positives, 4.3 (95% CI: 1.9–9.6) for blood recipients and 3.2 (95% CI: 2.0–5.1) for heavy drinkers. A statistically significant dose‐response relationship was observed between the risk of HCC and total alcohol consumption. The overall risk for HCC was also significantly elevated among smokers; however, there was no consistent dose‐response relationship between the risk and cigarette consumption. We conclude that HBV, blood transfusion and excessive alcohol drinking play important roles in the etiology of HCC in Osaka, Japan. Further investigation is needed to clarify the possible etiological role of smoking.
The 4th nation‐wide study of adult T‐cell leukemia/lymphoma (ATL) in Japan: Estimates of risk of ATL and its geographical and clinical features
Authors: Tajima K. ,   The T‐ and B‐Cell Malignancy Study Group,   Co‐Authors
Published: February 2007

AbstractTo estimate the annual incidence of adult T‐cell leukemia/lymphoma (ATL) by district in Japan, a large‐scale nationwide survey of ATL and of non‐Hodgkin's lymphoma was performed in 1988. Questionnaires for the registration of ATL and of T‐cell and non‐T‐cell lymphoma were distributed to the physicians in charge of this survey in 1,287 hospitals with 200 or more beds throughout Japan. From the positive rate of anti‐HTLV‐I antibody in adults, the annual incidence of ATL was estimated at 697, independently of the present survey. In fact, 657 cases (47% of the estimated number), newly diagnosed during the 2 years January 1986 to December 1987, were registered from 191 general hospitals throughout Japan. Major results obtained from the present survey are as follows: (1) among all ATL cases registered, 51% were from Kyushu and 29% were from metropolitan areas (Kanto, Chubu and Kinki) and most, but not all, patients with ATL in the metropolitan areas had come from the ATL‐endemic areas and settled in the metropolitan areas; (2) the estimated annual incidence rates of ATL per million adults were 40.4 in males and 26.4 in females in Kyushu, the overall risk of ATL being 1.5 times as high in males as in females; (3) the age‐specific incidence rate in Kyushu increased steeply with age until the age of 70, and then decreased markedly in both sexes; (4) the ratio of T‐cell versus non‐T‐cell lymphomas was 2.9 in Kyushu but 0.5 in other districts of Japan, however, this difference regressed to the average for the whole of Japan if ATL cases were excluded; (5) 26.5% of patients with ATL had a family history of cancer, and among these, 14 (8.2%) were ATL, 21 (12.2%) were lymphoma and 17 (9.9%) were hematopoietic malignancies, the incidence of which was markedly higher than in the general population; (6) with regard to clinicopathological features of ATL, there were more advanced cases in south Kyushu than in other districts, however, these differences were not statistically significant. To clarify the chronological changes and geographical variations in the annual incidence of ATL in Japan, continuous systematic nationwide surveillance is necessary and further nation‐wide studies are being prepared.
A simplified immuno‐enzymetric assay of the epidermal growth factor receptor in breast tumors: Evaluation in 282 cases
Authors: Grimaux M. , Mady E. , Remvikos Y. , Laine‐Bidron C. , Magdelenat H. 
Published: February 2007

AbstractThe epidermal growth factor receptor (EGF‐R) is currently being investigated in human clinical oncology, and particularly in breast cancer, as a potential prognostic factor and a biological target for therapy. As an alternative to the 125I‐EGF binding assay, we propose a sensitive immuno‐enzymetric assay (IEMA) suitable for EGF‐R assay in breast cancer. The assay is performed on solubilized extracts of the 105,000 g pellet of a tumor homogenate, allowing estrogen (ER) and progesterone (PR) assays to be made on the cytosol. The IEMA is performed on 96‐well plates coated with the monoclonal anti‐EGF‐R antibody RI, through an anti‐mouse IgG2b bridge. Trapped EGF‐R in the samples is covered by a second monoclonal antibody (MAb), 528, and revealed by an antilgG2a‐peroxidase complex. The sensitivity is I fmol/mg membrane protein, and the assay can be performed on tissue samples down to 50 mg. Two hundred and twenty primary ductal breast carcinomas assayed by this method showed a log normal distribution with a modal value of 8 fmol/mg prot., a mean at 18 and a median at 13 fmol/mg prot. EGF‐R‐rich tumors (>20 fmol/mg prot.) were highly correlated with the absence of estrogen receptors and/or with a high histological grade (SBR III). Our data demonstrate the validity of the IEMA assay of EGF‐R in human breast tumors.
Somatostatin receptors are present in small‐cell but not in non‐small‐cell primary lung carcinomas: Relationship to EGF‐receptors
Authors: Reubi J. C. , Waser B. , Sheppard M. , Macaulay V. 
Published: February 2007

AbstractSixteen primary human lung tumours were analysed for their content of somatostatin receptors using receptor autoradiography with somatostatin‐28 and somatostatin octapeptide analogues as radio‐ligands. Two out of 4 small‐cell lung carcinomas were somatostatin receptor‐positive, with a high density of homogeneously distributed receptors on tumour tissue only. Somatostatin receptors were characterized in one of the tumours in homogenate binding assay as saturable, high‐affinity binding sites (KD =0.53 nM) with a number of sites (Bmax) equivalent to 189 fmoles/mg protein. These sites were specific for somatostatin, since only biologically active somatostatin analogues but not unrelated peptides showed high‐affinity binding. Both receptor‐positive patients had limited disease; furthermore, the small‐cell lung carcinoma patient with the longest survival was receptor‐positive, while the one with the shortest survival was receptor‐negative. None of the 12 non‐small‐cell lung carcinomas (5 squamous carcinomas, 7 adenocarcinomas) contained somatostatin receptors. For comparison, epidermal growth factor receptors were found in all non‐small‐cell lung carcinomas. Neuroendocrine features (synaptophysin, chromogranin, neuronspecific enolase, protein gene product 9.5) were present in all small‐cell lung carcinomas but absent in non‐small‐cell lung carcinomas. Given the receptor‐mediated action of somatostatin in other neuroendocrine tumours, these data may have a bearing on the clinical application of somatostatin analogues in patients with small‐cell lung carcinomas.