bluuebunny/crossref_metadata_2025_split huggingface dataset:
Enhanced expression of human T‐cell leukemia/lymphoma virus in neoplastic T cells induced to proliferate by phorbol ester and interleukin‐2
Authors: Vyth‐Dreese Florry A. , De Vries Jan E. 
Published: February 2007

AbstractPeripheral blood T cells from a patient with T‐cell chronic lymphocytic leukemia (T‐CLL) failed to respond to mitogenic lectins or alloantigens but could be induced to proliferate by the addition of exogenous interleukin‐2 (IL‐2). The T‐CLL cells also proliferated in response to 12‐O‐tetradecanoyl phorbol‐13‐acetate (TPA), or to TPA in combination with phytohemagglutinin (PHA). These TPA‐mediated proliferative responses were transient, and only small but significant amounts of IL‐2 activity were generated. In contrast, no IL‐2 activity was produced after the T‐CLL cells had been stimulated with PHA only. The T‐CLL cells that were induced to proliferate with PHA and exogenous IL‐2 could be maintained in continous culture by the addition of exogenous IL‐2 at regular intervals. These continuously proliferating T‐CLL cells failed to produce IL‐2 constitutively. However, they could be induced to produce IL‐2 activity by stimulation with TPA or TPA plus PHA. Irradiation of the proliferating T‐CLL cells prior to incubation with TPA or TPA plus PHA resulted in a 9‐fold increase in IL‐2 activity, suggesting that the proliferating T‐CLL cells were able to consume the IL‐2 they produced. Studies on the presence of human T‐cell leukemia/lymphoma virus (HTLV) in the fresh and proliferating T‐CLL cells revealed that 12% of the fresh cells expressed the HTLV p19 structural core protein. HTLV p19 expression was strongly enhanced in the T‐CLL cells induced to proliferate by TPA (66%) and in the continuously growing IL‐2‐dependent T‐CLL cells (82%). In the latter culture, but not in the fresh T‐CLL cells, type‐C virus particles were observed. These results indicate that HTLV expression correlates with T‐CLL cell proliferation but not with IL‐2 production by these cells.
Modulation of K562 cells with sodium butyrate. Association of impaired NK susceptibility with sialic acid and analysis of other parameters
Authors: Werkmeister Jerome A. , Pross Hugh F. , Roder John C. 
Published: February 2007

AbstractNeuraminidase treatment of parental and butyrate‐induced K562 tumor cells was associated with an increase in natural killer (NK) susceptibility of these target cells. The degree of enhancement with neuraminidase was significantly greater for the NK‐resistant (NRR) butyrate‐differentiated K562 cells so that the relative difference between the parental NK‐sensitive (NKS) K562 line and its induced NKR variants, in terms of NK sensitivity, was no longer five‐ or six‐fold but only two‐fold. The predominant reason for the altered NK susceptibilities of the target cells after neuraminidase treatment was an increase in the target‐cell‐binding ability of these cells as assessed by a direct conjugate‐forming cell assay using Percoll‐enriched NK cells and cold target competition assays. The enhancement did not appear to be due simply to an increased membrane‐membrane attraction caused by a reduction of net negative cell surface charges since protamine sulphate, a positively charged molecule, had no effect on NK activity. Compared with the NKS parental K562 tumor cells, the NKR butyrate‐induced cells had 3.6‐to 4.0‐fold higher sialo‐transferase activities and were associated with significantly greater amounts of cell surface sialic acid detected both in sialyl glycoproteins (2.2‐ to 2.9‐fold higher) and particularly within ganglioside extracts (6.2‐ to 13.6‐fold higher). In conformity with the marked neuraminidase enhancement of NK‐mediated cytolysis of the butyrate‐induced targets, these NKR cells were associated with significantly enhanced levels of neuraminidase‐accessible sialic acid compared to the NKS parental K562 cell line. Other parameters such as sensitivity to superoxide radicals, intrinsic superoxide dismutase levels, altered membrane repair mechanisms and transferrin competition, were not significantly different between the NKS and NKR target phenotypes. Sugar inhibition studies demonstrated an enhanced inhibition against the butyrate‐induced cells with a variety of neutral sugars. The degree of inhibition with phosphorylated sugars was comparable between the parental and induced K562 tumor target cells and is consistent with our previous findings showing that these hexose phosphates may be inhibiting cytolysis at a step independent of target‐cell recognition.
In vitro production of rabbit macrophage tumor cell cytotoxin
Authors: Fisch Harvey , Gifford George E. 
Published: February 2007

AbstractRabbit pulmonary lavage cells, consisting mostly of macrophages (90–95%), cultured in the presence of LPS, secreted tumor cell cytotoxin that was similar to tumor necrosis serum cytotoxin. A similar cytotoxin was produced by phorbol‐ester‐pretreated rabbit bone marrow cells and by blood mononuclear cells when cultured in the presence of LPS. All cytotoxins had molecular weights of approximately 48,000 daltons by gel filtration and eluted from DEAE‐Sephadex between 0.28 and 0.32 m NaCl. All were stable to 56°C for 60 min, but labile to 70°C for 20 min. B16C3 melanoma cells and mouse embryo fibroblasts were resistant to the cytotoxins. By 3 h in culture, all effector cells secreted detectable cytotoxin levels. Kinetics of cytotoxin production differed for effector cells derived from the different tissues. No additional cytotoxin production could be demonstrated after 30 h in pulmonary lavage or bone marrow cell cultures, despite a change to fresh medium with LPS. Actinomycin D (1 μg/ml) added with LPS inhibited cytotoxin production (>95%) by pulmonary lavage cells. Delaying addition of actinomycin D after LPS treatment demonstrated that messenger RNA production for cytotoxin was completed by 2 to 6 h.
MHC imbalance and metastatic spread in Lewis lung carcinoma clones
Authors: Eisenbach Lea , Segal Shraga , Feldman Michael 
Published: February 2007

AbstractImbalance in the Kb and Db region encoded molecules is observed in Lewis lung carcinoma clones. The uncloned metastatic population and the D122 high‐metastatic clone show no expression of H‐2Kb products, while the non‐metastatic A9 clone expresses Kb products. Twenty‐nine new subclones of 3LL and A9 were analyzed for D‐end and K‐end membrane expression, primary growth rate and metastatic spread. We show that the imbalance in H‐2Kb to H‐2Db is correlated with metastatic properties of a given clone, but local tumor growth is not. A “low Kb/low D9” phenotype is nonmetastatic as is a “high Kb/high Db” phenotype; a “low Kb/high Db” is highly metastatic and a “medium Kb/high Db” is moderately metastatic. We find support for this notion of imbalance in experiments on MHC modulation by interferon and retinoic acid. Interferon increases both Kb and Db expression of A9 and D122 clones yet the net increase of Db was greater than Kb. This was associated with an increase in metastasis formation. Retinoic acid increases the expression of the Db gene product on the nonmetastatic A9, clone, without apparent changes in Kb expression. This treatment shifts the A9 to a high‐metastatic phenotype. The significance of this imbalance to the tumor — host relationship is discussed.
Plasminogen activator in normal and tumor‐bearing mice
Authors: Bruesch Margaret R. , Johnson Gail L. , Palackdharry Carol S. , Weber Michael J. , Carl Philip L. 
Published: February 2007

AbstractThe plasminogen activator levels of a series of murine tumors commonly used in cancer drug screening were determined and compared to the levels found in normal mouse tissues. Tumors high in plasminogen activator included the B16 and colon 26. The Lewis lung and M5076 carcinoma showed an intermediate level of activity, while the plasminogen activator activity in the L1210 leukemia and colon 38 was barely elevated above background. The specific activity of the enzyme (per μg protein) in extracts of B16 and colon 26 was three or four times higher than in the most active normal organs surveyed (kidney, lung, brain and intestine). The high level of plasminogen activator activity measured in extracts of the B16 tumor was reflected in a substantial elevation of the levels of fibrin degradation products in the serum of mice carrying this tumor. This result suggests that the tumor‐associated plasminogen activator activity is less subject to inhibitory controls in vivo than is the plasminogen activator of most normal tissues, since the total mass of the tumor was far less than the total mass of the fibrinolytically active tissues, and yet the bulk of the fibrin degradation products were caused by the tumor. We conclude that the high levels of plasminogen activator activity which are observed in many human tumors are found only in some of the transplantable murine tumors. Since this enzyme is active at an increased level in vivo in mice carrying the B16 tumor, plasminogen activator may be a suitable target for selective, enzyme‐activated chemotherapy with this tumor test system.
HLA and nasopharyngeal carcinoma in chinese —A further study
Authors: Chan S. H. , Day N. E. , Kunaratnam N. , Chia K. B. , Simons M. J. 
Published: February 2007

AbstractThis paper reports the results of 8 years of HLA typing of newly diagnosed nasopharyngeal carcinoma (NPC) patients among Chinese in Singapore, and compares the HLA profile of NPC cases with that of the normal Chinese population. Earlier results had indicated an association with A2 and BW46, but the heterogeneity of the earlier case series, which contained a proportion of long‐term survivors, obscured other aspects of the relationship. In this paper, the risk associated with A2 (relative risk = 1.5) and BW46 (relative risk = 1.9) is confirmed, showing a much higher relative risk in the presence of both antigens, and a risk is also demonstrated for B17 (relative risk = 2.1). Relative risks of less than unity are observed for All (relative risk = 0.5) and B13 (relative risk = 0.5). Data from family studies indicate the importance of the haplotype A2.BW46 in determining risk for NPC.
Protective effect of butylated hydroxytoluene against induction of gastric cancer by N‐methyl‐N′‐nitro‐N‐nitrosoguanidine in wistar rats
Authors: Tatsuta Masaharu , Mikuni Tomiko , Taniguchi Haruo 
Published: February 2007

AbstractThe effects of butylated hydroxytoluene (BHT) on the incidence and histology of gastric cancers induced by oral administration of N‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG) were investigated in Wistar rats. Oral administration of 1.0% BHT in regular chow pellets during treatment with MNNG for 25 weeks significantly reduced the incidence of gastric cancers in experimental week 40. BHT had no influence on the histological type of adenocarcinomas induced in MNNG‐treated rats. BHT alone induced slight glandular hyperplasia, but not moderate glandular hyperplasia or gastric cancer.
Sodium butyrate produces concordant expression of “early placental” alkaline phosphatase, pregnancy‐specific beta1‐glycoprotein and human chorionic gonadotropin beta‐subunit in a newly established uterine cervical cancer cell line (SKG‐IIIa)
Authors: Nozawa Shiro , Engvall Eva , Kano Shojiro , Kurihara Soju , Fishman William H. 
Published: February 2007

AbstractThe production of early and term placental alkaline phosphatase (ALP), human chorionic gonadotropin betasubunit (β‐hCG) and pregnancy‐specific beta1‐glycoprotein (SP1) was confirmed in the newly established uterine cervical cancer call line SKG‐IIIa. Treatment of these cells in culture with sodium butyrate caused an increase of all of these oncodevelopmental proteins. On the other hand, prednisolone treatment enhanced only term placental ALP, while it reduced early placental ALP, β‐hCG and SP1. These data suggested that such oncotrophoblastic proteins as early placental ALP, β‐hCG and SP1 were con‐cordantly modulated by butyrate and prednisolone. These findings may support the possibility of the reex‐pression of sets of development phase‐specific genes in cancer cells.
Effect of 13‐cis‐retinoic acid and 4‐hydroxyphenyl‐all‐trans‐retinamide on human tumor colony formation in soft agar
Authors: Meyskens Frank L. , Alberts David S. , Salmon Sydney E. 
Published: February 2007

AbstractWe studied the effects of 13‐cis‐retinoic acid (13cRA) and 4‐hydroxyphenyl‐all‐trans‐retinamide (4HPR) on the proliferation of clonogenic human tumor colony‐forming units (TCFU) from patient biopsies in soft agar. Continuous exposure (5 × 10−6M) to 13cRA and 4HPR reduced colony formation to less than 50% of control in 49% and 31% of cases, respectively. This suggests that these retinoids have antiproliferative activity against TCFU. Continuous exposure to 13cRA reduced the number of TCFU to 30% of control in 22.6% of cases while 4HPR reduced colony formation to less than 30% of control in only 10% of patients tested. Prospective in vitro/in vivo correlations for 13cRA indicated that clinical resistance was correctly predicted in 4 of 4 cases treated while clinical response was predicted in 2 of 2 cases (one minor and one partial response). These data suggest that retinoids may have modest antitumor effects and that inhibition of TCFU growth in vitro may be used to screen for such activity.
Effects of anti‐transferrin receptor antibodies on growth of normal and malignant myeloid cells
Authors: Taetle Raymond , Honeysett J. Michael , Trowbridge Ian 
Published: February 2007

AbstractThe effects of three monoclonal antibodies (B3/25, 43/31, and 42/6) reactive with human transferrin (Tf) receptors on growth of normal and malignant myeloid cells were examined using in vitro culture techniques. When added directly to cultures, all three antibodies caused dose‐dependent inhibition of normal granulocyte/macrophage progenitor (CFU‐GM) growth. Monoclonal antibody 42/6 was by far the most potent of the three, with an ID50 of < 5μg/ml. Identical effects were seen on CFU‐GM from three patients with chronic myelogenous leukemia. Growth of colonies from two myeloid leukemia cells lines (KG‐1, HL60) was also inhibited by all three antibodies, and these cells were generally more sensitive than normal CFU‐GM. Blast colony‐forming cells from three patients with acute non‐lymphocytic leukemia were relatively resistant to the antibodies, and CFU‐GM from a patient with myeloid metaplasia were resistant (ID50 > 50 μg/ml) to 42/6. In liquid culture, growth of the leukemic cell lines was inhibited by saturating concentrations of the three antibodies, although in both liquid and colony culture recovery was seen even after exposure to antibody for periods of up to 72 h. Analysis of the cell‐cycle status of these cells showed that the antibodies did not cause accumulation of cells in any particular phase of the cell cycle. Addition to cultures of large quantities of human Tf failed to reverse the inhibitory effects of the antibodies. Competitive binding studies on the leukemia cell lines showed that only 42/6 inhibited binding of Tf to its receptor, although all three antibodies inhibited cell growth. Addition of Fe chelate (as ferric nitriloacetic acid, FeNTA) failed to reverse the inhibitory effects of the antibodies on CFU‐GM and HL60 cells, but had variable effects on KG‐1 cell growth. FeNTA fully reversed inhibitory effects of 42/6 on KG‐1 cells. We conclude that monoclonal antibodies to Tf receptors can inhibit growth of both normal and malignant myeloid cells. Overall, no selectivity for malignant vs normal cells is apparent, although malignant cells from one individual were more sensitive to colony inhibition by 43/31 monoclonal antibody than normal CFU‐GM.
A mouse hepatocyte carbohydrate‐specific receptor and its interaction with liver‐metastasizing tumor cells
Authors: Cheingsong‐Popov R. , Robinson P. , Altevogt P. , Schirrmacher V. 
Published: February 2007

AbstractSpontaneous high‐metastatic variants (ESb) of the DBA/2 mouse lymphoma L5178Y which show heavy liver involvement were found to form rosettes in vitro with isolated autologous hepatocytes, whilst low‐metastatic sublines of the same tumor (Eb) did not. An analysis of the molecules involved in the hepatocyte:tumor cell interaction was performed by affinity adsorption and SDS‐polyacrylamide gel electrophoresis of 125I‐labelled membrane components from either the hepatocytes or the tumor cells. The hepatocytes were found to bind ESb tumor cells through lectin‐like hepatic binding proteins (HBP) with molecular weights of 52, 56 and 110 Kd and specificity for D‐galactosyl and N‐acetyl‐D‐galactosaminyl residues. More than 10 different cell surface glycoproteins of ESb tumor cells and none of Eb‐type tumor cells served as ligands in the hepatocyte interaction. The low‐metastatic subline Eb formed hepatocyte rosettes only after neuraminidase pretreatment, indicating that lectin binding carbohydrate structures existed in a cryptic form masked on these cells by sialic acid. Although lectin‐car‐bohydrate interactions have been found to play a crucial role in many intercellular recognition processes, this apparently is the first molecular description of such an interaction between organ‐derived normal parenchymal cells and tumor cells. The possible relevance of such an interaction for cancer metastasis is suggested by the finding that spleen‐selected ESb sublines differed from liver‐selected ones in their organotropism as well as in their ability to form hepatocyte rosettes.
Studies of the mechanisms for the induction of in vivo tumor immunity. VII. Development of specific antitumor immunity in progressors and regressors
Authors: Ting Chou‐Chik , Zhang Shu‐Ren 
Published: February 2007

AbstractThe present study was aimed at comparing the development of specific antitumor immunity between hosts with progressively growing tumors and hosts with regressing tumors. The experiments were performed with a Friend virus‐induced leukemia FBL‐3 in syngeneic C57BL/6 mice. The specific antitumor immunity was determined by in vitro cell‐mediated cytotoxicity assay and in vivo tumor neutralization test. Both the systemic immunity (demonstrated in spleen) and immunity developed at tumor site were examined. For progressors, the tumor site was in the peritoneal cavity. For regressors, it was in a subcutaneous site of both flanks. Testing by the cell‐mediated cytotoxicity assay showed that immune hosts and regressors had higher levels of systemic immunity than the progressors. However, when lymphocytes isolated from tumor sites were assayed, it was found that there was no remarkable difference between lymphocytes from progressor tumors (PTL) and lymphocytes from regressor tumors (RTL). Both lymphocyte populations were similar in profile analysis; they were characterized as T cells and possessed the same antigenic specificity. Nevertheless, when in vivo tumor transplantation experiments were performed, RTL were found to give protection against FBL‐3 challenge whereas PTL consistently failed to do so. On cytomorphological examination, the PTL were seen to contain large amounts of macrophages. The presence of macrophages in PTL appeared to have an inverse relationship to the in vivo protective effect. After removal of macrophages from PTL by Petri dish adherence, the non‐adherent PTL were found to give in vivo protection. Furthermore, thymocytes from progressors and macrophages isolated from the progressor tumors were found to suppress the in vivo T‐cell‐mediated immunity. These findings demonstrated that suppressor T cells and suppressor macrophages were present in tumor‐bearing hosts. These suppressor cells could interfere with the function of immune T cells at the efferent arm of the immune response.
Sucrase‐isomaltase: A marker of foetal and malignant epithelial cells of the human colon
Authors: Zweibaum Alain , Triadou Nicole , Kedinger Michèle , Augeron Chantal , Robine‐Léon Sylvie , Pinto Moïse , Rousset Monique , Haffen Katy 
Published: February 2007

AbstractThe presence of sucrase‐isomaltase (SI), a glycoprotein hydrolase normally restricted to the brush border membrane of the enterocytes of the small intestine, was investigated in tumours which developed in nude mice inoculated with six human colon carcinoma cell lines (HT‐29, Caco‐2, HRT‐18, HCT‐8R, SW‐480, and CO‐115). Foetal and normal adult human small intestines and colons were used as controls. SI was studied by (I) immunofluores‐cence with rabbit antibodies raised against purified human small intestine SI; (2) polyacrylamide gel elec‐trophoresis and immunoblotting; and (3) determination of the enzyme activity. SI was antigenically present, and enzymatically active, in all the tumours derived from Caco‐2 and HT‐29 cells. The presence of the enzyme was associated with that of typical brush borders at transmission electron microscopy examination. SI was absent from the tumours developed with the other four cell lines, as well as from the normal adult colon mucosa. SI was also present and active in the colons of mid‐gestation foetuses, ranging in ages between 20 and 28 weeks; it was absent from the colons of late‐gestation foetuses. The presence of SI in tumours derived from two cell lines suggests that this enzyme is a marker, so far unsuspected, of certain human colon cancers, and that the differentiation pattern of these particular cancers closely resembles that of the foetal colon.
Chromosomal aberrations in a case of T‐cell CLL with concomitant IgA myeloma
Authors: Zech L. , Hammarström L. , Smith C. I. E. 
Published: February 2007

AbstractFour consistent markers, involving chromosomes 8, 11, 14, 18, 21 and 22, were found in the majority of meta‐phases obtained after stimulation of peripheral blood and bone marrow from a patient with a T‐cell chronic lym‐phocytic leukemia (CLL) and a concomitant IgA/lambda myeloma with phytohemagglutinin (PHA), lipopolysac‐charide of E. coli(LPS) and S. aureus strain Cowan I bacteria (Cowan). A second malignant clone with three additional markers was observed after stimulation with Con‐canavalin A (Con A). A chromosome 14 aberration, inv(14) (q11‐q32), may be of significance in the T‐cell malignancy and may suggest a common clonal origin of the two tumors.
Ecotropic MuLV expression in radiation‐induced lymphomas of the RF, BALB/c and (BALB/c × RF)F1 mouse strains
Authors: Dorsch‐Häsler Karoline , Mayer Allen 
Published: February 2007

AbstractEndogenous ecotropic viruses isolated from radiation‐induced lymphomatous tissue of BALB/c mice have been shown to consist of a collection of variants as assayed by the mobility of virion structural proteins p30, p15, p12 and gp70 on SDS‐polyacrylamide gel electrophoresis (SDS‐PAGE) (Ellis et al., 1980a). In this study we show that a similar phenomenon occurs in RF mice, but only with regard to p15 and gp70, and not p30 and p12. Using the distinct and unvarying mobility of the RF viral p12 protein on SDS‐PAGE as a marker, we show that the RF‐derived ecotropic murine leukemia virus (MuLV) is expressed to the exclusion of the BALB/c‐derived ecotropic MuLV in F1 hybrid mice of the BALB/c X RF cross, and that variant viruses expressed in F1 radiation‐induced lymphomatous tissue display the pattern of variation characteristic of the RF, and not of the BALB/c, strain.