bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression and modulation by cytokines of the intercellular adhesion molecule‐1 (ICAM‐1) in human central nervous system tumor cell cultures
Authors: Guarini Ludovico , Temponi Massimo , Bruce Jeffrey N. , Bollon Arthur P. , Duigou Gregory J. , Moulton Thomas A. , Ferrone Soldano , Fisher Paul B. 
Published: February 2007

AbstractThe intercellular adhesion molecule (ICAM‐1) has been shown to be important in interactions involying cells of the immune system and to be upregulated in a number of cell culture systems by cytokines, including immune interferon (IFN‐γ) and tumor necrosis factor‐alpha (TNF‐α). In the present study, we have determined by fluorescence‐activated cell sorter (FACS) analysis and the anti‐ICAM‐I monoclonal antibody (MAb) CL203.4 the base‐line expression of ICAM‐I and its modulation by recombinant IFN‐β, IFN‐γ and TNF‐α in early passage (< 15) human central nervous system (CNS) tumor‐derived cell cultures. These cultures were established from various malignancies, including glioblastoma multiforme (GBM), astrocytoma (AST), ganglioglioma, medulloblastoma, meningioma and a pineal tumor. ICAM‐I expression was highest in the GBM‐ and AST‐derived cell cultures and was lowest in the ganglioglioma and normal pineal cell cultures. Variable ICAM‐I expression was found, however, in tumors of the same histological group. In several cell cultures the variable expression observed by FACS was substantiated by the intensity of the molecular species immunoprecipitated by the anti‐ICAM‐I MAb CL203.4 from these cells. All the cell cultures displayed variable but consistent increases in ICAM‐I expression following treatment with IFN‐γ or TNF‐α. In general, the degree of increase in ICAM‐I expression was greatest in cultures exposed to TNF‐α. Upregulation of ICAM‐I expression in an established glioblastoma multiforme cell line was of greater magnitude and more rapid following TNF‐α treatment (within 2 to 3 hr) than exposure to IFN‐γ (by 24 hr). In several cultures, IFN‐β also increased ICAM‐I expression and enhanced the increase induced by TNF‐α. The results of the present study indicate that variable expression of ICAM‐I is a common property of early passage cultures of CNS tumors and recombinant interferons and TNF‐α can differentially upregulate ICAM‐I expression in these CNS tumor cell cultures.
Characterization of a sialic‐acid‐rich mucus glycoprotein secreted by a premalignant human colorectal adenoma cell line
Authors: Corfield Anthony P. , Clamp John R. , Casey Angela D. , Paraskeva Christos 
Published: February 2007

AbstractThe human colonic cell line PC/AA, derived from an adenoma, retains in vitro colonic cell differentiation, notably the production of mucus glycoproteins. The PC/AA adenoma cells produce an extracellular gel layer in culture. The PC/AA gel could be isolated by extraction of the cell cultures with guanidine hydrochloride. The extracted material was purified by gel filtration and caesium chloride density‐gradient centrifugation and showed properties typical of mucus glycoproteins, namely, a carbohydrate content above 60% of dry weight rich in N‐acetylgalactosamine and sialic acid and low in mannose; an amino acid composition with high serine threonine and proline content; a molecular weight above 1,000 kDa on Sepharose CL 4B chromatography and on SDS‐polyacrylamide gel electrophoresis under reducing conditions (>200 kDa); a buoyant density of approximately 1.48 g/ml and the release of oligosaccharides by the alkaline β‐elimination reaction. Comparison of the gel mucus glycoprotein purified from premalignant PC/AA cells with normal human colon much showed that it has a higher sialic acid content. This suggests that higher sialic acid levels may precede the development of malignancy.
Steroid hormone receptor gene expression in human breast cancer cells: Inverse relationship between oestrogen and glucocorticoid receptor messenger RNA levels
Authors: Hall Rosemary E. , Lee Christine S. L. , Alexander Ian E. , Shine John , Clarke Christine L. , Sutherland Robert L. 
Published: February 2007

AbstractThe relative expression in human breast cancer cells of messenger ribonucleic acids (mRNA) encoding different steroid hormone receptors is unknown. Accordingly, mRNA levels in total RNA extracted from 13 human breast cancer cell lines were measured by Northern analysis employing complementary DNA probes for the human oestrogen (ER), progesterone (PR), androgen (AR), vitamin D3 (VDR) and glucocorticoid receptors (GR). The 7 ER+ lines expressed a single 6. 4 kilobases (kb) ER mRNA. Interestingly, low concentrations of ER mRNA were detected in the ER− cell lines, MDA‐MB‐330 and BT 20. PR mRNA, predominaintly a 13.5 kb species, was expressed in the 6 lines known to be ER+, PR+ by radioligand binding; however, one ER+ cell line, MDA‐MB‐134, failed to express PR mRNA. A 10.5 kb AR mRNA was expressed at significantly higher levels in ER+ than ER− cell lines. All cell lines expressed a single 4.6 kb mRNA for VDR and a single 7.4 kb mRNA for GR. ER and PR mRNA levels were positively correlated (p = 0.011) and each was positively correlated with androgen receptor (AR) mRNA levels (p < 0.009). ER, PR and AR mRNAs were negatively associated with GR levels (p < 0.012), while ER and AR mRNA levels were negatively correlated with mRNA for the epidermal growth factor receptor. In contrast, levels of VDR mRNA were unrelated to the concentration of any other steroid receptor mRNA. Our data demonstrate the coordinate expression of ER, PR and AR genes, and an inverse relationship between sex steroid hormone receptor and GR gene expression in human breast cancer cell lines.
Augmentation for intratumoral accumulation and anti‐tumor activity of liposome‐encapsulated adriamycin by tumor necrosis factor‐α in mice
Authors: Suzuki Shinya , Ohta So , Takashio Kazutoshi , Nitanai Hironobu , Hashimoto Yoshiyuki 
Published: February 2007

AbstractThe effect of recombinant human tumor necrosis factor‐α (rhTNF‐α) on anti‐tumor activity of adriamycin entrapped in small unilamellar liposomes (ADM‐Lip) has been studied using BALB/c mice bearing subdermal Meth‐A fibrosarcoma. Accumulation of i. v. injected ADM‐Lip, but not of free ADM, into tumor tissue was augmented by a single i. v. injection of rhTNF‐α. The maximum effect of rhTNF‐α was expressed when it was injected 1 hr before ADM‐Lip. This rhTNF‐α treatment did not result in increased accumulation of ADM‐Lip in normal organs. Based on these results, we treated mice bearing Meth‐A tumor with rhTNF‐α and then with ADM‐Lip 1 hr later. By 2‐cycle treatments using this regimen, tumor growth was markedly inhibited, and 5 out of 13 mice tested were cured of tumor, while treatment with rhTNF‐α alone, ADM alone, ADM‐Lip alone or rhTNF‐α plus ADM resulted neither in prolongation of survival time nor in cure of mice. Our results indicate that ADM‐Lip can express a potent and systemic anti‐tumor activity after pretreatment of animals with TNF, but only when administration of these drugs is appropriately timed.
Type‐II estrogen binding sites in a lymphoblastoid cell line and growth‐inhibitory effect of estrogen, anti‐estrogen and bioflavonoids
Authors: Scambia Giovanni , Ranelletti Franco O. , Panici Pierluigi Benedetti , Piantelli Mauro , Rumi Carlo , Battaglia Francesco , Larocca Luigi M. , Capelli Amaldo , Mancuso Salvatore 
Published: February 2007

AbstractType‐II estrogen‐binding sites (type‐II EBS) have been demonstrated in the human lymphoblastoid cell line IM‐9 using a whole‐cell assay with (6, 7‐3H) estradiol (3H‐E2) as tracer. Competition analysis showed that the anti‐estrogen tamoxifen and the flavonoids quercetin and rutin competed for (3H)‐E2 binding to type‐II EBS. Growth experiments demonstrated that diethylstilbestrol (DES) tamoxifen (TAM), quercetin and rutin exerted a reversible dose‐dependent inhibition of cell proliferation in the range of concentrations between 10 nM and 10 μM. The relative binding affinity of quercetin, rutin, DES and TAM for type‐II EBS correlated well with their potency as cell growth inhibitors. Moreover, hesperidin, a flavonoid which does not bind to type‐II EBS, was ineffective in inhibiting cell growth. Cell‐cycle analysis showed that the growth‐inhibitory effect of DES, TAM or quercetin was due to a blocking effect in the G0‐G1 phases. Our results suggest that high estrogen and anti‐estrogen concentrations and flavonoids may regulate IM‐9 cell growth through a common mechanism involving a binding interaction with type‐II EBS.
Nutritional factors and pancreatic cancer in the francophone community in montréal, Canada
Authors: Ghadirian P. , Simard A. , Baillargeon J. , Maisonneuve P. , Boyle P. 
Published: February 2007

AbstractIn a population‐based case‐control study of dietary risk factors for pancreatic cancer, a total of 179 cases and 239 controls were interviewed between 1984 and 1988. This study demonstrated an increased risk of pancreas cancer associated with high levels of reported energy intake. After adjustment for age, sex, response status, lifetime cigarette consumption and energy intake, there appeared to be an association with total fat intake (odds ratio in highest quartile relative to lowest quartile 2.24 [95% Confidence Interval (0.74, 6.73)] and, particularly, saturated fat [OR = 4.32, 95% CI(1.39,13.7)]. Although dietary cholesterol intake appeared to increase risk and a number of many micro‐nutrients were apparently associated with reductions of risk, none were statistically significant. The results are consistent with a role of nutritional factors in the etiology of pancreatic cancer. The magnitude of the risks involved emphasizes the necessity for larger studies of this topic.
The analysis of restriction fragment length polymorphism in human cancer: A review from an epidemiological perspective
Authors: Vineis Paolo , Caporaso Neil 
Published: February 2007

AbstractWe have reviewed published case‐control studies on the role of Restriction Fragment Length Polymorphism (RFLP) for specific loci in the causation of human cancer or as a prognostic factor. Five studies have been published on L‐myc polymorphism and prognosis for several types of cancer (lung, kidney, stomach or breast). Sixteen studies report on Ha‐ras polymorphism and the risk of cancers in the lung, breast, bladder, colorectum, brain, leukemias and melanoma. The results of the studies are conflicting. In addition, such studies raise important methodological issues: the choice of the cut‐off between “rare” and “common” alleles; the inclusion of prevalent cases; the distribution of the alleles in subgroups of the population, including different ethnic groups; a mechanistic interpretation of the role played by the polymorphism, including possible interaction with environmental exposures. These questions need to be answered before a cause‐effect relationship can be clearly established.
Characterization of NCAM expression and function in BT4C and BT4Cn glioma cells
Authors: Andersson A.‐M. , Moran N. , Gaardsvoll H. , Linnemann D. , Bjerkvig R. , Laerum O. D. , Bock E. 
Published: February 2007

AbstractThe neural cell adhesion molecule, NCAM, plays an important role in cell‐cell adhesion. Therefore, we have studied NCAM expression in the glioma cell lines BT4C and BT4Cn. We demonstrate that the 2 cell lines differ in their metastatic ability; while BT4C cells have a very low capacity for producing experimental metastases, that of BT4C cells is high. In BT4C cells NCAM is synthesized as 4 polypeptides with Mr's of 190,000, 140,000, 115,000 and 97,000. The 140,000, 115,000 and 97,000 polypeptides are glycosylated and for the 140,000 and 115,000 polypeptides sulfatation is observed. Conversely, no NCAM protein synthesis is observed in BT4Cn cells, even though NCAM mRNA is expressed. Thus, development of an increased metastatic capacity is accompanied by the disappearance of NCAM protein expression in this model system. The functional importance of NCAM expression was studied by a cell‐substratum binding assay in which the binding of BT4C and BT4Cn cells to NCAM immobilized to glass was assessed. We found that BT4C cells adhere specifically to NCAM, and that adhesion is inhibited by anti‐NCAM Fab'‐fragments, while no specific binding of BT4Cn cells to NCAM was observed. The BT4C and BT4Cn cell lines thus constitute an important new model system for the study of tumor invasion and metastasis and of the role of cell adhesion molecules in these processes.
Regional heterogeneity in breast carcinoma: Thymidine labelling index, steroid hormone receptors, dna ploidy
Authors: Meyer John S. , Wittliff James L. 
Published: February 2007

AbstractWe examined multiple samples of 65 primary breast carcinomas larger than I cm in diameter for thymidine labelling index (TLI), DNA index (DNAI, a measure of cellular DNA content by flow cytometry), and estrogen (ER) and progesterone (PgR) receptors by radioligand‐binding. One or more axillary metastases were also assayed in 11 patients. Two to 15 samples were successfully assayed for TLI from 59 tumors, 2‐31 samples for DNAI from 61 tumors, and 2‐15 samples from 55 tumors for ER and PgR. Criteria for heterogeneity were excess inter‐sample variance in comparison with intra‐sample variance at the p < 0.05 level for TLI and DNAI, and variation of clinically significant magnitude in assay results for ER and PgR. Sixty‐one percent of tumors were heterogeneous for TLI, 26% for DNAI, 24% for ER and 40% for PgR. High TLI disposed toward heterogeneity for TLI itself (p = 0.06), for ER (p = 0.04), and for PgR (p = 0.007). Young age favored heterogeneity for TLI (p = 0.12), ER (p = 0.002), and PgR (p = 0.04). Heterogeneity for DNAI was not related to age and TLI status but was more common in larger tumors (p = 0.08). After consideration of relationships between TLI, age, size, ER and PgR, TLI rather than age appears to be the more important determinant of heterogeneity for receptors. High TLI could lead to heterogeneity through increased numbers of cell divisions that favor emergence of variant stemlines, or by causing local vascular and humoral disparities through rapid growth. Regional heterogeneity can explain erroneous prognostic predictions in approximately 10% to 20% of breast carcinoma patients. We recommend multiple sampling of large breast carcinomas and analysis of axillary metastases for study of tumor markers.
Decreased tumorigenicity of a transplantable rat sarcoma following transfer and expression of an IL‐2 cDNA
Authors: Russell Stephen J. , Eccles Suzanne A. , Flemming Claudia L. , Johnson Caroline A. , Collins Mary K. L. 
Published: February 2007

AbstractThe notion that tumour‐cell‐derived IL‐2 might lead to paracrine stimulation of the host anti‐tumour response was tested in a transplantable rat sarcoma model. Three HSNLV clones induced to secrete different amounts of human IL‐2 following retroviral gene transfer showed reduced tumorige‐nicity and metastatic potential in athymic (nu/nu) and immunocompetent syngeneic rats which was directly related to the level of IL‐2 secretion. In contrast, the tumorigenicity of HSNLV clones secreting a biologically inactive form of IL‐2 (IL‐2Lys20) was unaltered. T‐lymphocyte‐mediated rejection of Zip I, the highest IL‐2 producer, was demonstrated histologically in hooded rats and infiltrating mononuclear cells were also observed in Zip I tumours growing in athymic rats. Tumours derived from IL‐2‐secreting HSNLV showed reduced or absent IL‐2 secretion in immunocompetent rats, sometimes with associated loss of the IL‐2 provirus, but continued to secrete IL‐2 in nude rats. The host response to Moloney‐helper‐virus‐infected HSNLV was also examined and the results represent a cautionary note to those undertaking experiments of a similar nature.
Establishment and characterization of five human malignant mesothelioma cell lines derived from pleural effusions
Authors: Manning Linda S. , Whitaker Darrel , Murch Ashleigh R. , Garlepp Michael J. , Davis Mark R. , Musk Arthur W. , Robinson Bruce W. S. 
Published: February 2007

AbstractMalignant mesothelioma (MM) is an aggressive tumour of the serosal cavities which is associated with exposure to asbestos. Studies of this tumour have been limited by a paucity of well‐characterized human MM cell lines. In this study, 5 human MM cell lines were established from pleural effusions of patients with this malignancy. All 5 patients were males with known crocidolite asbestos exposure, who had received no treatment for their disease and in whom the diagnosis was confirmed by cytology, histology and electron microscopy (EM). These lines have been in culture from 11 to 25 months, and all of them for more than 18 passages. The appearance of the cells in culture was extremely varied; in 3 of the lines they were spindle‐shaped with few vacuoles (JU77, LO68 and ONE58); in I line they had a thick, stellate shape with vacuoles (NO36) and in I they were very pleomorphic in both shape and size with irregular membranes and numerous vacuoles [DeHI28 (M)]. Upon reaching confluence, cells in 3 of the 5 lines assumed the cobblestone‐like pattern characteristic of epithelial‐type cells, whereas in the other 2 (LO68 and ONE58) they remained spindle‐shaped. All 5 lines demonstrated a loss of contact inhibition (i.e., piling) at confluence. Minimum doubling times varied significantly from 18 hr (JU77) to more than 30 hr [DeHI28 (M)]. Cytological examination showed characteristic mesothelial/mesothelioma morphology, and epithelial membrane antigen (EMA) and cytokeratin were demonstrated in cells from all 5 lines. These cells lacked CEA and epithelial mucin. The presence of cell junctions, glycogen and numerous long, thin, branching microvilli was readily demonstrable by EM. All lines had abnormal karyotypes, with the modal chromosome number varying from 40 to 80. Variable chromosome numbers, numerous structural rearrangements and unrecognizable marker chromosomes were readily observed; however, the only consistent change seen was del 6q2l in 4 of the 5 lines. The establishment of these 5 cultured human MM cell lines now provides an opportunity for comparative study of several aspects of the biology of MM in vitro as well as screening new treatment modalities.
α2, 6 sialylation of N‐acetyllactosaminic sequences in human colorectal cancer cell lines. Relationship with non‐adherent growth
Authors: Dall'olio Fabio , Malagolini Nadia , Stefano Giuseppina Di , Ciambella Manuela , Serafini‐Cessi Franca 
Published: February 2007

AbstractIn a previous work we found that human colorectal cancer tissues express increased levels of an α2,6 sialyltransferase (α2,6 ST) acting on N‐acetyllactosaminic sequences (E.C. 2.4.99.1). In this study we have taken advantage of the known specificity of elderberry bark lectin (Sambucus nigra agglutinin, SNA) for NeuAcα2, 6Gal/GalNAc structures to investigate the relationship between expression of α2,6 sialyltransferase activity and occurrence of α2,6‐sialylated oligosaccharide sequences in human colorectal cancer cell lines. Three cell lines with opposite adhesion properties were used in this study: SW 948 cells grow adherent to the culture flask surface and express very low levels of enzyme activity; COLO 205 cells grow in non‐adherent form and express the highest levels of α2,6 ST activity; A non‐adherent subline of SW 948 cells (SW 948 FL) was isolated and found to express high levels of α2,6 ST activity. By using SNA‐Sepharose chromatography we found that expression of α2,6 ST activity correlates with the extent of α2,6‐sialylation of N‐linked chains of glycoproteins but not with the presence of α2,6‐sialylated glycolipids.
Purification of an autoantigenic 75‐kDa human melanosomal glycoprotein
Authors: Vijayasaradhi Setaluri , Houghton Alan N. 
Published: February 2007

AbstractOnly a few autoantigenic human tumor antigens have been purified and characterized. We employed the monoclonal antibody (MAb) TA99 to isolate, purify and partially characterize an autoantigenic intracellular glycoprotein, gp75, from human melanoma cells. The gp75 antigen is the most abundant glycoprotein expressed in human melanocytes and pigmented melanomas and is the human homologue of the mouse brown locus gene product. Differential solubilization of melanoma membrane fraction and subcellular fractionation of pigmented melanoma cells showed that gp75 is an integral membrane protein localized to melanosomes. The gp75 glycoprotein eluted as a broad peak during ion exchange chromatography and appeared as a protein with broad pl (pl 5.5‐5.9), consistent with charge microheterogeneity. gp75 also exhibited heterogeneity of binding to concanavalin A. Tyrosine hydroxylase (tyrosinase) activity co‐purified with gp75 during membrane solubilization and anion exchange and Con A chromatography. However, most tyrosine hydroxylase activity could be dissociated from gp75 antigen during MAb TA99 affinity chromatography. TA99 did not immunoprecipitate or deplete tyrosine hydroxylase activity from lysates of human melanoma cells. Attempts to obtain N‐terminal amino acid sequence of purified gp75 were not successful due to blocked N‐terminus. Amino acid composition of gp75 was similar to that of tyrosinase. Physicochemical similarities and limited identity in the primary structure between gp75 and tyrosinase support the conclusion that the gp75 antigen does not exhibit tyrosine hydroxylase activity, but is a member of a tyrosinase‐related family of proteins.
Counteracting effects of dexamethasone and α2‐macroglobulin on inhibition of proliferation of normal and neoplastic rat hepatocytes by transforming growth factors‐β type 1 and type 2
Authors: Wollenberg G. K. , Lamarre J. , Semple E. , Farber E. , Gauldie J. , Hayes M. A. 
Published: February 2007

AbstractPrimary cultures of hepatocytes isolated from normal F‐344 rats or from F‐344 rats with hepatocellular carcinomas generated by a 2‐step model of chemical carcinogenesis were used to determine if dexamethasone (DEX) or α2‐macroglob‐ulin (α2M) modify the ability of transforming growth factors‐β type 1 (TGF‐β1) and type 2 (TGF‐β2) to inhibit labelling index of hepatocytes cultured continuously with or without epidermal growth factor (EGF). Both TGF‐β1 and β2 were equivalently potent inhibitors of S‐phase DNA synthesis in normal and neoplastic hepatocytes as determined by 3H‐thymidine autoradiography. Both DEX (1 to 100 μM) and α2M (50‐200 μm) partially counteracted the mito‐inhibitory effect of both TGF‐βs on the proliferation of normal and surrounding hepatocytes. In contrast, neoplastic hepatocytes cultured with DEX released much less immunoreactive α2M and were less able to overcome the inhibitory effect of TGF‐β than normal or surrounding hepatocytes. Purified bovine α2M partially counteracted the inhibition of TGF‐β1 or β2 of both surrounding and neoplastic hepatocytes. Both DEX and α2M were more effective against the mito‐inhibitory activity of TGF‐β2. Our data suggest that α2M released by DEX‐treated normal hepatocytes contributes to the counteraction of the TGF‐β effect by DEX. Our results support the hypothesis that glucocorticoids and growth‐factor‐binding proteins may have important roles in modulating the effects of TGF‐β on normal hepatocyte proliferation and suggest that under some conditions hepatocellular neoplasms can be more sensitive than normal hepatocytes to inhibition of proliferation by TGF‐β.