bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evidence that β1‐6 branched Asn‐linked oligosaccharides on metastatic tumor cells facilitate invasion of basement membranes
Authors: Yagel Simcha , Feinmesser Raphael , Waghorne Carol , Lala Peeyush K. , Breitman Martin L. , Dennis James W. 
Published: February 2007

AbstractIn previous studies we have shown that the ability of murine tumor cells to metastasize in situ is directly linked to expression of ‐GIcNAcβ1‐6Manαl‐6Manßi‐branched complex‐type Asn‐linked oligosaccharides in tumor‐cell glycoproteins. Here we demonstrate that cell‐surface expression of β1‐6 branched oligosaccharides in metastatic tumor cells is specifically associated with increased invasion of human amnion basement membranes in vitro. Compared to non‐metastatic SPI murine mammary carcinoma cells, 2 metastatic sublines expressed higher levels of β1‐6 branched oligosaccharides and were found to be invasive but poorly adhesive on the amnion basement membrane. Swainsonine, a non‐toxic inhibitor of β1‐linked oligosaccharide processing which blocks the pathway prior to initiation of the β1‐6 linked antenna, blocked metastatic tumor‐cell invasion and increased adhesiveness. Swainsonine and the metalloprotease inhibitor O‐phenanthroline inhibited invasion, apparently via independent mechanisms. O‐phenanthroline did not affect tumor‐cell adhesion to the amnion basement membrane and swainsonine did not block secretion of metalloproteases, β‐hexosaminadase or tissue plasminogen activator activity by the tumor cells. These results suggest that tumor‐cell invasion of basement membranes requires both secretion of hydrolase activities and expression of β1‐6 branched complex‐type oligosaccharides at the tumor cell surface, such oligosaccharides being associated with reduced tumor‐cell adhesion to extracellular matrix.
CD 16 surface molecules regulate the cytolytic function of CD3−CD16+ human natural killer cells
Authors: Moretta Alessandro , Tambussi Giuseppe , Ciccone Ermanno , Pende Daniela , Melioli Giovanni , Moretta Lorenzo 
Published: February 2007

AbstractMonoclonal (IgG) antibodies (MAbs) directed to CD 16 molecules efficiently induced lysis of the IgG‐binding P815 target cells. A similar effect was observed with selected anti‐CD2 MAbs. While combinations of 2 appropriate anti‐CD2 MAbs were required for induction of T lymphocyte activation, single stimulatory anti‐CD2 MAbs were sufficient for inducing cytolytic function in CD3−CDI6+ lymphocytes. In order to study possible regulatory mechanisms existing in the process of activation and induction of the cytolytic machinery of CD3−CDI6+ effector cells, we utilized the anti‐CDI6 OKNK MAb. Being of IgM isotype, the OKNK MAb does not allow cross‐linking between CD3−CDI6+ lymphocytes and target cells. Pre‐treatment of effector cells with OKNK MAb sharply inhibited the target cell lysis induced by either anti‐CD 16 (IgG) MAbs or stimulatory anti‐CD2 MAb. Moreover, a strong inhibitory activity of PHA‐induced target cell lysis and even of “spontaneous” lysis (at high effectontarget ratio) was observed. In contrast, in CD3+CDI6+ clones, OKNK MAb selectively inhibited the cell triggering induced by anti‐CD 16 MAbs (but not by anti‐CD3, anti‐CD2 MAbs or PHA). Our data indicate that CDI6 receptor molecules expressed by CD3−CD16+ lymphocytes down‐regulate cell responses to anti‐CD2 MAbs or PHA, and then exert a regulatory role in the cytolytic function of these cells.
Regulation of epidermal growth factor receptor by progestins and glucocorticoids in human breast cancer cell lines
Authors: Ewing Tania M. , Murphy Liam J. , Ng Mee‐Lian , Pang Grace Y. N. , Lee Christine S. L. , Watts Colin K. W. , Sutherland Robert L. 
Published: February 2007

AbstractHuman breast cancer cells secrete a number of autocrine peptides which modulate their proliferation rates. The known effects of steroid hormones on breast cancer cell proliferation may be mediated in part by altering the production of these growth factors and/or their interactions with cellular receptor sites. Receptors for epidermal growth factor (EGF), which also bind the autocrine growth factor, α‐transforming growth factor, are present on a number of breast cancer cell lines and it has previously been shown that T‐47D and MCF‐7 cells respond to progestins with an increase in the concentration of EGF receptors (EGF‐R). In the present study we examined the effects of both progestins and glucocorticoids on EGF binding in 10 human breast cell lines. Five of these lines were progesterone receptor positive and all lines expressed the glucocorticoid receptor (GR). All cell lines were initially incubated for 24 hr with increasing concentrations of the synthetic progestin, medroxyprogesterone acetate (MPA), and the level of specifically bound EGF was determined. An increase in specific binding of EGF was confirmed in two PR‐positive lines but, in addition, increases in EGF binding were observed in 4 PR‐negative cell lines. In these last lines the synthetic glucocorticoid, dexamethasone, was a more potent inducer of EGF binding than MPA, a known glucocorticoid agonist, while the high‐affinity PR ligand, ORG 2058, was without effect. Furthermore, MPA competed with dexamethasone for binding to GR in these cell lines, supporting the view that the induction of EGF binding by MPA in these cells was mediated via the GR. This conclusion was further supported by studies in which addition of the glucocorticoid and progestin antagonist, RU 486, inhibited the effect of ORG 2058 in two cell lines and completely abrogated the effect of dexamethasone in two other lines. Detailed binding studies revealed that the increase in EGF binding was accompanied by an increase in the concentration of EGF‐R. This effect was observed when EGF binding was assayed at either 0° or 37°C. Further studies demonstrated that the increases in EGF binding following ORG 2058 and dexamethasone treatment were accompanied by increases in EGF‐R mRNA levels. Our data illustrate that the binding of EGF by some human breast cancer cells can be regulated by both progestins and glucocorticoids acting vía their respective receptors and inducing increases in EGF‐R mRNA levels.
In vitro infection of cell lines with HTLV‐I and SIVmac results in altered intracellular free calcium concentration and increased membrane polarization
Authors: Wright K. A. , Olsen R. G. 
Published: February 2007

AbstractThis study was designed to determine whether retrovirus infection alters basal concentrations of intracellular free calcium, the magnitude of intracellular free calcium change upon receptor‐mediated cell‐stimulation, and cell membrane polarization. Two retrovirus‐infected cell lines were utilized: HTLV‐I‐infected MT‐2 cells and SIV‐infected H‐9 cells. Uninfected H‐9 cells were used as controls. The results show that the retrovirally‐infected cells had an increased basal concentration of intracellular free calcium when compared with the control cells and also a reduced magnitude of intracellular free calcium response to receptor‐mediated cell stimulants. The retrovirally‐infected cell membranes were also hyperpolarized when compared with the control cells.
Lymphocyte homing receptors and adhesion molecules in intravascular malignant lymphomatosis
Authors: Jalkanen S. , Aho R. , Kallajoki M. , Ekfors T. , Nortamo P. , Gahmberg C. , Duuvestun A. , Kalimo H. 
Published: February 2007

AbstractIntravascular malignant lymphomatosis (IML) is a highly malignant, recently recognized form of lymphoma. It is characterized by multifocal proliferation of malignant lymphocytes within small blood vessels, primarily in the central nervous system and skin, frequently resulting in circulatory disturbances. The cause of the impaired capability of the malignant lymphocytes to extravasate has remained unclear. We analyzed the presence of immunoreactivity for certain homing receptor and adhesion molecules associated with lymphocyte extravasation in 3 patients with this disease. Compared with nonneoplastic leukocytes, large malignant lymphocytes appeared either negative or only weakly positive for the leukocyte surface glycoprotein, CD 18 that is the beta chain of the CD 11 a/CD 18 complex (lymphocytefunction associated antigen‐1, LFA‐1), which mediates cell‐to‐cell adhesion of lymphocytes. On the other hand, antibody to one of the proposed ligands for this complex, intercellular adhesion molecule‐1, gave positive reactivity both on lymphocytes and on endothelial cells. Further, the malignant lymphoid cells stained positively with Hermes‐3 antibody, which recognizes a common structure of CD44 class of molecules involved in lymphocyte homing. It was also shown that HECA‐452 antigen, a marker of high endothelial venules (HEV) supporting lymphocyte extravasation, can be synthesized by an IML patient even at the site of inflammation but it is not prerequisite for extravasation of inflammatory lymphocytes. Our results suggest that the deficiency or absence of the adhesion molecule CD 11 a/CD 18 may contribute to the inability of the malignant lymphoid cells to extravasate in IML, and perhaps also to the high malignancy of this form of lymphoma.
Human yolk‐sac tumor antigen 2G10: Biochemical characterization and significance as a serum antigen
Authors: Tanaka Shigeki , Fujimoto Junichiro , Jshii Eizaburo , Hata Jun‐Ichi 
Published: February 2007

AbstractThe biochemical characterization of human yolksac tumor (YST) antigen 2G10, detected by monoclonal antibody (MAb) M912‐2G10, was studied. Previous results indicated that glycolipids having a nonreducing terminal N‐acetyllactosamine structure were the epitope of 2G10 on human erythrocytes. In this study, the glycoprotein nature of 2G10 on the infantile embryonal carcinoma line, MTE, was investigated. 2G10 activity, measured by a new enzymelinked immunosorbent assay (2G10‐ELISA), was recovered in residual fractions of MTE from which glycolipids were removed. Chromatographically, 3H‐galactoselabelled 2G10 on MTE had a molecular weight (mw) of about 580 kDa, which decreased after pronase or alkalineborohydride treatment. Our results indicate the glycoprotein nature of 2G10 on MTE. Furthermore, 2G10, both on erythrocytes and on MTE, was sensitive to galactosidase but not to neuraminidase and fucosidase, suggesting that terminal galactose is involved in the antigenic structure. It was also found by 2G10‐ELISA that 2G10 sheds from tumor cells. Shedding occurs in nude mice transplanted with MTE as well as in patients with germ‐cell tumors (GCTs). The serum level of 2G10 in nontumor patients was low, but high levels were detected in patients with YSTsand with GCTshaving YST components. Immunohistochemically, the presence of 2G10‐positive YST components was shown in patients who had high serum levels of 2G10. Sera from other urogenital and childhood solid tumors did not have elevated 2G10. The mw of shed 2G10 was lower than that of 2G10 on the cell surfaces. Our results clearly indicate the usefulness of serum 2G10 as a tumor marker for GCTshaving YST components.
Amplification of c‐myc and c‐erbB‐2 proto‐oncogenes in human solid tumors: Frequency and clinical significance
Authors: Gutman M. , Ravia Y. , Assaf D. , Yamamoto T. , Rozin R. , Shiloh Y. 
Published: February 2007

AbstractMolecular probes for cellular protooncogenes have recently been extensively used in order to search for functional and structural alterations in tumor tissues. Variable, and sometimes contradictory, results have been obtained regarding the frequency and clinical significance of amplification of the cmyc and cerbB‐2 protooncogenes in different series of human solid tumors. We addressed this question by performing Southern blotting analysis on 131 primary adult solid tumors of various tissues and 5 metastases of unknown origin, using molecular probes for both genes. Amplification of cmyc was found in 5 of the primary tumors, and amplification of cerbB‐2 in 5 others. In 2 tumors of the latter group, the cerbB‐2 gene was also rearranged. The distribution of these 10 tumors with regard to clinical stage and course of the disease did not point to an association between the amplification events and specific stage or prognosis. We concluded that, in this series, the amplification of both protooncogenes was occasional and was not a prognostic marker.
Expression of the pS2 gene in normal, benign and neoplastic human stomach
Authors: Luqmani Yunus , Bennett Caroline , Paterson Iain , Corbishley Catherine M. , Rio Marie‐Christine , Chambon Pierre , Ryall Glenys 
Published: February 2007

AbstractThe expression of the estrogenregulated breastcancerassociated pS2 gene was examined in 75 stomach resections taken from 45 patients. The 600‐base pS2 mRNA was found in all of the 47 nonneoplastic samples at varying levels: in the histologically normal group we observed a Poissontype distribution, whereas 79% of the tissues exhibiting dysplastic features expressed high levels of transcript. Tumour samples expressed relatively lower pS2 mRNA, with only 18% having high levels and 43% with no detectable expression. These differences were not correlated to tumour grading, stage or site. No amplification or rearrangement of the pS2 gene was found. Immunohistochemical analysis of formalinfixed paraffin sections, using a polyclonal antibody against pS2 protein, showed specific staining of both cytoplasm and membrane of epithelial cells in the neck region of antral and body glands as well as in luminal secretions. Immunoreactivity was observed in the subnuclear region of foveolar cells, with specialized gland and goblet cells in atrophic gastritis being negative. Heterogeneous but strong focal cytoplasmic staining was seen in tumour cells as well as in dysplastic epithelium. Two gastric cell lines, KATO III and MKN‐45, derived from poorly differentiated adenocarcinomas also expressed pS2, whereas 3 other lines from well differentiated parental tumours did not. Genomic analysis revealed a BamHI polymorphism in Kato III cells and in the nonexpressing MKN‐28 cells. Immunostaining to pS2 protein was also demonstrated in the cytoplasm of KATO III cells, but neither these nor any of 30 tissues examined showed any positivity with a monoclonal antibody (MAb) to estrogen receptor. Our results suggest that pS2 is normally expressed in human stomach, possibly in association with secretory activity, and becomes downregulated during malignancy.
Is chronic sunlight exposure important in accounting for increases in melanoma incidence?
Authors: Gallagher Richard P. , Elwood J. Mark , Yang C. Paul 
Published: February 2007

AbstractMost attempts to relate changes in patterns of sunlight exposure to the rise in incidence of malignant melanoma have concentrated on the positive association between intermittent exposure to sunlight and risk of melanoma. The Western Canada Melanoma Study, however, also detected a significant inverse association between melanoma and chronic or longterm occupational sun exposure in men, with the lowest risk (OR = 0.5) in those with maximum occupational exposure, suggesting that chronic exposure may be protective. Data obtained from Canadian census figures indicated that since 1951 there has been a substantial reduction in the number of males engaged in outdoor occupations in Canadian society. These observations suggest that part of the increase in the incidence of melanoma in lowsunlight areas may be due to a reduction over the past 40 years of the size of this group of individuals “protected” by their exposure to UV light.
Correlation of HLA‐D/Ii antigen expression in breast carcinoma with local lymphohistiocytic infiltration reveals considerable dysregulation in a subset of tumors
Authors: Koretz Karin , Moldenhauer Gerhard , Majdic Otto , Möller Peter 
Published: February 2007

AbstractNon‐neoplastic mammary glands and 203 carcinomas of the breast were examined immunohistochemically for expression of HLA‐DR, ‐DP, and ‐DQ molecules and the HLA‐D‐associated invariant chain (li). According to the reaction of normal breast epithelium in the course of chronic inflammation, these antigens were found to be induced in 120 carcinomas. In 106 of these the order was li ≥ HLA‐DR ≥ HLA‐DP ≥ HLA‐DQ. The extent of induction of these sequentially expressed antigens correlated with the density of local lympho‐histiocytic infiltration (li: p = 0.003; HLA‐DR: p = 0.0005; HLA‐DP: p = 0.0000005; HLA‐DQ: p= 0.01). Therefore, li/ HLA‐D antigen expression of carcinoma cells in local association with inflammation was regarded as an adequate reaction. The presence of these antigens in the absence of inflammation was regarded as “inadequate hyper‐expression”, and was found in 14 cases involving li, in 8 involving HLA‐DR, and in 1 case each involving ‐DP and ‐DQ molecules. In contrast, 20 cases expressed minimal/no li despite heavy inflammatory infiltration. This “inadequate hypo‐expression” was also found in 25 cases involving HLA‐DR, in 30 involving ‐DP and in 40 involving ‐DQ determinants. Combining the 2 variants showed that at least 54 cases (26.6%) were characterized as being dysregulated. “Adequate vs. inadequate li/HLA‐D antigen expression” did not correlate with tumor grading and might therefore be an independent parameter.
Urinary excretion of N‐nitrosamino acids and nitrate by inhabitants of high‐ and low‐risk areas for stomach cancer in Poland
Authors: Zatonski W. , Ohshima H. , Przewozniak K. , Drosik K. , Mierzwinska J. , Krygier M. , Chmielarczyk W. , Bartsch H. 
Published: February 2007

AbstractUrine samples were collected from 96 inhabitants of a high‐risk rural area and a low‐risk urban area for stomach cancer in Poland, according to the following protocol: (1) when they were undosed; (2) after ingestion of proline 3 times a day; and (3) after ingestion of proline together with vitamin C 3 times a day. The samples were analyzed for N‐nitrosamino acids and nitrates, as indices of exposure to preformed and endog‐enously formed N‐nitrosamines. The median values of N‐nitrosoproline (NPRO) and N‐nitrosothiazolidine 4‐carboxylic acid (NTCA) excreted in the urine of undosed subjects were not different between the two areas; but N‐nitrososarcosine and 3‐(N‐nitroso‐N‐methylamino)propionic acid levels were 3‐ to 4‐fold higher in subjects of the high‐risk area. After intake of proline, the NPRO level increased (p < 0.02) only in subjects in the high‐risk area; intake of vitamin C tended to inhibit this increase in NPRO and lowered the levels of other nitrosamino acids. The urinary level of nitrates was 1.4‐fold, but significantly higher among subjects in the high‐risk area than among those in the low‐risk area; nitrate levels were not correlated with the amounts of cured meat or types of vegetables consumed. Urinary nitrate levels and excretion of NPRO, NTCA and the sum of all nitrosamino acids analyzed showed positive, though modest, correlations. These results indicate a higher potential for endogenous nitrosamine formation, possibly by intragastric nitrosation among subjects in the high‐risk rural area.
Monoclonal antibody against human squamous‐cell‐carcinoma‐associated antigen
Authors: Tatake Revati J. , Amin Kishore M. , Maniar Hina S. , Jambhekar Nirmala A. , Srikhande Sumati S. , Gangal Sudha G. 
Published: February 2007

AbstractMouse monoclonal antibody (MAb) 3F8E3 (lgG3k) was developed against the head and neck cancer cell line LICR‐LON‐HN2. Subjected to indirect immunofluorescence, the MAb reacted exclusively with SCC cell lines and showed no reactivity with normal or transformed mouse and human non‐SCC cell lines and hematopoietic cell lines. The radiolabeled MAb showed an affinity constant of 1.8 × 108 M−1 with HN2 cells and identified 2.07 × 104 sites/cell by Scatchard analysis. It identified 2 peptides from membrane extracts of HN2 cells by Western blotting. Avidin‐biotin‐complexed im‐munoperoxidase staining on cryostat sections of tumors from various tissues revealed that 3F8E3 reacted mainly with the membrane antigens of well differentiated SCC cells of oral cavity, larynx, esophagus, lung, uterine cervix, metastatic nodes of patients with oral cancer, and dysplastic cells in oral leukoplakia. The MAb did not react with poorly differentiated cells of Ca esophagus, adenocarcinoma of breast, stomach and colon, renal‐cell carcinoma and soft‐tissue sarcoma.
Preservation of chromosome and DNA characteristics of human colorectal adenocarcinomas after passage in nude mice
Authors: Lefrançois Danielle , Olschwang Sylviane , Delattre Olivier , Muleris Martine , Dutrillaux Anne‐Marie , Thomas Gilles , Dutrillaux Bernard 
Published: February 2007

AbstractTwenty‐seven human colorectal adenocarcinomas were implanted s.c. into nude mice. A comparative study of chromosomes and DNA between fresh tumor (FT) and xenografted tumor cells (XT) could be performed in 9 cases. Losses or deletions were consistently found in FTs as well as in XTs, particularly on chromosomes 17 and/or 18. This was correlated with loss of heterozygosity for these chromosomes. Comparison between corresponding FT and XT karyotypes showed great similarities. However, the tendency toward polyploidization, which exists in FTs, appeared to be more pronounced in XTs. Passage in nude mice makes it possible to repeat cytogenetic analyses in order to obtain interpretable metaphases. Xenografting not only increases the number of tumorigenic cells, but also eliminates human normal stromal or blood cells and gives unambiguous data on allelic loss.
Unique patterns of brain metastasis produced by different human carcinomas in athymic nude mice
Authors: Schackert G. , Price J. E. , Bucana C. D. , Fidler I. J. 
Published: February 2007

AbstractThe purpose of this study was to develop an in vivo model to study the growth pattern and biological behavior of brain metastases produced by different human carcinomas. To do so, human tumor cells from 8 different carcinomas of the colon, breast, kidney and lung were injected into athymic nude mice either by a direct intracerebral route or into the internal carotid artery. All carcinoma cells invaded through the blood‐brain barrier and produced progressively growing lesions in the brain parenchyma. Unique patterns of growth were discernible among the carcinomas. Human colon carcinomas produced multiple lesions that spread by extension. Lung carcinoma cells produced widespread lesions throughout the brain. A very high degree of vascularization was associated with lesions produced by renal‐cell carcinoma. The influence of estrogen on the growth of estrogen‐receptor‐positive human breast carcinoma cells was well demonstrated in this model. We conclude that the athymic nude mouse can be a useful model for studies of the biology and perhaps therapy of brain metastases produced by human carcinoma cells.
Clustering of discrete cell properties essential for tumorigenicity and metastasis. II. Studies of syrian hamster embryo fibroblasts transformed by rous sarcoma virus
Authors: Deichman G. I. , Kashleva H. A. , Kluchareva T. E. , Matveeva V. A. 
Published: February 2007

AbstractTumorigenic and metastasizing activities (TGA; MA) and susceptibility, or resistance to H202 and PGE‐releasing activity (H2OR2 + PGEs+ phenotype) have been examined in 6 Syrian hamster embryo cell strains transformed in vitro with Rous sarcoma viruses (Schmidt‐Ruppin and Prague strains). Early observations of extremely high level of TGA and even MA of RSV‐SR‐transformants never selected in vivo have been confirmed. The correspondence of these properties with a high level of expression of H2OR2 + PGEs+ phenotype and its clustering character were demonstrated in 4 RSV‐SR trans‐formants, while significantly lower expression of all these characteristics, including TGA, was observed in 2 RSV‐Prague transformants. High level of spontaneous MA was noticed in some RSV‐SR transformants. A tumor cell line induced in vivo by RSV‐SR did not differ from the cell strain transformed in vitro by RSV‐SR. inhibition of H2OR2 + PGEs+ phenotype in one of RSV‐SR transformants was obtained with non‐toxic doses of BCNU and indomethacin, leading to a marked decrease of TGA.