bluuebunny/crossref_metadata_2025_split huggingface dataset:
Preserved foods and nasopharyngeal carcinoma: A case‐control study among singapore chinese
Authors: Lee Hin Peng , Gourley Lynn , Duffy Stephen W. , Esteve Jacques , Lee James , Day Nicholas E. 
Published: February 2007

AbstractThe association between the consumption of preserved foods in infancy, childhood and adulthood and the risk of nasopharyngeal carcinoma was investigated in a case‐control study among Singapore Chinese: 200 cases (73% male) were compared with 406 hospital controls (71% male). Significantly increased risks were observed in association with frequent adult consumption of salted soy beans (OR 7.3 for consumption 4 or more times per week, compared with never), canned pickled vegetables (p = 0.01; OR 4.5 for 4 or more times per week), “sze chuan chye”, a salted Chinese tuber, (OR 2.4 for 4 or more times per month) and “kiam chye”, salted mustard greens (OR 2.7 for 4 or more times per week). A protective effect of high vitamin‐E intake in adulthood was observed (OR 0.5 for the highest third of the control range, as compared with the lowest).
Identification of a novel neutralization epitope on envelope GP46 antigen of human t‐cell‐leukemia virus‐type‐II (HTLV‐II)
Authors: Tanaka Yuetsu , Tanaka Reiko , Hoshino Hiroo 
Published: February 2007

AbstractHaving observed that multiple neutralization epitopes of human T‐cell‐leukemia‐virus‐type‐l (HTLV‐I) envelope gp46 clustered in a region between amino acids 187 and 199, we speculated that a region of HTLV‐II gp46 corresponding to the HTLV‐I‐neutralization region may contain HTLV‐II‐specific neutralization epitopes. To test this, we immunized a NZW rabbit and BALB/c mice with a synthetic peptide containing the HTLV‐II gp46 amino acids 182 to 199 (pep 182–199) conjugated to OVA. The serum from the rabbit reacted to the HTLV‐II gp46 and neutralized HTLV‐II‐mediated syncytium formation. One monoclonal antibody (MAb), M2E186NI, generated from the BALB/c mice, stained specifically the surface of HTLV‐II‐positive cells and reacted with HTLV‐II gp46 by Western blot. This MAb was of the IgA isotype and inhibited HTLV‐II‐ but not HTLV‐I‐mediated syncytium formation at a final antibody concentration of 200 μ/ml; it also neutralized an HTLV‐II‐VSV pseudotype virus specifically. Epitope mapping by ELISA using overlapping synthetic peptides indicated that the neutralization epitope recognized by the M2E186NI MAb was located between HTLV‐II gp46 amino acids 186 and 192, corresponding to the sequence Leu‐Gln‐His‐Val‐IIe‐Leu‐Gln‐Pro. These new observations will be helpful in developing vaccines against HTLV‐II infection.
Epithelial‐to‐mesenchymal transition in hpv‐33‐transfected cervical keratinocytes is associated with increased invasiveness and expression of gelatinase a
Authors: Gilles Christine , Polette Myriam , Piette Jacques , Birembaut Philippe , Foidart Jean‐Michel 
Published: February 2007

AbstractThe invasive potential of a set of HPV‐33‐ and HPV‐33+ras‐transfected cervical keratinocytes was investigated. These cell lines were previously separated into 2 groups according to their behavior on collagen rafts. Cell lines from the first group reconstituted CINIII‐like lesions, whereas cell lines from the second group reconstituted epithelia comparable to microinvasive carcinomas. They were thus postulated to represent distinct stages of cervical carcinogenesis. The present results have shown that lines from group I, which have conserved an epithelial morphology in monolayer, (i) could not invade matrigel when tested in a modified Boyden chamber assay, (ii) produced solely gelatinase B and (iii) were unable to activate exogenous gelatinase A. On the other hand, lines from group II associated epithelial‐to‐mesenchymal transition (acquisition of elongated morphology, vimentin positivity) with high in vitro invasive potential and with the ability both to produce and to activate gelatinase A. These results strongly support the hypothesis that the epithelial‐to‐mesenchymal transition and the associated events might be implicated in the progression to the metastatic phenotype.
Expression and functional activity of fibroblast growth factors and their receptors in human pancreatic cancer
Authors: Leung Hing Y. , Gullick William J. , Lemoine Nicholas R. 
Published: February 2007

AbstractWe have analysed expression of the first 7 members of the family of heparin‐binding fibroblast growth factor (FGFs) and their 4 high‐affinity receptors (FGFRs) in human pancreatic carcinoma cell lines, both at the mRNA and protein levels. In cell lines expressing FGFRs, 2 typical patterns were observed: (i) expression of FGFR‐1, −3 or −4 along with the expression of at least one FGF; (ii) co‐expression of FGFR‐3 and FGFR‐4 in the absence of FGF expression. Using RT‐PCR, transcripts representing multiple isoforms of both extracellular and intracellular domains of FGFR‐1 were detected in the cell line PT45. A novel extracellular domain variant of FGFR‐1 was predicted to encode the first immunoglobulin loop in a potentially secreted form. Protein expression of the splice variants of FGFR‐1 was confirmed by immunoprecipitation with specific antibodies in radiolabelled ligand cross‐linking experiments. The type I carboxyl end and the α subtype extracellular domain were detected in the PANC‐1 cell line, while the type I carboxyl terminus and the γ subtype extracellular domain were expressed in the PT45 cell line. Expression of FGF‐2 in PT45 was also detected by immunoprecipitation using 3 different anti‐FGF‐2 antibodies. Apart from the 18‐kDa product, higher molecular weight isoforms, namely 22‐ and 23‐kDa isoforms, were expressed. In an assay of anchorage‐independent growth, exogenous FGF‐2 stimulated a maximum 15‐fold and 10‐fold increase in colony formation by the cell lines MIA PACA‐2 and PANC‐1 respectively. Treatment of monolayer cultures of the same cell lines did not promote growth. However, a specific neutralising antibody against FGF‐2 reduced cell proliferation of MIA PACA‐2 cells by 50%.
AN association between high Ly‐6A/E expression on tumor cells and a highly malignant phenotype
Authors: Katz Ben‐Zion , Eshel Rinat , Sagi‐assif Orit , Witz Isaac P. 
Published: February 2007

AbstractMurine Ly‐6 is a molecule expressed by various cells, including several types of hematopoietic cells such as pluripotent stem cells, and activated T cells. Ly‐6 is also expressed on tumor cells originating from a variety of tissues. Preliminary observations suggested that the expression of Ly‐6A/E is up‐regulated on highly tumorigenic variants of polyoma‐virus(PyV)‐transformed BALB/c 3T3 cells as compared with weakly tumorigenic variants. On the basis of these observations, we sorted PyV‐transformed A3C cells or DA3 mammary adenocarcinoma cells into stable sub‐populations expressing high or low levels of membrane or mRNA Ly‐6A/E. In vivo studies indicated that the high‐Ly‐6A/E‐expressing cells in both tumor systems expressed a considerably more malignant phenotype (higher efficiency in local tumor production as well as in lung colonization) than low‐Ly‐6A/E expressors. Since the high‐Ly‐6A/E expressors did not exhibit any growth advantage in vitro over low Ly‐6A/E expressors, we concluded that interactions of the former cells with micro‐environmental factors operating in vivo (e.g., Ly‐6A/E ligands) conferred upon these cells a highly malignant phenotype. Apart from the difference in Ly‐6A/E expression, no other phenotypic characteristics distinguished highly from weakly malignant tumor cells. Similarly to T cells, where antibodies to Ly‐6 transduce (or co‐transduce) a proliferative signal, antibodies to Ly‐6A/E were found to transduce a mitogenic signal to high‐Ly‐6A/E‐expressing tumor cells but not to low‐Ly‐6A/E expressors. Taken together, these results show that Ly‐6A/E expression is directly or indirectly associated in vivo with a highly malignant phenotype of 2 types of non‐lymphoid murine tumors.
Globo‐series carbohydrate antigens are expressed in different forms on human and murine teratocarcinoma‐derived cells
Authors: Krupnick Jason G. , Damjanov Ivan , Damjanov Andrea , Zhu Zheng M. , Fenderson Bruce A. 
Published: February 2007

AbstractThe glycolipids of human teratocarcinoma‐derived cell line NCCIT were compared with those of 5 murine teratocarcinoma‐derived cell lines. Glycolipid antigens were identified by cell surface immunofluorescence and high‐performance thin‐layer chromatography (HPTLC) immunostaining with a panel of monoclonal anti‐carbohydrate antibodies. Human NCCIT embryonal carcinoma (EC) cells contained extended globo‐series glycolipids Gb5 (galactosyl globoside) and GL7 (sialyl galactosyl globoside) recognized by antibodies to stage‐specific embryonic antigens 3 and 4 (SSEA‐3 and −4). SSEA‐4 was not detected by immunofluorescence on the surface of any of the 5 murine teratocarcinoma‐derived cell lines examined; however, SSEA‐3 was detected on the surface of murine cell lines resembling primitive endoderm (JC44, NF‐PE) and trophectoderm (E6496D). HPTLC analysis revealed a large amount of globoside (Gb4) in these differentiated cells, which may account for their labeling with anti‐SSEA‐3 antibody. Globo‐series glycolipids were also detected in murine EC cells; however, differences were noted between the 2 cell lines examined. F9 cells contained primarily Gb4 and Forssman glycolipid, whereas NF‐I cells contained only minor amounts of Gb4 and lacked Forssman glycolipid entirely. Our results, coupled with the known distribution of Forssman antigen in the egg cylinder‐stage mouse embryo, suggest that F9 and NF‐I murine EC cells are replicas of cells at different stages of development of the embryonic ectoderm. Glycolipids of normal mouse embryos were examined for comparison. Gb4 and Forssman glycolipid were present in both embryonic and extra‐embryonic tissues, whereas Gb5 and GL7 were restricted to visceral yolk sac and placenta. Our results demonstrate that human and murine teratocarcinoma‐derived cells both synthesize extended globo‐series glycolipids; however, oligosaccharide chain elongation takes different pathways in the 2 species. These differences reflect species‐related and cell type‐specific patterns of glycosylation.
Tumor cells suppress cytokine‐induced nitric‐oxide (no) production in cerebral endothelial cells
Authors: Murata Jun‐Ichi , Corradin Sally Betz , Janzer Robert Charles , Juillerat‐Jeanneret Lucienne 
Published: February 2007

AbstractNitric oxide (NO) produced by endothelial cells (EC) has been shown to exert cytotoxic activity on tumor cells. In order to analyze events involved in brain metastasis, the modulation of NO production in rat‐brain‐derived EC was investigated. NO release was increased by tumor necrosis factor‐α (TNF‐α), interferon‐γ (IFN‐γ), interleukin‐1β, lipopolysaccharide or forskolin in EC2I9 cells, a rat‐brain‐microvessel‐derived EC line. Dexamethasone decreased NO release by cytokine‐activated EC219 cells. Tumor cells (DHD/K12/PROb, a rat coloncarcinoma cell line) were highly adherent to EC2I9 cells, and adhesion was not modified by TNF‐α plus IFN‐γ, or by dexamethasone. Addition of tumor cells or tumor‐cell‐conditioned medium significantly inhibited NO release induced by any of the stimuli examined, but only if added during the initial phase of endothelial‐cell activation. Tumor‐derived suppression of NO release was also observed in primary cultures of cerebral EC. NO synthase (NOS) activity in cytosol extracts of the cerebral EC line was Ca2+‐independent and required both NADPH and tetrahydrobiopterin. NOS activity was increased by TNF‐α and IFN‐γ, and significantly reduced by tumor‐cell‐conditioned medium. These results suggest that rat colon‐carcinoma cells may have developed a protective mechanism involving the release of (a) soluble factor(s) which inhibit(s) NO production by cerebral EC.
Increased risk of colorectal cancer among smokers: Results of a 26‐year follow‐up of us veterans and a review
Authors: Heineman Ellen F. , Zahm Shelia Hoar , McLaughlin Joseph K. , Vaught Jimmie B. 
Published: February 2007

AbstractTo clarify the relationship between tobacco use and risk of colorectal cancer, we evaluated a cohort of 248,046 American veterans followed prospectively for 26 years. In comparison with veterans who had never used tobacco, the risk of death was significantly increased for colon cancer and rectal cancer among current and former cigarette smokers and among pipe or cigar smokers, controlling for social class and occupational physical activity. Rectal‐cancer risk was also significantly elevated among users of chewing tobacco or snuff. For both sites, risk increased significantly with pack‐years, earlier age at first use, and number of cigarettes. These results reinforce 2 recent reports of the association of cigarette smoking and colorectal cancer in men and women. Inconsistencies in the findings of earlier epidemiologic studies appear to be due in large part to differences in length of follow‐up or in choice of controls. Studies with at least 20 years of follow‐up or population‐based controls have tended to find elevated risk with tobacco smoking, while those with shorter follow‐up or hospital controls have not. This, plus the strength and consistency of the association of smoking and colon polyps, suggest that smoking may primarily affect an early stage in the development of colon cancer. If this association is causal, tobacco use may be responsible for 16% of colon‐cancer and 22% of rectal‐cancer deaths among these veterans.
Identification and characterization of autocrine‐motility‐factor‐like activity in oral squamous‐cell‐carcinoma cells
Authors: Ishisaki Akira , Oida Shinichiro , Momose Fumio , Amagasa Teruo , Rikimaru Koichi , Ichijo Hidenori , Sasaki Satoshi 
Published: February 2007

AbstractA human oral squamous‐cell‐carcinoma cell line, HOC313, was found to produce a factor which stimulates cell motility in an autocrine manner. The motility factor of HOC313 cells also promoted the locomotory activity of B16 murine melanoma cells reported to be sensitive to autocrine motility factor (AMF). HOC313 cells were found to express a large amount of AMF receptor mRNA. In addition, the cell motility activity of HOC313 cells was completely blocked by pertussis toxin, a known inhibitor of AMF activity, suggesting that the motility factor of HOC313 cells may be AMF or a closely related factor. Immunocytochemical analysis has revealed that the AMF‐like factor of HOC313 cells diminishes the cell‐surface expression of adhesive molecule E‐cadherin. These results suggest that down‐regulation of E‐cadherin may be involved in the cell‐motility activity induced by the AMF‐like factor of HOC313 cells.
Bcl‐2 expression is associated with lymph node metastasis in human ductal breast carcinoma
Authors: Sierra Angels , Lloveras Belen , Castellsagué Xavier , Moreno Loli , García‐Ramirez Marta , Fabra Angels 
Published: February 2007

AbstractThe Bcl‐2 proto‐oncogene product blocks apoptosis. We retrospectively studied Bcl‐2 expression in 124 primary tumors from patients diagnosed with T1 (2 cm or less) breast carcinoma with (T1N1) or without (T1N0) lymph‐node metastasis. Bcl‐2 protein was detected by immunohistochemistry on paraffinembedded tissue sections. Multivariate logistic regression modeling was used to estimate prevalence odds ratios for lymphnode metastasis. Bcl‐2 was widely expressed among T1 tumors showing a strong positive relationship with estrogen (F.R)‐ and progesterone (PR)‐receptor‐positive tumors. However, a significant inverse correlation was seen between Bcl‐2 expression and histological grade, Bcl‐2 being absent in the majority of Tl undifferentiated tumors (grade‐Ill carcinomas). Furthermore, Bcl‐2 was more frequently expressed in T1N1 cases (72.2%) than in T1N0 specimens (45.7%). The odds for lymph‐node metastasis in the Bcl‐2‐positive group was 3.6 times larger than that in the Bcl‐2‐negative group. The co‐expression of PR significantly modified the effect of Bcl‐2 on the odds for lymph‐node metastasis, suggesting the existence of a synergistic interaction between the 2 parameters. We studied the percentage of dead cells in primary tumors by in situ DNA fragmentation (FDNA), and found an inverse correlation between Bcl‐2 expression and FDNA. This supported the hypothesis that Bcl‐2 extends cell survival. In conclusion, our study provides evidence that Bcl‐2 expression is involved in breast‐cancer progression, at least in a subset of well‐differentiated and PR‐positive tumors. © 1995 Wiley‐Liss, Inc.
EGF receptor and p185erbB‐2‐specific single‐chain antibody toxins differ in their cell‐killing activity on tumor cells expressing both receptor proteins
Authors: Wels Winfried , Beerli Roger , Hellmann Peter , Schmidt Mathias , Marte Barbara M. , Kornilova Elena S. , Hekele Armin , Mendelsohn John , Groner Bernd , Hynes Nancy E. 
Published: February 2007

AbstractMany human tumors over‐express erbB‐2 and EGF receptors. The membrane localization of these receptor tyrosine kinases make them appropriate targets for directed tumor therapy. We have used recombinant DNA technology to produce single‐chain antibody exotoxin A (scFv‐ETA) fusion proteins which specifically bind the erbB‐2 and EGF receptors. The scFv portion is composed of the heavy‐ and light‐chain variable domains of monoclonal antibodies which recognize the extracellular portion of each receptor. We have previously described the anti‐tumor activity of the bacterially produced scFv(FRP5)‐ETA directed to the erbB‐2 receptor. In this paper we describe the characteristics of scFv(225)‐ETA, a protein which binds the EGF receptor. The bacterially produced recombinant protein binds to the receptor with high affinity and inhibits the in vitro growth of the EGF receptor over‐expressing tumor cell lines A431 and MDA‐MB468. Combination treatment with scFv‐(FRPS)‐ETA and scFv(225)‐ETA led to an additive inhibitory effect on the in vitro growth of A431 cells. SKBR3 cells expressing low levels of EGF receptor but high levels of p 185erbB‐2 were not affected by scFv(225)‐ETA treatment but were sensitive to scFv(FRP5)‐ETA. Stimulation of SKBR3 cells and HCII RI#11 mouse mammary epithelial cells expressing the human erbB‐2 with EGF led to an increase in scFv(FRP5)‐ETA activity, showing that the EGF‐induced activation of erbB‐2 can potentiate the action of the erbB‐2‐directed toxin. Treatment of athymic nude mice with scFv(FRP5)‐ETA and the combination of both scFv‐ETA proteins led to the transient arrest of growth of established A431 tumors. scFv(22S)‐ETA treatment alone was the most effective, leading to tumor shrinkage during the course of treatment, whereas treatment with the parental monoclonal antibody 225 led to retarded tumor growth. © 1995 Wiley‐Liss, Inc.
Cervical cancer and herpes simplex virus type 2: Case‐control studies in Spain and Colombia, with special reference to immunoglobulin‐G sub‐classes
Authors: Muñoz Nubia , Kato Ikuko , Bosch F. Xavier , De Sanjosé Silvia , Sundquist Vivi‐Anne , Izarzugaza Isabel , Gonzalez Luis Carlos , Tafur Luis , Gili Miguel , Viladiu Pablo , Navarro Carmen , Moreo Pilar , Guerrero Eloisa , Shah Keerti V. , Wahren Britta 
Published: February 2007

AbstractTwo casecontrol studies, including 449 histologically confirmed cases of cervical intraepithelial neoplasia (CIN) III and 425 controls, and 2 studies on invasive cervical cancer, involving 316 histologically confirmed cases and 330 population controls, were conducted in Colombia and Spain to assess the role of herpes simplex virus type 2 (HSV‐2) in cervical neoplasia. Antibodies to this virus were also measured in the sera of 931 husbands of cases and controls. A serological assay using typespecific antigens, glycoprotein C for type I (gC‐1) and glycoprotein G for type 2 (gG‐2) was employed. Immunoglobulin‐G (IgG) subclasses, IgG1 and lgG3r were measured in women positive for HSV‐2 antibodies. No increase in risk of CIN III or invasive cancer was found in women whose sera or whose husbands' sera were positive to HSV‐2. However, compared with women negative to HSV‐2, the risk of CIN III progressively increased with increasing levels of IgG1. The trend was statistically significant in Colombia. There was also a statistically significant increasing trend in risk of invasive cancer with levels of IgG1 in Spain. The levels of lgG3 and its ratio to lgG1, which may indicate recurrent infections, were not associated with the risk of either type of cancer. When the association with lgG1 was analyzed by human papillomavirus (HPV) DNA status, as determined by polymerase chain reaction, the trend was clearer in women whose HPV status was not determined or in those with negative HPV DNA. These results suggest that the role of HSV‐2 is merely marginal and do not support the hypothesis that recurrent HSV‐2 infections are of importance for cervical neoplasia.
Comparison of immunohistochemistry and RT‐PCR for detection of CD44v‐expression, a new prognostic factor in human breast cancer
Authors: Dall Peter , Heider Karl‐Heinz , Sinn Hans‐Peter , Skroch‐Angel Petra , Adolf GÜNther , Kaufmann Manfred , Herrlich Peter , Ponta Helmut 
Published: February 2007

AbstractIn different human tumors, splice variants of the surface glycoprotein CD44 (CD44v) are correlated with advanced stages of tumor growth and metastatic potential. In breast cancer and colon cancer, expression of epitopes encoded by exon v6 on primary tumors is an independent prognostic factor for poor patient survival. Two different screening methods for the detection of CD44 variants in tumors have been applied: immunohistochemistry (IHC) and semi‐quantitative reverse transcription PCR (RT‐PCR). In this study, we have compared the predictive capacity and the applicability of both approaches, using 31 human breast‐tissue specimens (normal and neoplastic). IHC reveals lack of expression of CD44v on normal ductal epithelial cells but strong expression on myoepithelial cells. The majority of tumors express CD44 epitopes encoded by several variant exons. RT‐PCR detects splice variants in normal epithelium, probably derived from RNA expressed in the myoepithelium. In tumors, RT‐PCR reveals expression of a wide range of splice variants, including new ones that are not detected in normal breast tissue, e.g. ones that contain all variant exons. The conclusion of this comparison is that IHC is the better method for breast‐tumor sample screening but that the increased sensitivity of RT‐PCR can help to distinguish CD44v‐positive from CD44v‐negative tumors in cases where only a few tumor cells express variants or where epitopes are masked.