bluuebunny/crossref_metadata_2025_split huggingface dataset:
Viral infections and chemical exposures as risk factors for hepatocellular carcinoma in Vietnam
Authors: Cordier S. , Thuy Le Thi Bich , Verger P. , Bard D. , Dai Le Cao , Larouze B. , Dazza M. C. , Quinh Hoang Trong , Abenhaim L. 
Published: February 2007

AbstractA case‐control study investigating risk factors for hepatocellular carcinoma (HCC) was conducted in Hanoi, in the north of Vietnam, between 1989 and 1992. Male cases of HCC (152) diagnosed in 2 hospitals were included. Hospital controls (241) admitted mainly to abdominal surgery departments were frequency‐matched to cases for sex, age, hospital and place of residence (Hanoi, province). Odds ratios adjusted for matching variables and other potential confounders were estimated using unconditional logistic regression, or exact non‐parametric statistical inference when numbers were small. Positivity for hepatitis B surface antigen (HBsAg) was the main risk factor for HCC in this sample. Five subjects (3 cases, 2 controls) had been infected by hepatitis C virus (HCV), and none of them were carriers of HBsAg, giving an OR of 38 associated with HCV infection among HBsAg‐negative subjects. Alcohol drinking was associated with HCC and interacted with HBsAg positivity. Agricultural use of organophosphorous pesticides (30 liters/year or more) and military service in the south of Vietnam for 10 years or more were also associated with an increased risk of HCC. This study confirms the major role played by HBV infection and its association with HCC in south‐east Asia. It also suggests how other factors such as alcohol consumption or exposure to chemicals may interact with HBV infection.
Cancer incidence trends in women at high risk of human immunodeficiency virus (HIV) infection
Authors: Rabkin Charles S. , Biggar Robert J. , Baptiste Mark S. , Abe Toshi , Kohler Betsy A. , Nasca Philip C. 
Published: February 2007

AbstractTo determine the types and rates of tumors which may be associated with HIV infection in women, we used cancer incidence data from New York and northern New Jersey. We examined changes in incidence of selected cancers in women aged 20‐49 years and compared groups differing in incidence of AIDS. Black women were compared to white women in New York City and in the remainder of New York State; for cervical cancer, rates were also compared for Blacks and Whites in northern New Jersey. The incidence of Kaposi's sarcoma in women increased in New York City, beginning in 1982 for Blacks and in 1984 for Whites, but remained stable in the remainder of New York State. The incidence of non‐Hodgkin's lymphoma in New York women doubled in Blacks after 1982 whereas incidence trends in Whites were unchanged. No consistent variation was seen in the incidence of Hodgkin's disease. Cervical cancer in New York and northern New Jersey Blacks declined over the same period by approximately 40% for invasive tumors and 50% for in situ lesions. The HIV epidemic is associated with substantial excesses of Kaposi's sarcoma and non‐Hodgkin's lymphoma in women. The absence of Kaposi's sarcoma in upstate New York women suggests the existence of a geographically restricted co‐factor(s) for Kaposi's sarcoma in addition to HIV. If HIV affected cervical cancer incidence through 1988, its impact was small compared to the striking decreases which followed widespread adoption of Papanicolaou screening.
Diet and colorectal adenomas: A case‐control study in majorca
Authors: Benito E. , Cabeza E. , Moreno V. , Obrador A. , Bosch F. X. 
Published: February 2007

AbstractA case‐control study on dietary factors and colorectal adenomas was conducted in the island of Majorca, Spain, from April 1987 to February 1990. Subjects were interviewed using a food frequency questionnaire. Nutrient and caloric intake was estimated using local food composition tables. The risk of colorectal adenomas was related to the consumption of sugar and pastries. Consumption of vegetables was highly protective, irrespective of the cooking procedures. Analyses by nutrients identified as protective factors fiber from fruits and vegetables, magnesium and zinc, and vitamins C, B6 and folic acid. No excess risk was found for alcohol drinking, intake of saturated fats or animal protein. Of the non‐dietary factors, sedentariness in the workplace and urban residence were the only risk factors identified.
Cytogenetic analysis of epithelial renal‐cell tumors: Relationship with a new histopathological classification
Authors: van den Berg E. , van der Hout A. H. , Oosterhuis J. W. , Störkel S. , Dijkhuizen T. , Dam A. , Zweers H. M. M. , Mensink H. J. A. , Buys C. H. C. M. , de Jong B. 
Published: February 2007

AbstractRenal‐cell carcinomas (RCC) are clinically, histologically and cytogenetically very heterogeneous. The present histological WHO classification shows no clear correlation between histologic subtypes and specific chromosomal abnormalities. In 1986, a new classification was proposed by Thoenes and Störkel based on the cell type from which the tumor arises. They distinguish 5 cell types: clear‐cell, chromophilic, chromophobic, ductus Bellini and oncocytic. Results of 105 primary tumors show that, in this new classification, there is a correlation between different subtypes of renal‐cell tumor and specific chromosomal abnormalities at a microscopic and/or molecular level. The clear‐cell compact type shows structural aberrations of chromosomes 1, 3, 4, 5q, 6, 10q, 11 q and 12q, together with polysomy of chromosomes ×, 4, 5, 7, 10, 12, 15, 16, 19, 20, 21 and 22, monosomy of chromosomes 3, 8, 9, 13, 14, and loss of Y. The main characteristics of the chromophilic tubulo‐papillary type are trisomies 7 and 17, and loss of the Y‐chromosome. Chromophobic carcinoma seems to be correlated with, inter alia, polysomy 7, trisomies 12, 16, 18, 19, structural abnormalities of 11q, and telomeric associations. Oncocytomas do not reveal any specific chromosomal anomaly, except for trisomy 7. Loss of heterozygosity on 3p is only found in the clear‐cell compact type. Some specific chromosomal abnormalities correlate with a particular grade of the tumor. These correlations support the hypothesis that specific chromosomal abnormalities play a role in the histogenesis and oncogenesis of RCC. They may be important for tumor diagnosis and clinical prognosis.
Metalloproteinase and timp expression by the human breast carcinoma cell line 8701‐BC
Authors: Alessandro R. , Minafra S. , Pucci‐Minafra I. , Onisto M. , Garbisa S. , Melchiori A. , Tetlow L. , Woolley D. E. 
Published: February 2007

AbstractIt is widely accepted that collagenolytic enzymes are required to facilitate the invasion and spread of tumour cells into host tissues. Immunohistochemical, zymographic and PCR analyses have produced evidence that the recently established human mammary carcinoma cell line, 8701‐BC, expresses several metalloproteinases (MMP‐1, ‐2, ‐9 and ‐10) and their tissue inhibitors (TIMP‐1 and ‐2). Application of these different techniques has led to several observations, both complementary and dissimilar. Whereas PCR analysis showed that mRNA was detected for each of the proteins, the immunolocalization study demonstrated that MMP‐1, MMP‐2, MMP‐9 and TIMP‐1 production was restricted to only a proportion of the tumour cells, with no evidence of MMP‐3 or TIMP‐2 synthesis. Such observations suggested phenotypic heterogeneity within the cell line, which was further examined by use of the tumour cell clones BC‐3A and BC‐61 derived from the parental 8701 ‐BC line. Comparative studies using zymography and PCR analysis demonstrated differences in MMP‐2 and MMP‐10 expression between the 3 cultures. The data indicate that the 8701 ‐BC cell line retains an inherent capacity for metalloproteinase and TIMP expression, with the production of both interstitial collagenase (MMP‐1) and the 2 basement‐membrane‐degrading enzymes (MMP‐2 and MMP‐9) representing an aggressive collagenolytic pheno‐type. The concomitant production of TIMP‐1 by these cell cultures, and the apparent phenotypic heterogeneity displayed by these lines, suggest that metalloproteinase dysregulation may represent an important feature of clonal heterogeneity. Although the 8701‐BC and BC‐61 cells were much more invasive than those of the BC‐3A clone, as judged by the penetration of “Matrigel”, it has not yet been possible to relate this invasive potential to the metalloproteinase and TIMP profiles reported here for each cell line.
Retinoic‐acid‐induced augmentation of molecular species carrying sialosyl lewisa antigen in colorectal‐carcinoma cell cultures
Authors: Liepkalns V. A. , Icard‐liepkalns C. 
Published: February 2007

AbstractIn order to study the effects of vitamin‐A metabolites on long‐term carcinoma‐antigen secretion, colorectal‐carcinoma cells SWIII6 were cultured on membrane filters in totally synthetic media with 0 to 2.6 μM retinoic acid (RA). RA altered cell division, cell size and soluble‐sialosyl Lea (S‐Lea) secretion and S‐Lea accumulation within cells and apical‐membrane domains. Cultures treated with RA for 10‐12 days grew to lower cell densities (60% of controls) and contained more protein per cell (140% of controls). RA treated cells also had 5‐fold higher levels of S‐Lea in cells and secreted 9‐fold more S‐Lea into culture media assayed per 24 hr by (ELISA) 19‐9 monoclonal antibody binding. As total media S‐Lea increased, polarity of non‐lipid S‐Lea antigen secretion increased toward the interior (apical) media. High‐performance thin‐layer immunobinding showed that ganglioside S‐Lea was higher in RA‐fed cells, but could not be detected in apical media of RA‐fed or control cells after 24 hr. Western blots indicated that non‐lipid sialosyl Lewisa was bound to 150‐ to 180‐kDA molecular species principally in cells, but 210‐ to 300‐kDa molecular species appeared in the non‐lipid extract of media. Thus, the above RA alterations, monitored by 3 immunochemical techniques, include up to 9‐fold stimulation of “constitutive” 150‐ to 300‐kDa sialosyl‐Lewisa secretion, but ganglioside Lewisa is sorted differently and retained by apical membranes.
Adhesion to carcinoembryonic antigen by human colorectal carcinoma cells involves at least two epitopes
Authors: Jessup J. M. , Kim J. C. , Thomas P. , Ishii S. , Ford R. , Shively J. E. , Durbin H. , Stanners C. P. , Fuks A. , Zhou H. , Hansen H. J. , Goldenberg D. M. , Steele G. 
Published: February 2007

AbstractCarcinoembryonic antigen (CEA) may be involved in both cell‐cell and cell‐substrate adhesion. Our purpose was to determine whether epitopes involved in the homophilic binding of human colorectal carcinoma cells to CEA participated in adhesion to basement membrane proteins. Three human colorectal adenocarcinoma cell lines and one CHO cell line transfected with CEA cDNA were tested in a solid‐phase adhesion assay. The 2 CEA‐expressing carcinoma cell lines (KM‐12c and CCL 188) and the transfectant, but not the parental CHO line, bound to CEA. The CEA‐non‐producing carcinoma line (Clone A) did not bind to CEA. All colorectal carcinoma cell lines, the transfectant and the parental CHO line bound to laminin, while the colorectal carcinoma lines bound to type‐IV collagen. MAbs to epitopes on CEA that cross‐react with non‐specific cross‐reacting antigen (NCA) inhibited adhesion of CEA‐expressing cells to CEA. MAbs to non‐cross‐reactive epitopes of CEA did not block adhesion to CEA. When the inhibitory anti‐CEA antibodies were compared in a competitive radioimmunoassay, 2 distinct epitopes were identified. Epitope I is in the N‐terminal domain and defined by MAbs MN3, T84.1 and C110, whereas epitope II is located in the repeating loop domains and is recognized by antibodies MN15, PR3B10 and NPI. None of the antibodies to epitope I or II blocked adhesion by KM‐12c or CCL 188 cells to laminin or type‐IV collagen. Thus, at least 2 different regions on CEA participate in adhesion to CEA but not to collagen or laminin by CEA‐expressing human colorectal carcinoma cells.
Spontaneous development of a chromosomal translocation 5;14 in an epstein‐barr‐virus‐associated b‐cell lymphoma in a SCID mouse
Authors: Glaser Ronald , Theil Karl S. , Bonneau Robert H. , Sheridan John F. , Vasquez Marco , Allen Carl M. 
Published: February 2007

AbstractC.B‐17 SCID mice were inoculated with human peripheral blood leukocytes (PBLs) from normal Epstein‐Barr virus (EBV)‐seropositive and ‐seronegative donors. Confirmation of a functioning human immune response was demonstrated by the detection of human antibody after inoculation with rotavirus, tetanus toxoid, or EBV. One group of animals inoculated with PBLs from an EBV‐seropositive donor developed immunoblastic lymphomas approximately 9 weeks after transplantation. Confirmation of the species and sex of origin of the tumor cells was established using a spontaneous cell line prepared from the tumor. At passage I, the tumor‐cell line (AGTI) showed 15% of the metaphases with a translocation involving chromosomes 5 and 14. A lymphoblastoid cell line (AGLCL) established from the same PBLs from the same donor at the time of inoculation of the mice had a normal female karyotype. The AGLCL and a clone of AGTI cells were analyzed for rearrangement of immunoglobulin heavy chain (IgH) genes; both cell lines showed rearrangement of both IgH alleles. The results outlined in this report suggest that a spontaneous chromosomal translocation involving chromosome 14 occurred in normal PBLs in the SCID mouse.
Different expression patterns of oncogenes and proto‐oncogenes in hereditary and carcinogen‐induced tumors of xiphophorus
Authors: Mäueler Winfried , Schartl Angelika , Schartl Manfred 
Published: February 2007

AbstractHereditary melanoma in Xiphophorus hybrids carrying the melanoma‐inducing Tu‐Sd locus is caused by transcriptional activation of the Xmrk gene that resides at the Tu‐Sd locus and encodes a novel member of receptor tyrosine kinases (RTK). In this study, a total of 27 hereditary melanomas from various hybrid genotypes harbouring 7 different Tu alleles were also found to over‐express the corresponding Xmrk alleles. The level of over‐expression correlated with the degree of malignancy of the melanoma. In addition, Xsrc expression was high in many malignant melanomas. Expression patterns and levels of the Xiphophorus EGF‐receptor gene (Xerb B), the c‐myc (Xmyc), and the PDGF (Xsis) gene(s) were not intriguing. Transcription of the ras gene(s) may be correlated to secondary events of melanoma progression. Expression patterns of Xfms, the Xiphophorus CSF‐I receptor homologue, can be explained by different contents of infiltrating macrophages in the tumors. In carcinogen‐induced tumors including one melanoma no significant expression of the Xmrk oncogene could be detected. Xsrc expression, however, was strikingly high. This indicates that activation of oncogenes other than Xmrk is instrumental in tumorigenesis of neoplasia of non‐hereditary origin.
Determination of the specificities of monoclonal antibodies recognizing members of the CEA family using a panel of transfectants
Authors: Daniel S. , Nagel G. , Johnson J. P. , Lobo F. M. , Hirn M. , Jantscheff P. , Kuroki M. , von Kleist S. , Grunert F. 
Published: February 2007

AbstractCarcinoembryonic antigen (CEA), one of the most clinically important tumor markers, is mainly used in the post‐surgical surveillance of patients with colorectal carcinomas. CEA belongs to a large protein family, which includes cross‐reacting antigens, e.g., non‐specific cross‐reacting antigens (NCAs) and biliary glycoprotein (BGP) as well as pregnancy‐specific glycoproteins (PSGs). The genes encoding these proteins can be subdivided into the CEA and PSG subgroups. The members of the subgroups share antigenic determinants and show high similarity in amino‐acid sequences. Their derived secondary structures show them to belong to the Immunoglobulin superfamily. Due to the close relationship of the members of the CEA subgroup, it is very difficult to distinguish between the individual members with MAbs. Here we have used flow cytometric analysis of transfectants expressing individual members of the CEA subgroup as an alternative approach to determine the specificities of 13 MAbs. This allows us to examine the specificities of these antibodies for members of the CEA family, even of those which have not yet been characterized at the protein level. In addition, binding of the MAbs to NCAs expressed by polymorphonuclear cells (PMN) was tested by Western‐blot analysis, immunoprecipitation and flow cytometry.Four antibodies bound exclusively to NCA‐50/90 and one MAb (80H3) only to NCA‐95. MAb 4/3/17 recognizes CEA and BGP on the surface of transfectants and NCA‐160 from granulocytes. We assume that NCA‐160 is a product of the BGP gene. On granulocytes, which do not express CEA, MAb 4/3/17 is specific for NCA‐160 (BGP).Mutual inhibition of the MAbs binding to NCA‐50/90 revealed 3 different epitope groups.
Inhibition of tumor growth and enhancement of metastasis after transfection of the γ‐interferon gene
Authors: Lollini Pier‐Luigi , Bosco Maria C. , Cavallo Federica , De Giovanni Carla , Giovarelli Mirella , Landuzzi Lorena , Musiani Piero , Modesti Andrea , Nicoletti Giordano , Palmieri Gabriella , Santoni Angela , Young Howard A. , Forni Guido , Nanni Patrizia 
Published: February 2007

AbstractCells from the spontaneous metastatic TS/A mammary adenocarcinoma of a BALB/c mouse were transfected with the murine γ‐interferon (IFN‐γ) gene. Six clones (IFN‐γ clones) releasing between 2 and 6,000 international units (IU) of IFN‐γ/ml culture medium, were compared to TS/A parental cells (TS/A‐pc) and to cells transfected with neomycin resistance gene only (NEO cells). Autocrine IFN‐γ up‐regulated membrane expression of H‐2 class‐1 and Ly‐6 glycoproteins, but did not alter cellular proliferation in vitro. All IFN‐γ clones gave rise to progressive tumors with a growth rate significantly slower than that of tumors induced by TS/A‐pc and NEO cells, and inversely correlated with the amount of IFN‐γ secreted. TS/A‐pc and NEO tumors displayed a marginal reactive infiltrate, whereas those formed by IFN‐γy clones were massively infiltrated mostly by macrophages. In T‐ and NK‐deficient mice the growth of tumors formed by I FN‐y clones was not enhanced. In vitro tests showed that IFN‐γ clone cells were markedly more lysed by macrophages than TS/A‐pc and NEO cells, while they remained poorly sensitive to NK and LAK cells. These data as a whole suggest that the development of solid tumors by IFN‐γ clones is primarily hampered by macrophages and not by T‐lymphocytes or NK cells. When spontaneous metastatic ability was compared, 2 IFN‐γ clones releasing 2‐4 IFN‐γ lU/ml were significantly more metastatic, while most IFN‐γ clones appeared to be as metastatic as NEO cells. By contrast, following intravenous challenge, all IFN‐γ clones produced 5‐10 times more experimental metastases than NEO cells. The higher metastatic ability of IFN‐γ clones was attributed to increased resistance to NK cells since, in NK‐depleted BALB/c mice, metastatic spread of IFN‐γ clones was not enhanced, whereas a 50‐fold increase in the number of metastases was found upon injection of NEO cells.
Presence of CD4+ T suppressor cells in mice rendered unresponsive to tumor antigens by intravenous injection of irradiated tumor cells
Authors: Rakhmilevich Alexander L. , North Robert J. , Dye Earl S. 
Published: February 2007

AbstractWe used in vivo and in vitro assays to determine whether suppressor cells are generated in mice rendered unresponsive to tumor‐specific antigens by intravenous (i.v.) injection of non‐replicating tumor cells. The results show that a single i.v. injection of 2 × 107 irradiated P815 tumor cells resulted in the induction of a state of specific unresponsiveness to tumor‐associated antigens, as revealed by the inability of the treated mice to achieve immunologically‐mediated regression of an intradermal P8 15 tumor containing C. parvum, or to generate effector T cells capable of causing rejection of a P815 tumor in T‐cell‐deficient (T × B) test recipients. Failure to respond to tumor antigens was associated with the presence in spleen of CD4+ T cells capable, on passive transfer, of suppressing adoptive T‐cell‐mediated tumor regression in T × B recipients. However, the same CD4+ suppressor cells failed to inhibit the generation of tumor‐specific cytotoxic T lymphocytes (CTL) in vitro. On the contrary, spleen cells from mice made unresponsive by i.v. injection of tumor cells were primed to generate CTL in response to tumor antigens in vitro. Taken together, our results suggest that unresponsiveness induced by i.v. injection of tumor antigens is an active process mediated, at least in part, by CD4+ T suppressor cells, and that these cells coexist in the spleen with antigen‐primed effector T cells with a capacity to generate tumor‐specific CTL when released from suppression in vitro.
Activation of cytolytic activity in peripheral blood
Authors: Galligioni Enzo , Quaia Michele , Spada Antonella , Monfardini Daniela Silvio 
Published: February 2007

AbstractOur purpose was to evaluate the ability of blood monocytes of renal cancer patients to become cytotoxic against fresh, autologous tumor cells. Fresh target cells were obtained by mechanical and enzymatic dissociation of tumor and normal renal tissue. The A375 cell line, derived from a human melanoma, and the SW626 cell line, derived from a human ovarian carcinoma, were used as positive target cell controls. Monocytes from renal cancer patients and normal volunteers were activated in vitro with lipopolysaccharide (LPS), or muramyl tripeptide (MTP‐PE), or multilamellar vesicle liposomes containing MTP‐PE (MLV‐MTP‐PE), with or without a pre‐incubation with r‐IFN‐γ, and tested for cytotoxicity in a 72‐hr 111Indium‐release assay. All patients were tumor‐free at the time of the monocyte study. No difference in cytotoxic activity was observed between monocytes from healthy volunteers and those from cancer patients. Freshly dissociated tumor cells were as susceptible to tumoricidal monocytes as the 2 cell lines. Moreover, no cell population appeared to be resistant to activated monocytes, which were cytotoxic to both allogeneic and autologous fresh tumor cells. Activated monocytes maintained their ability to discriminate between normal and neoplastic cells and were not cytotoxic against autologous or allogeneic normal non‐neoplastic cells. Our data indicate that MLV MTP‐PE liposomes activate peripheral blood monocytes from cancer patients to a tumoricidal status against fresh, dissociated non‐cultured autologous tumor cells.