bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cancer incidence and mortality among teenagers in vaud, switzerland, 1974–1992
Authors: Levi Fabio , La Vecchia Carlo , Randimbison Lalao , Te Van‐Cong 
Published: February 2007

AbstractData from the Vaud Cancer Registry, Switzerland, were used to analyse incidence and mortality from cancer in teenagers (aged 10 to 19 years) over the period 1974–1992. A total of 113 males and 87 females were registered. Of these, 23% were lymphomas, 16% leukaemias, about 15% central nervous system neoplasms, 10% germ cell tumours and bone neoplasms and 8% soft tissue sarcomas. The overall incidence rate (age‐adjusted, world standard population) for all cancers combined was 167 per million boys and 128 per million girls. In both sexes, there was some indication of rising trends over time, to reach 196 per million males and 141 per million females in 1986–1992. The only types of cancer showing consistent upward trends in both sexes were lymphomas. A total of 53 cancer deaths were certified, due to leukaemias in about 40% of cases in both sexes and to lymphomas and brain tumours in 15%–20%. The overall mortality rate at age 10–19 years (age‐standardised, world standard) was 47 per million boys and 31 per million girls, and no trend in mortality was observed over time. The 2 main findings of our analysis are (i) the absence of major trends in cancer incidence in adolescents, with the sole exception of a possible increasing incidence of lymphomas, and (ii) the lack of appreciable trends in mortality, in view of the declines in cancer mortality observed in children and young adults over the same calendar period. © 1995 Wiley‐Liss, Inc.
Characterization of mature and immature Rad LV‐Induced thymic T‐cell lines for tumorigenesis and mhc‐class‐I gene expression
Authors: Bashi Orna , Ehrlich Rachel 
Published: February 2007

AbstractClass‐I‐MHC molecules are divided into class‐la molecules, which play major roles in recognition of virus‐infected cells, graft rejection and immune responses against tumors, and class‐lb molecules, which are less polymorphic and may be responsible for presenting unique classes of peptides. Our report characterizes RadLV‐induced thymic T‐cell lines that differ both in their tumorigenic potential and in the level of protein for class‐la and TL genes. The PDI.I cell line is CD4−CD8+ and expresses relatively high levels of class‐l as compared with the CD4+CD8+ PDI.2 cell line. These class‐I‐expression levels correlate with thymocytes and splenic T cells of the same phenotype, except that normal cells fail to express TL3b. Interferon‐treated PDI.2 cells demonstrate significantly lower levels of class‐l expression than do interferon‐treated PDI.I cells, and were shown to contain large amounts of degraded class‐l mRNA, at least some of which was TL in origin. These RNA products were not detected in PDI.I cells, suggesting the existence of a mechanism controlling cell‐specific and gene‐specific mRNA stability. Such RadLV‐induced cell lines provide a means for obtaining stage‐specific T cells, which can be used for studying the regulation of class‐l gene expression during T‐cell differentiation, as well as factors that differentially regulate class‐la and class‐lb expression and are potentially useful for studying T‐cell differentiation in general. © 1995 Wiley‐Liss, Inc.
Glycosylation of a novel member of the immunoglobulin gene superfamily expressed in rat carcinoma cell lines
Authors: Chadéneau Corinne , Le Moullacguy Cornu Béatrice , Meflah Khaled , Denis Marc G. 
Published: February 2007

AbstractMAb E4 recognizes a 66‐kDa glycoprotein, pE4, which is a member of the immunoglobulin gene superfamily. This protein is expressed at the cell surface in rat colon and mammary carcinomas, but only in trace amounts in normal adult rat tissues. Since expression of aberrant carbohydrate structures is often associated with malignant transformation, glycosylation of pE4 was analyzed. Reactivity of lectins with pE4 suggested the absence of N‐acetylneuraminic acid, terminal galactose and O‐linked glycan, and the presence of N‐linked glycans. Tunica‐mycin treatment reduced the binding of MAb E4 to cancer cells suggesting that the E4 epitope is at least partially glycosylated. Digestions with neuraminidases, O‐glycosidase and peptide‐N‐glycosidase F confirmed these results. Pronase treatment abolished the binding of MAb E4, indicating that E4 epitope involves not only a carbohydrate determinant but also a peptide moiety. Mild periodate oxidation abolished the binding of MAb E4, indicating that non‐reducing terminus carbohydrates are part of the E4 epitope. Neutral sugar analysis revealed the absence of galactose and the presence of fucose. Since fucose is sensitive to periodate oxidation, this sugar could be the carbohydrate part of the determinant recognized by MAb E4. Reactivity of lectins specific for fucose indicated the presence of ø(1‐6)‐fucose on pE4. © 1995 Wiley‐Liss, Inc.
Direct transforming activity of TGF‐β on rat fibroblasts
Authors: Vossbeck Heinke , Höfler Brigitte Strahmpetra , Bauer Georg 
Published: February 2007

AbstractTreatment of NRK 536 fibroblasts with EGF and transforming growth factor type beta (TGF‐β) is known to lead to the reversible induction of the transformed phenotype in a large percentage of cells. Maintenance of the transformed state is dependent on the continuous presence of the cytokines. Here we show that treatment of these cells with TGF‐β alone leads to the formation of a small percentage of colonies, the majority of which stably retain the transformed phenotype after removal of the cytokine. Colony induction is dependent on the concentration of TGF‐β originally present. Stably transformed cells grow in soft agar without further addition of exogenous TGF‐β, and exhibit criss‐cross morphology in monolayer culture and a diffuse actin pattern. Transformation of NRK 536 cells can be demonstrated only for individualized cells treated with TGF‐p in soft agar, as treatment in monolayer leads to the induction of apoptosis in newly transformed cells by neighboring normal cells. Transformation of NRK 536 fibroblasts by TGF‐β is not due to the induction of point mutations by TGF‐β. © 1995 Wiley‐Liss, Inc.
The human immunodeficiency virus(HIV) inhibitor 9‐(2‐phosphonylmethoxyethyl)adenine (pmea) is a strong inducer of differentiation of several tumor cell lines
Authors: Balzarini J. , Verstuyf A. , Hatse S. , Goebels J. , Sobis H. , Vandeputte M. , De Clercq E. 
Published: February 2007

Abstract9‐(2‐phosphonylmethoxyethyl)adenine (PMEA) is the prototype compound of a series of acyclic nucleoside phosphonate derivatives endowed with potent and selective anti‐retroviral activity in vitro and in vivo. We have now found that PMEA is also a potent inducer of differentiation of a number of tumor cells, including human erythroleukemia K562 cells, rat choriocarcinoma RCHO cells and human acute promyelocytic leukemic HL‐60 cells. At 10 μM PMEA, rat RCHO cell cultures could be almost fully differentiated, and at 50 μM PMEA, approximately 50% of the K562 cells could be triggered to produce hemoglobin. The differentiating activity of butyric acid was at least partially additive to that of PMEA when both drugs were combined in K562 cell cultures. PMEA needs to be present for at least 2 or 3 days in the K562 cell cultures to achieve optimal differentiating activity. This suggests that either a PMEA metabolite and/or its anti‐metabolic effects may be responsible for differentiation of the tumor cells. © 1995 Wiley‐Liss, Inc.
Muscle wasting associated with cancer cachexia is linked to an important activation of the atp‐dependent ubiquitin‐mediated proteolysis
Authors: Llovera Marta , Garcia‐Martinez Cèlia , Agell Neus , Lopez‐Soriano Francisco J. , Argiles Josep M. 
Published: February 2007

AbstractRats bearing the Yoshida AH‐130 ascites hepatoma for 7 days showed an important decrease in muscle mass—over 30% in gastrocnemius and extensor digitorum longus (EDL)—in relation to non‐tumour‐bearing controls, which is associated with an increased proteolytic rate‐in in vitro incubation. In order to identify the precise biochemical process which was involved, we measured different proteolytic systems in incubated EDL muscles. The capacity for intralysosomal proteolysis, as measured by sensitivity to methylamine, was not increased in tumour‐bearing rats, suggesting that the mechanism involved in the increased proteolytic rate was extralysosomal. Incubations using the Ca2+ ionophore A23187 revealed no change in the activity of calcium‐dependent proteases as a consequence of tumour growth. Finally, muscle incubation in an ATP‐depleted medium allowed us to conclude that energy‐dependent proteases were involved in the activation of muscle proteolysis in tumour‐bearing rats. In particular, the ubiquitin‐dependent proteolytic system is involved, since there is an important increase in ubiquitin conjugates in the skeletal muscle of tumour‐bearing rats. It may thus be suggested that extralysosomal ATP‐and ubiquitin‐dependent proteases underlie the biochemical mechanism of muscle wastage associated with cancer cachexia. © 1995 Wiley‐Liss, Inc.
Anti‐gastrin antibodies raised by gastrimmune inhibit growth of the human colorectal tumour AP5
Authors: Watson Susan A. , Michaeli Dov , Grimes Steven , Morris Teresa M. , Crosbee David , Wilkinson Mark , Robinson Graham , Robertson John F. R. , Steele Robert J. C. , Hardcastle Jack D. 
Published: February 2007

AbstractThe neutralising ability of rabbit anti‐gastrin‐17 (G17) anti‐serum raised by Gastrimmune, an immunogen constructed of the N‐terminal portion of human G17 conjugated to diptheria toxoid (DT), was evaluated. The anti‐serum (denoted anti‐G17: DT) was shown to displace 125[I] G17 from the gastrin receptors on AR42 cells. The therapeutic effect of the rabbit anti‐G17:DT anti‐serum was evaluated on a freshly derived human colorectal cancer cell line, AP5, which was shown to express both gastrin receptors and gastrin immunoreactivity as assessed by immunocytochemistry. Rabbit anti‐G17:DT anti‐serum was shown to block basal in vitro growth of AP5 cells when used at an antigen binding capacity of 3.75 × 10−9 M. The same dilution of anti‐serum completely reversed growth stimulated by human G17 at concentrations of 1 × 10−8 and 1 × 10−9 M but did not inhibit growth at 1 × 10−8 M G17. When AP5 was grown as a xenograft in nude mice, the sensitivity to the proliferative effect of human G17 was maintained. In addition, the basal growth of AP5 xenografts was significantly reduced by i.v. infusion of rabbit anti‐G17:DT anti‐serum when compared to treatment with rabbit anti:DT control anti‐serum. Thus anti‐G17:DT antibodies raised by Gastrimmune may be of clinical value in gastrin‐sensitive tumours. © 1995 Wiley‐Liss, Inc.
O6‐methylguanine‐DNA methyltransferase activity in breast and brain tumors
Authors: Preuss Ilka , Eberhagen Ingrid , Haas Simone , Eibl Robert H. , Kaufmann Manfred , Minckwitz Gunther Von , Kaina Bernd 
Published: February 2007

AbstractThe DNA repair protein O6‐methylguanine‐DNA methyltransferase (MGMT) is a main determinant of resistance of tumor cells to the cytostatic activity of chemotherapeutic alkylating agents (methylating and chloroethylating nitrosoureas) and is effective in protecting normal cells against genotoxic and carcinogenic effects resulting from DNA alkylation. Therefore, the level of expression of MGMT is significant for the response of both the tumor and the non‐target tissue following application of nitrosoureas in tumor therapy. To determine the expression of MGMT in tumor tissue, we have assayed MGMT activity in 68 breast carcinomas and 38 brain tumors. There was a wide variation of MGMT expression in breast carcinomas ranging from below the level of detection up to 863 fmol/mg protein. About 4% of breast tumors did not display detectable MGMT, 15% had activity lower than 100 fmol/mg protein, and 26% expressed more than 500 fmol/mg. The mean level of expression was 321 fmol/mg. In brain tumors (astrocytoma WHO grade I, II, and III, and glioblastoma WHO grade IV) the MGMT activity was generally lower than in breast tumors, ranging from below the level of detection up to 238 fmol/mg. The mean level of expression was 55 fmol/mg. Five percent of the brain tumors had no detectable MGMT activity. The MGMT repair activity correlated well with the amount of MGMT protein present in tumor samples, as shown by Western‐blot analysis, indicating that loss of MGMT repair activity is due to inability of these tumor cells to synthesize the protein. © 1995 Wiley‐Liss, Inc.
Epstein‐barr virus (EBV) in malaysian upper‐aerodigestive‐tract lymphoma: Incidence and sub‐type
Authors: Peh Suat C. , Sandvej Kristian , Pallesen Gorm 
Published: February 2007

AbstractEpstein‐Barr virus (EBV) type B, a less potent transformer of B lymphocytes than type A, has rarely been detected in EBV‐associated neoplasms except in AIDS‐related lymphomas, in which about 50% of the cases contained this sub‐type. In this study we analyzed the association of EBV and the distribution of virus sub‐types in Asian non‐Hodgkin's lymphoma (NHL) of the upper aerodigestive tract. We studied archival material of 29 NHL cases from Malaysia. B‐ and T‐cell associated antigens were demonstrated by immunohistochemistry, and EBV early RNA EBER‐1 was demonstrated using the RNA in situ hybridization technique. EBV was detected in the majority of tumour cells in 11/13 T‐NHL but in only 1/16 B‐NHL. EBV was sub‐typed by single‐step polymerase chain reaction of the EBNA‐2 gene. This was successful in 9/10 cases of EBER‐I‐positive tumours and all contained type‐A virus only. Our results showed a preponderance of T‐cell lymphoma of the upper aerodigestive tract in the ethnic Chinese group of Malaysian patients, and EBV was strongly associated with T‐NHL but not with B‐NHL. Our results suggest that type‐A EBV is the prevalent sub‐type in Asian NHL of the upper aerodigestive tract, similarly to findings in Asian nasopharyngeal carcinoma. © 1995 Wiley‐Liss, Inc.
Incidence and prognostic significance of vascular and neural invasion in squamous cell carcinomas of the esophagus
Authors: Sarbia Mario , Porschen Rainer , Borchard Franz , Horstmann Olaf , Willers Rainhart , Gabbert Helmut E. 
Published: February 2007

AbstractThe prognostic influence of blood‐vessel invasion (BVI), lymphatic‐vessel invasion (LVI) and neural invasion (NI) was evaluated retrospectively in a series of 161 patients with squamous cell carcinoma (SCC) of the esophagus who underwent esophageal resection. Evidence of BVI, LVI and NI was found in 32.9%, 48.5% and 26.1%, respectively. Incidence of BVI, LVI and NI was significantly higher in high pT categories (pT3 and pT4) than in low pT categories (pTI and pT2) and in patients with distant metastases than in patients without distant metastases. Incidence of LVI and NI in lymph‐node‐positive patients was significantly higher than in lymph‐node‐negative patients. The 5‐year survival rate was significantly lower in patients with BVI or LVI than in patients without BVI or LVI. Patients with evidence of NI showed no significant differences in 5‐year survival from patients without evidence of NI. By stepwise multivariate Cox regression analysis, BVI and LVI were shown to be independent prognostic factors. A search for vascular invasion may therefore provide additional prognostic precision in SCC of the esophagus. © 1995 Wiley‐Liss, Inc.
Resistance‐associated factors in human small‐cell lung‐carcinoma GLC4 sub‐lines with increasing adriamycin resistance
Authors: Versantvoort C. H. M. , Withoff S. , Broxterman H. J. , Kuiper C. M. , Scheper R. J. , Mulder N. H. , De Vries E. G. E. 
Published: February 2007

AbstractPrevious studies have shown that the in vitro‐selected adriamycin‐resistant human small‐cell lung‐carcinoma cell line GLC4‐ADR150 displays multidrug resistance as the result of 3‐fold decreased DNA‐topoisomerase II (topo II) activity and a 6‐fold reduction in adriamycin accumulation. Not the MDRI gene, but the MRP gene, was over‐expressed in this cell line. The aim of our study was to establish which of these drug‐resistance‐associated factors are already involved in drug resistance occurring at early steps of selection with adriamycin. To address this question, changes in expression of topo IIα/topo IIβ, MRP and drug accumulation were measured along with adriamycin resistance (from 2‐ to 10‐ to 150‐fold) and in a partial revertant cell line (10‐fold resistant). Topo IIα and IIβ mRNA and protein levels were decreased in the resistant sub‐lines, except in the 10‐fold‐resistant cell line. Cellular daunorubicin accumulation was decreased 1.2‐ to 5‐fold with increasing resistance. MRP mRNA was over‐expressed in all resistant sub‐lines, with a marked increase in the 10‐fold‐resistant cells (level of expression as high as in the GLC4‐ADR150 cells). Expression of an ATP‐binding 190‐kDa membrane protein and Western‐blot analysis with anti‐MRP anti‐serum ASPKE, was in accordance with the expression of MRP mRNA in all cell lines. Expression of MRP mRNA and protein, however, was not proportional with the decrease in drug accumulation in all resistant sub‐lines. This study also shows that drug accumulation, topo II and MRP expression were all changed at the earliest stage of resistance development of GLC4 cells upon adriamycin selection. © 1995 Wiley‐Liss, Inc.
Glycosylation of β‐1 integrins in B16‐F10 mouse melanoma cells as determinant of differential binding and acquisition of biological activity
Authors: Veiga Silvio S. , Chammas Roger , Cella Nathalie , Brentani Ricardo R. 
Published: February 2007

AbstractStudying B16‐F10 cells we could identify β‐1 integrins as laminin, fibronectin and collagen receptors. Gradient ionic strength elution analysis of affinity chromatography showed differential interactions between laminin‐binding β‐1 integrins (two β‐1 polypeptides of 105 and 120 kDa) and fibronectin and collagen‐binding β‐1 integrins (elution of one major β‐1 polypeptide of 120 kDa) and their respective ligands. To evaluate this diversity we submitted B16‐F10 extracts to IEF and SDS‐PAGE and found that one β‐1 integrin formed acidic and larger isoforms, while another formed basic and smaller isoforms. To study this difference we also submitted material eluted from WGA‐Sepharose columns to IEF but now only the acidic β‐1 isoform was found. Extracts of B16‐F10 treated with neuraminidase showed only the basic β‐1 isoform, suggesting that terminal sialic acid residues may be responsible for this acidic pattern, an interpretation supported by the fact that MAA (Maackia ammurensis agglutinin) reacts only with the acidic isoform. Differential glycosylation of β‐1 integrin isoforms in B16‐F10 was also demonstrated since the smaller lamininbinding β‐1 integrin isoform reacted only with GNA (Galanthus nivalis agglutinin), whereas the mature larger form reacted with DSA (Datura stramonium agglutinin) and MAA; thus this heterogeneity of β‐1 chains is essentially due to variable glycosylation. Autoradiography and immunoblotting analysis of material separated by 2‐dimensional electrophoresis show that only the processed forms of β‐1 integrins are expressed at the cell surface. © 1995 Wiley Liss, Inc.
Tenascin‐C in serum: A questionable tumor marker
Authors: Schenk Susanne , Muser Jürgen , Vollmer Günter , Chiquet‐Ehrismann Ruth 
Published: February 2007

AbstractIn normal adult tissue tenascin‐C (TN‐C) is usually expressed at low levels. However, it is strongly induced in many tumors as well as in other pathological conditions often associated with inflammation. To evaluate the diagnostic significance of TN‐C, we established a sensitive sandwich ELISA to determine TN‐C levels in serum. Furthermore, we investigated the distribution of TN‐C variants in serum and found the large TN‐C isoforms to be predominant. We measured TN‐C in sera from 15 healthy persons, 75 tumor patients and 84 patients selected due to their elevated levels of the acute‐phase protein C‐reactive protein (CRP), which is a very specific marker for infection and inflammation. It was found that sera from cancer patients can have elevated TN‐C levels; however, the increase was more pronounced in persons with high levels of CRP. There appeared to be a correlation of TN‐C levels with the levels of CRP. In view of these facts, the diagnostic value of TN‐C levels in serum as a potential tumor marker seems to be questionable, since our data show that TN‐C levels can be elevated as a consequence of infection and inflammation. © 1995 Wiley‐Liss, Inc.
Human papillomaviruses in 91 oral cancers from indian betel quid chewers—high prevalence and multiplicity of infections
Authors: Balaram Prabha , Nalinakumar K. R. , Abraham Elizabeth , Balan Anita , Hareendran N. K. , Bernard Hans‐Ulrich , Chan Shin‐Yen 
Published: February 2007

AbstractIndia has one of the world's highest incidences of oral cancer. The habit of chewing betel quid is widespread and is suspected to play a role in the etiology of this disease. Studies in many other countries have also pointed to a role for human papilloma‐viruses (HPVs) in the etiology of some oral cancers. In this study we analyzed biopsies from 91 Indian oral cancer patients, most of whom were betel quid chewers, by PCR amplification and direct DNA sequencing. HPV DNA was detected in 74% of these lesions, of which 41% had multiple HPV infections. Among the lesions from different oral sites, lesions of the tongue had the highest rate (9 of 11) of HPV infection. These HPV prevalences are among the highest ever reported in oral cancers. As to individual HPV types, prevalences of HPV‐6, HPV‐II, HPV‐16 and HPV‐18 were 13%, 20%, 42% and 47%, respectively. No additional known or novel HPV types were detected. To understand the unexpectedly high prevalences of the “low‐risk” types HPV‐6 and HPV‐11, we compared the subtypes and variants that were found in oral cancers against those from benign genital warts from the same patient population but found no differences. The high prevalence of HPV in the oral cancers of these Indian patients suggests that viral infection is an important etiological component, with betel quid probably causing additional mutagenic steps in the carcinogenic process. © 1995 Wiley‐Liss, Inc.
αv‐Integrins in human melanoma: Gain of αvβ3 and loss OF αvβ5 are related to tumor progression in situ but not to metastatic capacity of cell lines in nude mice
Authors: Danen Erik H. J. , Jansen Kees F. J. , Van Kraats Annemieke A. , Cornelissen Ine M. H. A. , Ruiter Dirk J. , Van Muijen Goos N. P. 
Published: February 2007

AbstractWe investigated the expression of αv‐integrins in different stages of human cutaneous melanocytic tumor progression. We observed that αvβ5 was the αv‐integrin expressed in all common nevocellular nevi, in 78% of dysplastic nevi, in 63% of early primary melanomas, in 43% of advanced primary melanomas, and in 33% of melanoma metastases. Hence, loss of αvβ5 expression was related to melanocytic tumor progression. In line with earlier reports, αvβ3 was exclusively detected in advanced primary melanomas and metastases (24% and 50% respectively). Staining with anti‐αv monoclonal antibodies (MAbs) in lesions where both αvβ3 and αvβ5 were absent showed that alternative αv‐integrins were expressed in advanced primary melanomas and metastases. By FACS analysis, we determined expression of αvβ5 and αvβ3 in 4 human melanoma cell lines with different metastatic capacities after s.c. inoculation into nude mice. One of the non‐metastatic and both highly metastatic cell lines expressed αvβ5 at their surface. Surprisingly, αvβ3 was detected exclusively in the non‐metastatic cell lines. Absence of αvβ3 in the highly metastatic cell lines was confirmed by lack of immunoprecipitation from 35S‐methionine‐labeled cells and by absence of immunohistochemical staining on primary and metastatic xenograft lesions. Our findings indicate that αvβ5 expression is often lost in advanced stages of melanocytic tumor progression in situ, while αvβ3 is acquired, but that a decrease in αvβ5 and an increase in αvβ3 expression are not necessarily related to the metastatic behavior of human melanoma cells in nude mice. © 1995 Wiley‐Liss, Inc.