bluuebunny/crossref_metadata_2025_split huggingface dataset:
Distribution of VRA09, an ovarian tumor‐associated antigen, distinguishing borderline serous tumors
Authors: Voeltzel Thibault , Duvillard Pierre , Ghillani Pascale , Bénard Jean , Bohuon Claude , Bellet Dominique , Bidart Jean‐Michel 
Published: February 2007

AbstractWe recently reported the characterization of an antigen designated VRA09, identified by a monoclonal antibody and overexpressed on the surface of vincristine‐resistant human ovarian carcinoma cells. In the present study, we analyze the distribution of this antigen in normal and tumor tissues. Its pattern of expression appears to differ from that described for other drug‐resistance‐ and/or tumor‐associated antigens. In normal tissues, the antigen has a restricted histological distribution and appears to be localized in mesoderm‐derived tissues. In tumor tissues, VRA09 expression was mainly detected in serous ovarian tumors. Indeed, VRA09 is strongly expressed in papillary serous cystadenocarcinomas and their metastases, and more specifically in the basement membranes of serous tumors of borderline malignancy. In contrast, no immunostaining was observed in normal ovarian tissue or benign tumors. The detection of this antigen may help to identify serous ovarian tumors by distinguishing tumors of low malignancy from cystadenocarcinomas.
Elevated levels of benzene‐related compounds in the urine of cigarette smokers
Authors: Ong C. N. , Lee B. L. , Shi C. Y. , Ong H. Y. , Lee H. P. 
Published: February 2007

AbstractBenzene exposure causes leukemia and lymphomas. Recent epidemiological findings have also shown an association between cigarette smoking and an increased risk of leukemia. However, further evidence is required to document the biological plausibility of this association. In evaluating this link, it is important to note that cigarette smoke contains benzene and various pyrolytic compounds, among other carcinogens. This study aims to determine the uptake of benzene by measuring 3 benzene‐related compounds in cigarette smokers and non‐smokers. Urinary concentrations of catechol (CAT), hydroquinone (HQ), and trans,trans‐muconic acid (tt‐MA) were measured by high‐performance liquid chromatography (HPLC) with fluorimetric and UV detection, respectively. The results showed that these compounds were present in all urine samples. However, the concentrations were significantly higher in smokers than in non‐smokers. The mean level of urinary tt‐MA was 0.19 ± 0.09 mg/g creatinine for 46 male smokers and the corresponding value for 40 non‐smokers was 0.14 ± 0.07 mg/g creatinine. The mean concentrations of HQ and CAT were 0.81 ± 0.4 and 3.51 ± 2.6 mg/g creatinine for smokers, and 0.45 ± 0.4 and 1.94 ± 1.2 mg/g creatinine for non‐smokers, respectively. These results suggest that cigarette smoking is associated with a significant additional exposure to benzene and its related compounds. Furthermore, significant correlations were observed between the concentrations of cotinine, the metabolite of nicotine, and the above compounds. These findings suggest that the exposure originated from cigarette smoking.
Tomatoes and risk of digestive‐tract cancers
Authors: Franceschi Silvia , Bidoli Ettore , Vecchia Carlo La , Talamini Renato , D'Avanzo Barbara , Negri Eva 
Published: February 2007

AbstractIn view of the persisting uncertainty concerning possible mechanisms by which high vegetable and fruit intake decreases cancer risk, foods with divergent values for potentially important micronutrients are a priority for investigation. Tomatoes are low in beta‐carotene, but high in lycopene, an active antioxidative agent. In order to assess the effect of tomatoes on risk of cancers of the digestive tract, data were analyzed from an integrated series of case‐control studies conducted between 1985 and 1991 in northern Italy, where tomato intake is high but, also, heterogeneous. The overall dataset included the following histologically confirmed cancer cases: oral cavity and pharynx, 314; esophagus, 85; stomach, 723; colon, 955; and rectum, 629; and a total of 2,879 controls admitted to hospital for acute non‐neoplastic or non‐digestive conditions, unrelated to long‐term dietary modifications. Multivariate odds ratios (OR) and 95% confidence interval (CI) for subsequent quartiles of intake of raw tomatoes were derived, after allowance for age, sex, study center, education, smoking and drinking level, and tertile of total caloric intake. There was a consistent pattern of protection for all sites (OR in the upper quartile ranging between 0.4 and 0.7), most notably for gastrointestinal neoplasms. All trends in risk were highly significant. The beneficial effect of raw tomatoes in this population may be partly due to the fact that they constitute perhaps the most specific feature of the Mediterranean diet. However, if it is true that tomatoes protect against digestive‐tract cancers, this is of interest from both a scientific and a public health viewpoint.
Loss of polarity and De novo expression of the β1 family of integrins in thyroid tumors
Authors: Vitale Mario , Bassi Vincenzo , Illario Maddalena , Fenzi Gianfranco , Casamassima Adele , Rossi Guido 
Published: February 2007

AbstractThe expression and cell‐membrane distribution of the β1 family of integrins (very‐late‐activation antigens, VLA) were investigated in benign and malignant human thyroid tumors. We compared tissue samples of normal glands, nodular goiters, adenomas and carcinomas. We also examined 3 thyroidcarcinoma cell lines cultured in vitro. The expression of subunits of the β1 family of integrins was assessed by flow cytometry and specific antibodies in dispersed single‐cell suspensions and by immunofluorescence on frozen tissue sections. In contrast to the heterogeneity of the expression of β1 integrins observed in other tumors, thyroid neoplastic lesions showed a remarkably constant VLA profile. In all tumors, benign as well as malignant, and in carcinoma cell lines, all sub‐units of β1 integrins were expressed at high levels. While sub‐units α1, α3, α5, α6 and occasionally α2 were also present in a cell sub‐set of normal glands and nodular goiters, expression of α4 was restricted to neoplastic lesions; this integrin can be therefore considered an antigen associated with thyroid tumors. It has been reported that in normal glands and in nodular goiters, the expression of β1 integrins is restricted to the basal‐cell membrane. Immunofluorescence on tissue sections showed instead that, in adenomas and carcinomas, the polarized distribution of these integrins on the cell membrane is lost.
Generation of an antitumour immune response to a murine mesothelioma cell line by the transfection of allogeneic mhc genes
Authors: Leong Clement C. , Robinson Bruce W. S. , Garlepp Michael J. 
Published: February 2007

AbstractWe have determined whether transfection and expression of allogeneic MHC genes in a murine mesothelioma cell line can generate an anti‐tumour immune response. The MHC genes encoding H‐2Kb and H‐2Dd were transfected into the mesothelioma cell line AC29 (derived from CBA mice, H‐2k) and transfectant clones isolated. Each of five H‐2Kb and 4 H‐2Dd transfectant clones were unable to form tumours in CBA mice, although they had maintained their ability to form tumours in F1 crosses of CBA ± C57b1/10 or CBA ± BALB/c, respectively. Thus the tumours expressing the transfected MHC genes were rejected only in an allogeneic setting. Mice without tumours after transfectant challenge were inoculated on the opposite flank with 1 ± 106 parental AC29. There was no evidence of systemic immunity to the parental cell line since tumours formed at the same rate as in naive mice. The mixing of allogeneic MHC transfectants with parental AC29 did, however, retard the growth of parental tumour. Our study illustrates that the expression of allogeneic MHC molecules on a highly immunosuppressive and non‐immunogenic murine malignant mesothelioma cell line was able to stimulate rejection of tumour cells but was incapable of generating a systemic protective response against the parental cell line.
DNA of lymphoma‐associated herpesvirus (HVMF1) in SIV‐infected monkeys (Macaca fascicularis) shows homologies to EBNA‐1, ‐2 and ‐5 genes
Authors: Li Su Ling , Biberfeld P. , Ernberg I. 
Published: February 2007

AbstractWe have characterized a new Epstein‐Barr‐virus(EBV)‐like herpesvirus associated with lymphomas of SIV‐infected cynomolgus (Macaca fascicularis) monkeys and propose that this virus is designated herpesvirus macaca fascicularis I (HVMFI). Genomic regions in HVMFI of potential significance for tumor pathogenesis were analyzed by Southern blotting, PCR and sequencing, and compared with human EBV DNA. Virus from 7 SIV‐associated lymphomas and one lymphoma‐derived cell line were shown to share homology with the EBNAI‐ and EBNA2‐coding regions of EBV, while some homology to EBV‐LMPI was detectable only at low‐stringency hybridization. Homologous regions to the long internal repeat (IRI; BamHI W), the EBERI and 2 and the latent origin of DNA replication (oriP) could also be demonstrated in HVMFI. These coding regions, except IRI, showed restriction‐enzyme maps different from those of EBV. Sequencing of the EBNA5 homologous region of HVMFI DNA, corresponding to exons W1 and W2, showed 65% homology to the EBV exons W1 and W2, and 80% to the whole region including the intron. Since EBNA5 has been reported to bind tumor‐suppressor proteins p53 and Rb in vitro, the HVMFI homology could be important for the lymphomagenic capacity of this monkey herpesvirus.
Carcinogenic risk of dark VS. light liquor
Authors: Day Gina L. , Blot William J. , McLaughlin Joseph K. , Fraumeni Joseph F. 
Published: February 2007

AbstractA previous report suggested that the cancer risk associated with hard liquor is greater among users of dark liquors, which may contain more potentially carcinogenic compounds than light liquors. To test this hypothesis, we examined alcohol consumption data obtained by interview with 921 cases and 900 controls who participated in 1984–1985 in a population‐based case‐controls study of oral and pharyngeal cancer conducted in 4 areas of the United States. Among heavy liquor drinkers (30+ drinks/week), odds ratios were 13.2 (95% Cl = 5.2–33.5) for those who usually drank light liquors vs. 4.6 (95% Cl = 2.7–7.9) for those who usually drank dark liquors, with higher risks for light vs., dark liquors at each anatomical subsite. This analysis provides no support for the notion that dark liquors are more carcinogenic than light liquors or that non‐ethanolic ingredients of alcoholic beverages are major contributors to the excess risk of oral and pharyngeal cancer. © 1994 Wiley‐Liss, Inc.
Expression of the FGFR1 gene in human breast‐carcinoma cells
Authors: Jacquemier Jocelyne , Adelaide José , Parc Patricia , Penault‐Llorca Frédérique , Planche Jacqueline , Delapeyriere Odile , Birnbaum Daniel 
Published: February 2007

AbstractFibroblast growth factors (FGF) constitute a family of at least 9 members which act through high‐affinity tyrosine‐kinase receptors encoded by 4 distinct genes. In humans, the FGFRI gene is located in chromosomal region 8pl2. Its amplification and expression were examined in a panel of 110 breast carcinoma samples by Southern‐ and Northern‐blot analyses. FGFRI was amplified in 9% and overexpressed in about 15% of the tumors studied. In situ hybridization experiments were performed on tissue sections of normal breast and tumors with a high level of FGFRI expression. In both normal and tumoral tissues, FGFRI RNA was detected in the epithelial cells. Overexpression of FGFRI seems to be associated with small, well‐differentiated diploid tumors. © 1994 Wiley‐Liss, Inc.
Growth advantage of human leiomyoma cells compared to normal smooth‐muscle cells due to enhanced sensitivity toward insulin‐like growth factor I
Authors: Van Der Ven Leo T. M. , Gloudemans Ton , Roholl Paul J. M. , Van Buul‐Offers Sylvia C. , Bladergroen Bellinda A. , Welters Marij J. P. , Sussenbach John S. , Otter Willem Den 
Published: February 2007

AbstractHuman uterine leiomyomas exhibit increased IGF‐I binding compared to myometrium, while both tissues show IGF‐I gene expression. In this study we have examined the functional importance of these findings by testing the presence of IGF‐I in 15 leiomyoma biopsies and in 18 myometrium biopsies and the capacity of smooth‐muscle cells cultured from these tissues to react to IGF‐I. The mean IGF‐I peptide concentration in leiomyomas was 3 times higher than in myometrium. This resulted from increased IGF‐I uptake in leiomyomas rather than from increased synthesis, as these tissues contain higher concentrations of type‐IIGF receptors, as detected by immunohistochemistry, and equal levels of IGF‐I mRNA. Blocking IGF‐I transport with cytochalasin‐B and with the type‐I IGF receptor blocking antibody αIR3 in cultured cells induced decreased immunostaining intensity for IGF‐I in most myometrium and leiomyoma cultures, indicating that the detected IGF‐I is internalized. Depending on the culture conditions, IGF‐I administration yielded increased survival or a higher proliferation rate in leiomyoma cultures than in myometrium cultures, indicating the increased importance of exogenous IGF‐I for the growth of transformed smooth‐muscle cells. We conclude that the increased concentrations of type‐I IGF receptors in leiomyoma compared to myometrial smooth‐muscle cells are functional with respect to the enhanced internalization of IGF‐I and that they provide these tumor cells with a growth advantage compared to their normal counterparts. © 1994 Wiley‐Liss, Inc.
Growth inhibition of human colorectal‐carcinoma cells by interleukin‐4 and expression of functional interleukin‐4 receptors
Authors: Lahm Harald , Schnyder Bruno , Wyniger Josiane , Borbenyi Zita , Yilmaz Aysim , Car Bruce D. , Fischer Jürgen R. , Givel Jean‐Claude , Ryffel Bernhard 
Published: February 2007

AbstractThe growth‐inhibitory effect of interleukin‐4 (IL‐4) was investigated in a panel of 7 human colorectal‐carcinoma cell lines. In 5 cell lines (HT29, WiDr, LS41 IN, LS513, LS1034) a dosedependent reduction of proliferation was documented. At 100 U/ml, IL‐4 inhibited thymidine incorporation between 45 and 75% and MTT conversion (26 to 41%). The ability of LS513 and WiDr cells to form colonies after IL‐4 treatment was reduced by 85 and 62% respectively. LS513 was the most sensitive cell line, with IL‐4 inducing half‐maximal inhibition at 5 to 6 U/ml. The inhibitory effect of IL‐4 was completely neutralized by anti‐IL‐4 antibodies. Northern‐blot analysis revealed the presence of IL‐4‐receptor (IL‐4R) mRNA in all cell lines. The membrane expression of the 130‐kDa IL‐4R was assessed by FACS, utilizing an anti‐IL‐4R monoclonal antibody and was confirmed by biotinylated IL‐4 binding. Our results attribute an important role for IL‐4 as a negative regulator of colorectal‐carcinoma cell growth, thus indicating a possible avenue for intervention in this disease. © 1994 Wiley‐Liss, Inc.
Use of analgesics and risk of renal cell cancer
Authors: Chow Wong‐Ho , McLaughlin Joseph K. , Linet Martha S. , Niwa Shelley , Mandel Jack S. 
Published: February 2007

AbstractAlthough heavy or long‐term use of analgesics has been related to risk of renal cell cancer in several studies, evidence for such an association remains inconclusive. In a populationbased case‐control study including 440 renal cell cancer cases, spouses of an additional 151 cases, and 691 controls, we assessed renal cell cancer risk associated with lifetime consumption among those who reported during in‐person interviews regular (at least 2 or more times per week for I month or longer) use of analgesics. Odds ratios (OR) were computed using logistic regression analyses. No excess risk was associated with regular use of aspirin, acetaminophen, phenacetin or combinations of these agents, nor did risks rise with increasing cumulative intake of these analgesics. A non‐significant increased risk (OR = 2.1, 95% CI = 0.6–6.9) was observed among women who used only acetaminophen‐containing analgesics, but little excess was seen in men. Earlier studies reported a link to phenacetin‐containing analgesics, but no one reported exclusive use of phenacetin‐containing drugs in our study. The findings suggest that use of analgesics is not likely to play a major role in renal cell cancer development and that for cases diagnosed in the late 1980s or later, after the earlier withdrawal of phenacetin‐containing drugs from the market, a hazard from this analgesic no longer exists. © 1994 Wiley‐Liss, Inc.
Vascular endothelial growth factor and glioma angiogenesis: Coordinate induction of VEGF receptors, distribution of VEGF protein and possible In vivo regulatory mechanisms
Authors: Plate Karl H. , Breier Georg , Weich Herbert A. , Mennel Hans D. , Risau Werner 
Published: February 2007

AbstractWe have previously suggested that tumor angiogenesis in human gliomas is regulated by a paracrine mechanism involving vascular endothelial growth factor (VEGF) and flt‐I (VEGF‐receptor I). VEGF, an endothelial‐cell‐specific mitogen, is abundantly expressed in glioma cells which reside along necrotic areas, whereas fit‐I, a tyrosine‐kinase receptor for VEGF, is expressed in tumor endothelial cells, but not in endothelial cells in normal adult brain. Recently, a second tyrosine‐kinase receptor which binds VEGF with high affinity, designated KDR or flk‐I, has been described. We performed in situ hybridization for VEGF mRNA, flt‐I mRNA and KDR mRNA on serial sections of normal brain, low‐grade and high‐grade glioma specimens. We show that KDR mRNA is co‐expressed with flt‐I in vascular cells in glioblastoma but not in low‐grade glioma. Since flt‐I and KDR are not expressed in endothelial cells in the normal adult brain, the coordinate up‐regulation of 2 receptors for VEGF appears to be a critical event which controls tumor angiogenesis. Immunocytochemistry with a monoclonal anti‐VEGF antibody revealed significant amounts of VEGF protein in the same glioma cells that expressed VEGF mRNA. The largest amount of VEGF immunoreactivity, however, was detected on the vasculature of glioblastomas, the site where VEGF exerts its biological functions. These findings suggest that VEGF is produced and secreted by glioma cells and acts on tumor endothelial cells which express VEGF receptors. To further characterize VEGF‐producer cells in vivo, we investigated cellular proliferation, immunoreactivity to the p53 tumor‐suppressor gene product and epidermal‐growth‐factor‐receptor(EGFR) expression on serial sections by immunocytochemistry. VEGF‐producer cells did not show increased cellular proliferation, p53 immunoreactivity or EGFR immunoreactivity as compared with glioma cells which did not express VEGF. Our studies therefore do not demonstrate evidence for a growth advantage of VEGF‐producer cells in vivo or VEGF induction by p53 mutation or EGFR over‐expression. © 1994 Wiley‐Liss, Inc.
Accumulation in “normal” lungs of live tumorigenic cells during sub‐cutaneous growth of weakly and highly metastasizing tumors and their In vitro sensitivity to growth regulation by normal fibroblasts
Authors: Deichman Galina I. , Gurova Katherina V. , Dyakova Natalia A. 
Published: February 2007

AbstractThe main purposes of the study were: (I) in vivo comparison of accumulation of live tumorigenic cells (LTC) in macroscopcally normal lungs of animals bearing 6 s.c. Syrian hamster sarcomas differing in spontaneous metastasizing activity (SMA); (2) in vitro examination of the sensitivity of these cell strains to the growth‐regulating signals of normal fibroblasts. Cell strains used differed in SMA from very weak (WM) to extremely high (HM). The numbers of LTC doses in “normal” lung tissue of tumorbearing animals were determined in s.c. transplantation tests by titrating single‐cell suspensions prepared from the lung tissues of 5 tumor‐bearing animals, for each cell strain, every 5 days during 30 days of s.c. tumor growth, until the appearance of the first spontaneous lung metastases. The sensitivity of WM and HM cells to growth‐regulating signals of normal hamster embryo fibroblasts (HEFs) was examined by in vitro co‐culturing during 6 days with daily determination of 3H‐TdR incorporation in the WM and HM cells grown with or without contact with HEFs. The data presented demonstrate (I) the surprisingly similar efficiency in the occupation of macroscopically normal lung tissues by live tumorigenic cells of WM and HM strains, disseminating spontaneously from the s.c. tumors; (2) the significantly lower sensitivity of HM cells, in contrast to WM, to growth inhibition by contact with HEFs and especially their marked ability to usurp the growth‐stimulating signals of normal HEFs. © 1994 Wiley‐Liss, Inc.
Initiated stem cells in murine intestinal carcinogenesis: Prolonged survival, control by nk cells, and progression
Authors: Altmann G. G. , Lala P. K. 
Published: February 2007

AbstractWeekly injections of dimethylhydrazine (DMH) (25 mg/kg), or azoxymethane (AOM) (8 mg/kg) to young adult male CDI mice for 1–2 months produced generalized intestinal crypt hyperplasia, which we measured in duodenum in terms of number of interphase and mitotic cells present in crypts. As shown earlier, the crypts expanded because of the presence of a hyperproliferative “initiated” crypt subpopulation which was also sensitive to natural killer (NK) cells. Hyperplasia was thus present as long as NK activity was suppressed by the carcinogen treatment. After interruption of the treatment for periods of 1, 2, 3, 6 and 10 months in the various groups, hyperplasia soon regressed as a result of elimination of the subpopulation by the recovering NK cells. When NK activity was once again eliminated during the terminal days of these “interruption periods” (by injections of anti‐asialo GM‐l antibody, αAGM‐l), the original hyperplasia was fully reconstituted, apparently from stem cells of the subpopulation which survived up to 10 months in their crypt base location. These “initiated stem cells” represented, then, the original carcinogenic insult during the pre‐cancerous period. They also appeared to be the source of the eventual neoplasia, as treating the animals with mutagens during the interruption periods produced specific changes in crypt base histology: new “crypt base basophilic” (CBB) cells appeared which produced large accumulations as well as microscopic tumors when NK activity was suppressed (by αAGM‐l). Some of the initiated stem cells were apparently transformed into neoplastic ones which remained under NK control, the NK cells preventing the establishment of their progeny. Further experiments indicated that, although the initiated stem cells are not eliminated by normal NK activity, activated NK cells can kill them, thereby eliminating the potential source of neoplasia. © 1994 Wiley‐Liss, Inc.