bluuebunny/crossref_metadata_2025_split huggingface dataset:
Radiation leukemia virus (RadLV)‐induced leukemogenesis is associated with an increased number and activity of thymic macrophages
Authors: Messika E. , Gallily R. , Yefenof E. 
Published: February 2007

AbstractThe radiation leukemia virus (RadLV) is a chronic leukemia retrovirus that induces thymlc lymphomas in C57BL/6 mice after a latency of 3 to 6 months. During the pre‐leukemic (PL) period, the number of thymic macrophages gradually increased up to 100 fold. Of the cells in a RadLV‐induced lymphoma, 0.3% were large macrophages packed with infected lymphoma cells. These thymic lymphoma macrophages (TLM) also ingested RadLV‐induced lymphoma cells in vitro. red RadLV‐induced lymphoma lines could activate and fix C3 fragments through the alternative complement pathway (ACP). C3‐bound lymphoma cells elicited an oxidatlve burst (OB) response in TLM but not in bone‐marrow macrophages (BMM). However, IL4 treatment of BMM rendered them capable of responding with an OB following triggering by C3‐opsonized cells. Thymic macrophages (TM) responded moderately with OB to C3‐opsonized cells and this response was elevated If the TMs were treated by rlL4. The OB reaction of the TLMs could be partially inhibited by anti‐LFA‐1 or anti‐MALA‐2 antibodies, and was completely inhibited by antl‐CR3 antibodies. These results suggest that IL4 can prime macrophages for triggering an OB reaction and that the interaction between C3‐opsonized cells and IL4‐primed macrophages is mediated primarily through CR3.
Reactivity against herpes simplex virus in patients with head and neck cancer
Authors: Larsson P‐A. , Edström S. , Westin T. , Nordkvist A. , Hirsch J. M. , Vahlne A. 
Published: February 2007

AbstractThe relation between herpes simplex virus (HSV) and head and neck cancer was examined. A total of ninety patients were analyzed for IgG antibodies against HSV. Antibody titers were established with an enzyme‐linked immunosorbent assay and antibodies against specific HSV‐antigens were analyzed by Western blot. These patients' seroreactivity was compared to that of an age‐matched control group of patients with arteriosclerotic disease in their lower limbs, a disease also closely related to heavy tobacco consumption. Prevalence of antibodies against HSV was around 90% and did not differ significantly between cancer patients and controls, but antibody titers against HSV were significantly higher in the cancer patients. The cancer patients also reacted more constantly (80%) in Western blot analysis against the early immediate protein, ICP‐4, than controls (50%). This suggests a different course of an earlier herpetic infection in these patients with a prolonged exposure to early immediate HSV‐proteins which may be related to an increased risk of developing head and neck cancer. We propose that heavy smoking may contribute to this phenomenon.
Increased expression of laminin receptors during myeloid differentiation
Authors: Federico M. H. H. , Maria D. A. , Sonohara S. , Yamamoto M. , Katayama M. L. H. , Brentani M. M. 
Published: February 2007

AbstractVariation of laminin receptor levels (LNR) during myeloid‐cell differentiation and in acute leukemia were investigated by 125I‐laminin‐binding determination during HL60 cell differentiation and in cells of patients with different types of leukemia, characterized according to the FAB classification. LNR levels in HL60 cells increased during differentiation, being significantly higher in cells exposed to phorbol myristate acetate (PMA) and ethanol (55,391 ± 27,845 and 29,314 ± 6,435 sited cell respectively) as compared with HL60 controls (8,549 ± 4,000 siteskell). The control cells do not adhere to laminin‐coated surfaces, but differentiation with PMA results in their rapid adherence on this substratum. Short treatment with PMA does not increase the number of adherent cells or the receptor expression. Granulocytes also presented equally high LNR concentration (29,739 ± 13,516 sites/cell). The lymphoid cells (lymphocyte, acute lymphoid leukemia and chronic lymphocytic leukemia) shared low LNR numbers (<6,500 sites/cell). Myeloid cells displayed a wide range of LN receptors with higher levels being associated with the more differentiated FA9 subgroups. 125I‐laminin binding to lymphoid or myeloid leukemic cells was mainly inhibited by P1 fragments, whereas granulocytes and differentiated HL60 cells displayed a dual binding pattern for laminin fragments P1 and E8. These results were confirmed by assays using 125I‐labelled P1 and E8 fragments. We conclude that magnitude of LNR levels and variation in expression of P1 and E8 receptors appear to be linked to lineage and maturation status in hematopoietic cells.
Pooled analysis of 3 european case‐control studies of ovarian cancer: II. Age at menarche and at menopause
Authors: Franceschi Silvia , La Vecchia Carlo , Booth Margaret , Tzonou Anastasia , Negri Eva , Parazzini Fabio , Trichopoulos Dimitrios , Beral Valerie 
Published: February 2007

AbstractThe role of age at menarche and at menopause on epithelial ovarian cancer risk was re‐assessed in a combined analysis of 3 hospital‐based case‐control studies conducted in Italy, the United Kingdom and Greece, which produced a total of 1, 140 cases and 2,724 controls. In the overall dataset, there was no evidence of an association with age at menarche: compared with women whose menarche occurred at age I5 or over, the relative risk (RR) estimates were 1.0[95% confidence interval (CI) 0.8 to 1.2] for those with menarche at ages 12 to 14, and 1.0 (95% CI 0.8‐1.2) for those with menarche below age 12. There was no consistent interaction between age at menarche and study centre or age at diagnosis. In relation to age at menopause, compared with women whose menopause occurred at age 44 or earlier, the RR was 1.4 between 45 and 49, 1.6 between 50 and 52 and 1.9 above 52. The strength of the association was apparently (but not significantly) greater in the British than in the Greek or Italian dataset. The effect of age at menopause tended to be long‐lasting and, if anything, to increase across subsequent age‐groups. The large dataset, and the replication of results in different studies, provide more definite and precise information than previously available on the absence of appreciable effect of age at menarche on subsequent ovarian cancer risk in developed countries. For age at menopause, there was a direct and consistent trend in risk, but the association was relatively weak, with RRs below 2 even between extreme categories.
Roles of ovaries and testes in hepatocellular tumorigenesis induced in mice by 3′‐methyl‐4‐dimethylaminoazobenzene
Authors: Yamamoto Reiko , Iishi Hiroyasu , Tatsuta Masaharu , Tsuji Motomu , Terada Nobuyuki 
Published: February 2007

AbstractThe roles of gonads in tumorigenesis induced in mouse liver by 3′‐methyl‐4‐dimethylaminoazobenzene (3′‐Me‐DAB) were investigated. C57BL/6 × DS‐F1 mice which were 10, 12, 14, 16 and 18 days old were treated i.p. with 3′‐Me‐DAB. Nodular lesions induced in the liver were classified into adenomatous nodules and hepatocellular carcinomas. Adenomatous nodules were composed of a mixture of eosinophilic, basophilic, vacuolated and foamy hepatocytes in various proportions and compressed the adjacent parenchyma. These adenomatous nodules were of monoclonal origin. Carcinomas had a trabecular structure. The incidence, numbers per mouse and areas of adenomatous nodules and carcinomas in male and female mice aged 16‐64 weeks were compared. Adenomatous nodules were first detected in males and females aged 24 and 52 weeks, respectively, and their incidences were much higher in males than in females of the same age. The number of adenomatous nodules per mouse and their size were also higher in males. The first carcinoma was found in a 52‐week‐old male, but no carcinomas were found in females even at 64 weeks of age. The effects of castration 23 days after birth on the appearance of nodular lesions in the livers of 32‐ to 64‐week‐old mice were examined. Castration of males did not affect the incidence of adenomatous nodules, but reduced the incidence of carcinomas. It also decreased the number of adenomatous nodules per mouse. Castration of females reduced the time before appearance of adenomatous nodules and increased their incidence, number per mouse, and area. A carcinoma appeared in a 64‐week‐old castrated female, but no similar lesion was found in intact females of the same age. These results indicate that tumorigenesis induced in mouse liver by 3′‐Me‐DAB is enhanced by the testes and suppressed by the ovaries.
Butyric monosaccharide ester‐induced cell differentiation and anti‐tumor activity in mice. Importance of their prolonged biological effect for clinical applications in cancer therapy
Authors: Pouillart Philippe , Cerutti Italina , Ronco Gino , Villa Pierre , Chany Charles 
Published: February 2007

AbstractThe interest of butyric salts is based on their capacity to promote differentiation of malignant cells and inhibition of tumor development. The phenotypic modifications are rapidly reversible and require the continuous presence of butyric salts in the target area, which raises problems for therapeutic applications. We show here that the covalent binding of n‐butyric acid on natural polyhydroxylated compounds such as monosaccharides, especially 3‐ or 6‐O‐butanoyl‐ 1,2‐O‐iropro‐pylidene‐α‐D‐glucofuranose, retains the majority of the biological properties of n‐butyric acid. The delayed degradation of these covalent compounds is associated with an improved maintenance of cell differentiation and anti‐tumor protection in mice. These butyric complexes thus seem potentially useful for therapeutic applications.
Impact of interleukin‐2‐receptor‐targeted cytotoxins on a unique model of murine interleukin‐2‐receptor‐expressing malignancy
Authors: Bacha Patricia A. , Forte Serene E. , McCarthy Donna M. , Estis Leonard , Yamada Gen , Nichols Jean C. 
Published: February 2007

AbstractDAB486IL‐2 is a genetically engineered fusion protein consisting of a portion of diphtheria toxin fused to human IL‐2. It is specifically cytotoxic for tumor cells which bear high‐affinity IL‐2 receptors (IL‐2R). DAB389IL‐2 is a similarly constructed hybrid protein which is smaller than DAB486IL‐2 and is slightly more potent in vitro. We have developed a murine model of IL‐2R‐expressing malignancy to study the in vivo efficacy of these genetically engineered cytotoxins. Following intravenous administration of CP3 cells, C57BL/6 mice develop tumors which are lymphatic in distribution. When mice are injected i.v. with 106 CP3 cells, 90% of the animals show signs of observable tumor by day 10 to 20; death occurs in 50% of untreated animals by day 30. Intravenous treatment of mice with DAB486IL‐2 (10 μg daily for 10 days), beginning 24 hr after administration of CP3 cells, increases mean survival time by approximately 50%. In comparative studies, DAB389IL‐2 is more potent in vivo than DAB486IL‐2, with approximately 90% of treated animals with no evidence of tumor at 60 days. The mechanism of action of tumor inhibition by DAB486IL‐2 is specific, since treatment of animals which have 1L‐2R‐negative EL4 tumors has not resulted in increased survival time. In addition, treatment of such tumors with DAglu53B486IL‐2, a fusion protein which can bind to the IL‐2R but is incapable of inhibiting protein synthesis, is ineffective.
Regulation of protein kinase a activation and prostaglandin E2‐stimulated migration of lewis lung carcinoma clones
Authors: Young M. Rita , Young Melvin E. , Lozano Yvonne , Coogan Michael , Bagash Jamila M. 
Published: February 2007

AbstractLewis lung carcinoma (LLC) clones were used in in vitro models for dissemination to identify mechanisms regulating the stimulation of metastatic LLC‐LN7 migration by prostaglandin E2 (PGE2) or forskolin plus 3‐isobutyl‐I‐methyl‐xanthine (IBMX), and the lack of responsiveness to generated cAMP in non‐metastatic LLC‐C8 cells. The regulatory subunits of protein kinase A (PKA) from LLC‐LN7 cells bound more 8‐N3‐32P‐cAMP, even though production of regulatory subunits was equal to that in LLC‐C8 cells. Protein kinase C (PKC) differentially regulated PKA activation in the LLC variants. PKC activation inhibited PGE2‐stimulated migration by LLC‐LN7 cells. Inhibition of PKC with staurosporine stimulated LLC‐LN7 cell migration to a level comparable with that induced by PGE2. However, PGE2 did not further stimulate the migration of staurosporine‐treated cells. The PGE2 or staurosporine stimulation of LLC‐LN7 cell migration was dependent on PKA activation. The effects that modulation of PKA and PKC had on LLC‐LN7 cell migration paralleled the effects on endogenous protein phosphorylation. LLC‐LN7 cell autophosphorylation was stimulated to a similar degree by PGE2, forskolin plus IBMX, staurosporine, or the combination of staurosporine and forskolin plus IBMX. In contrast, neither migration nor autophosphorylation was stimulated in nonmetastatic LLC‐C8 cells by cAMP elevation or by PKC inhibition. Autophosphorylation, although not migration, of LLC‐C8 cells was stimulated by forskolin plus IBMX when PKC activity was inhibited. These results suggest that the increased PKA response of metastatic LLC‐LN7 cells is contributed by an increased binding of cAMP by the PKA regulatory subunits and a reduced level of regulation by PKC.
Tumor progression in human malignant melanoma is associated with changes in α6/β1 laminin receptor
Authors: Natali Pier Giorgio , Nicotra Maria Rita , Cavaliere Renato , Giannarelli Diana , Bigotti Aldo 
Published: February 2007

AbstractCells of the melanocytic lineage have been shown to be capable of producing laminin and to lose this property during transformation. In the present study, we have evaluated immunohistochemically whether these changes are paralleled by an altered expression of the α6/β1 laminin receptor. Results of this analysis have shown that while nevic cells display high levels of the receptor, this heterodimer undergoes a progressive decrease in expression in cutaneous melanomas of increasing invasiveness. A loss or unco‐ordinated expression of the α1/β complex is present in the majority of the metastatic foci at different body sites. The present results show that during transformation the α6/β1 laminin receptor undergoes quantitative alterations and deregulated expression of the 2 subunits. Although the functional relevance of these changes remains unknown, their occurrence in association with modifications of other cellular and extracellular macro‐molecules associated with tumor progression, strongly suggests a role in human melanoma progression.
Serological discrimination between HTLV‐I and HTLV‐II antibodies by elisa using synthetic peptides as antigens
Authors: Washitani Yukiko , Kuroda Naotaka , Shiraki Hiroshi , Nishimura Youko , Yamaguchi Kazunari , Takatsuki Kiyoshi , Fernando Leonor P. , Fang Chyang T. , Kiyokawa Hiroyuki , Maeda Yoshiaki 
Published: February 2007

AbstractUsing the peptides from amino acids 100‐130 of the HTLV‐I gag protein, 175‐199 of the HTLV‐I env protein and the corresponding peptides of HTLV‐II (amino acids 106 to 135 of the gag protein and 171 to 196 of the env protein), we tested for reactivity against antibodies by enzyme immunoassay in sera from HTLV‐I and HTLV‐II carriers. The peptides derived from the env proteins have high specificity for antibody binding. The peptide based on amino acids 175‐199 of HTLV‐I reacted with antibodies in sera from all HTLV‐I carriers, and the peptide composed of amino acids 171‐196 of HTLV‐II reacted with antibodies in sera from all HTLV‐II carriers. For the peptides derived from the gag proteins, we observed some cross‐reactivity in sera from persons with anti‐HTLV‐I and anti‐HTLV‐II, due to antibody binding to the peptide corresponding to 12 amino acids from the C‐terminal end of the gag protein. Separate enzyme immunoassays that used the four synthetic peptides as antigens clearly distinguished between serum with antibodies to HTLV‐I or HTLV‐II in various individuals and excluded false positive results using the particle agglutination assay that used a whole‐virus lysate of HTLV‐I as antigen.
Depot‐medroxyprogesterone acetate (DMPA) and risk of liver cancer
Authors:   THE WHO COLLABORATIVE STUDY OF NEOPLASIA AND STEROID CONTRACEPTIVES, Mati J. G. , Kenya P. , Kungu A. , Gatei D. , Silpisoronkosol Suporn , Pardthaisong Tieng , Sahapong Virote , Theetranont Choti , Boosiri Banpot , Chutivongse Supawat , Virutmasen Pramuan , Wongsrchanalai Chansuda , Sindhvananda Sermsri , Koetsawang Suporn , Rachawat Daungdao , Koetsawang Amom , Anthony P. P. , Thomas David B. , Noonan Elizabeth A. , Ray Roberta M. , Rosenblatt Karin A. , Stanford Janet L. , Holck Susan , Farley Timothy M. M. , Rosenblatt Karin A. , Thomas David B. 
Published: February 2007

AbstractA hospital‐based case‐control study was conducted to assess the possible relationship between use of depot‐medroxy‐progesterone acetate (DMPA), an injectable progestational contraceptive, and the development of liver cancer in 2 developing countries where hepatitis B is endemic. Information about prior DMPA use and potential confounders was ascertained during personal interviews with 71 cases and 530 controls from 3 hospitals in Thailand and 1 hospital in Kenya. No significant association between liver cancer and DMPA use was observed in Kenya (RR = 1.64, 95% CI = 0.4‐0.6) or Thailand (RR = 0.33, 95% CI = 0.1‐1.O). No consistent changes in risk were observed with duration of use, time since last use, or time since first use. No significant associations were observed between DMPA use and risks of either hepatocellular carcinoma or cholangiocarcinoma. These findings suggest that risk of liver cancer in areas where hepatitis B is endemic is not appreciably altered by the use of DMPA.
p53 Protein alterations in human testicular cancer including pre‐invasive intratubular germ‐cell neoplasia
Authors: Bártkov´ Jir̂ina , Bártek Jir̂í , Lukáŝ Jir̂ina , Vojtêŝek Bor̂ivoj , Staŝková Zdenka , Rejthar Aleŝ , Kovar̂ík Jan , Midgley Carol A. , Lane David P. 
Published: February 2007

AbstractExpression of the p53 oncoprotein was examined in a wide range of primary human testicular germ‐cell tumours using a new mouse monoclonal antibody (MAb) BP53‐11 raised and characterized in this study, in parallel with a polyclonal rabbit antiserum CM‐1. Immunohistochemistry on paraffin sections showed positive nuclear reaction in at least a fraction of malignant cells in 90 (84%) out of 107 cases studied. Aberrant accumulation of the p53 protein was found among testicular tumours of all major histological types, although generally a higher percentage of positive cases and a higher proportion of p53 over‐expressing nuclei within individual lesions was observed in embryonal carcinomas when compared with seminomas. The typical heterogeneous staining pattern characteristic of histological specimens was also found in a cultured cell line derived from a human embryonal carcinoma. In contrast to immunohistochemically undetectable levels in normal tes‐tes and morphologically normal tissue areas in the tumour‐bearing testes, the accumulation of the p53 protein was clearly identified in a high proportion (59% of cases) of the pre‐invasive lesions with positive atypical intratubular germ cells often found in the tissue adjacent to invasive tumours. Altered expression of the p53 protein is therefore a unifying feature of the majority of invasive male germ‐cell tumours and the change resulting in high levels of p53 appears to be a relatively early step in the human testicular cancer pathogenesis.
Diet and bladder cancer in Spain: A multi‐centre case‐control study
Authors: Riboli Elio , González Carlos A. , López‐Abente Gonzalo , Errezola Manuel , Izarzugaza Isabel , Escolar Antonio , Nebot Manuel , Hémon Bertrand , Agudo Antonio 
Published: February 2007

AbstractA multi‐centre case‐control study on bladder cancer and diet was carried out in 5 regions of Spain. We report results on 432 male cases and 792 matched controls. Usual dietary habits were investigated by means of an interview‐based dietary history questionnaire. Bladder‐cancer cases were selected from the registers of 12 hospitals located in the study areas. Each case was matched by sex, age and area of residence to 2 controls, one identified in the same hospital and one drawn from population lists. Descriptive analyses indicated that the average dietary pattern was typical of Mediterranean populations: a high P/S ratio, high intake of fish, fruits and vegetables and moderate or low intake of meat and dairy products. Relative risks for specific foods and nutrients were adjusted for tobacco smoking and energy intake. Subjects in the highest quarter of intake of saturated fat had a significantly increased risk of bladder cancer (RR for highest quarter = 2.25; 95% CI = 1.42 to 3.55). Moderate increases in risk for high intake of mono‐unsaturated fats and calcium, and a slight decrease for iron were also found, but these disappeared after adjustment for saturated fat. Intake of vitamin E was related to slightly reduced risk (RR for highest quarter = 0.72; 95% CI = 0.48 to 1.09) which was not modified by adjustment for fat. No association was found with intake of retinol or carotene. These results, along with those of previous studies, suggest that saturated fat intake may influence the occurrence of bladder cancer.
Prediction of antifolate efficacy in a rat sarcoma model
Authors: Li Wei Wei , Lin James T. , Chang Y. M. , Schweitzer Barry , Bertino Joseph R. 
Published: February 2007

AbstractA methylcholanthrene‐induced rat sarcoma propagated both in vitro and in vivo was used to examine the usefulness of a rapid biochemical in situ assay that measures thymidylate synthase (TS) activity in whole cells to predict sensitivity and resistance to the folate antagonists methotrexate (MTX), 10‐ethyl‐10‐deazaaminopterin (10‐EDAM) and trimetrexate (TMTX). There was an excellent correlation between the effects of these drugs on inhibiting TS and cytotoxicity as measured by a clonogenic assay, when the exposure time was 4 hr, and those when the rat sarcoma cell line was employed (p < 0.001). When tumor‐cell suspensions were prepared from the rat sarcoma propagated in vivo, they were less sensitive to these antifolates, but the relative effectiveness of the 3 antifolates was similar: TMTX ≫ 10‐EDAM > MTX. As expected, continuous exposure (10 to 12 days) produced cytotoxicity at a much lower dose of these drugs. When the 3 drugs were tested for anti‐tumor effectiveness in rats bearing this tumor, the tumor regression measured was best with TMTX; 10‐EDAM was intermediate in effectiveness as compared with MTX. These results indicate that the in situ TS assay and clonogenic assay may be used to predict anti‐tumor efficacy of antifolates in vivo in this rat sarcoma.