bluuebunny/crossref_metadata_2025_split huggingface dataset:
Pooled analysis of 3 european case‐control studies of epithelial ovarian cancer: III. Oral contraceptive use
Authors: Franceschi Silvia , Parazzini Fabio , Negri Eva , Booth Margaret , La Vecchia Carlo , Beral Valerie , Tzonou Anastasia , Trichopoulos Dimitrios 
Published: February 2007

AbstractThe relationship between use of oral contraceptives (OCs) and other contraceptive methods and the risk of ovarian cancer was examined in a combined analysis of 3 hospital‐based case‐control studies conducted in Italy, the United Kingdom, and Greece, for a total of 971 ovarian cancer cases and 2,258 controls under age 65. Compared with never‐users, the combined multivariate relative risk (RR) for ever‐users was 0.6 (95% confidence interval, CI = 0.4‐0.8) and the estimates were consistent in the 3 datasets. The protection was also similar across strata of age and parity. Considering various measures of OC use, available in the Italian and British data‐sets only, the protection conveyed on ovarian cancer risk increased with the duration of use and persisted in the medium‐long period: the RR in women reporting their last OC use ≧15 years prior to diagnosis was 0.5 (95% CI = 0.2‐1.0). The risks in ever‐users were appreciably lower in those women who reported their first OC use before 25 years of age (RR = 0.3 for first use before age 25. 0.8 for first use at age 25‐34 and 0.7 at 35 years or after). Such findings emerged similarly from Italian and British data. This combined analysis, besides offering further quantitative estimates of the protective effects of OCs on ovarian cancer risk in European populations, provides useful insights into the time pattern of the relationship between OC use and ovarian carcinogenesis, suggesting that the protection persists for 15 years or more after cessation of use and may be larger for use at younger age.
Severe cachexia in mice inoculated with interferon‐γ‐producing tumor cells
Authors: Matthys Patrick , Dukmans Roger , Proost Paul , Van Damme Jo , Heremans Hubertine , Sobis Halina , Billiau Alfons 
Published: February 2007

AbstractNude mice were inoculated with CHO/IFN‐γ cells, a line of Chinese hamster ovary tumor cells, that had been genetically engineered to produce murine IFN‐γ. Severe cachexia, as evident from body weight loss and reduced food intake, occurred in these mice, but not in those injected with CHO/ control cells, i.e. the original, non‐IFN‐γ‐producing line. The essential role of IFN‐γ in the pathogenesis of cachexia was confirmed by the demonstration that monoclonal antibodies (MAbs) against IFN‐γ, given prior to injection of the tumor cells, prevented cachexia. In addition to IFN‐γ, the presence of the tumor cells was also required for cachexia to develop. As evident from pair‐feeding experiments, reduced food intake could only partially account for the rapid and extensive body‐weight loss. Cachexia was characterized by a marked reduction in the amount of interscapular fat tissue. Injected tumor cells exclusively invaded intraperitoneal adipose tissue and elicited an inflammatory cell infiltrate, indicating that interscapular fat loss was due to humoral factors. Our data suggest that, among the humoral factors responsible for cancer‐associated cachexia, IFN‐γ plays a prominent role.
c‐myc Gene in a murine plasmocytoma without visible chromosomal translocations moves to chromosome 12f1 with pvt‐1 and rearranges with IgH enhancer‐Sμ sequences
Authors: Ohno Shinsuke , Migita Shunsuke , Murakami Seishi 
Published: February 2007

AbstractThe DCPC 21 plasmocytoma lacks any of the MPC‐associated chromosomal translocations. However, the c‐myc gene has been transposed to the IgH locus on chromorome 12 by an Ig switch‐region‐mediated recombination mechanism. DNA sequencing analysis, further, revealed that this recombination is consistent with an insertion of the IgH enhancer (Eμ)‐Sμ sequences, 2341 bp in length, into the c‐myc 5′‐flanking region, resulting in 5′: c‐myc 5′‐flanking‐Eμ‐Sμ‐c‐myc 5′‐flanking‐c‐myc exon‐1 : 3′ segment. In situ molecular hybridization of DCPC 2I metaphase chromosome spreads using a Pvt‐1 probe demonstrated that Pvt‐1 has also moved to the FI sub‐band region of chromosome I2 where the IgH genes are located. These results indicate that the c‐myc gene has been inserted into the IgH locus together with the Pvt‐I, regardless of whether plasmocytoma has cytogenetically identifiable translocations. The possible interaction between c‐myc activation and Pvt‐I in the development of MPCs is discussed.
An autocrine motility factor secreted by the dunning R‐3327 rat prostatic adenocarcinoma cell subtype AT2.1
Authors: Evans Christopher P. , Walsh Douglas S. , Kohn Elise C. 
Published: February 2007

AbstractTumor cell locomotion is an integral part of the metastatic process. We present a new autocrine motility factor (AMF) derived from the serum‐free conditioned medium of the Dunning R‐3327 rat prostate adenocarcinoma AT2.1 tumor cell subline AT2.1‐AMF, prepared by concentration of components ≧30 kDa in size and washed free of low‐molecular‐weight growth factors, stimulated motility of AT2.1 cells in modified Boyden chamber migration assays. This stimulated migration was dose‐dependent, and by checkerboard analysis was both chernotactic and chemokinetic. AT2.1‐AMF activity was labile to heat, acid, base, reduction, oxidation, and proteases. Lyophilization and treatment with 6M urea caused a mild decrease (<20%) in migration‐stimulating capability. Tumor‐cell specificity was demonstrated for AMF of AT2.1 and AT3.1 Dunning sublines, and the A2058 human melanoma cell lines. AT2.1 cell migration to AT2.1‐AMF was inhibited by 2 hr pre‐treatment with cholera toxin (0.1 μg/ml) or forskolin (100 μM), but not altered by 2 hr pre‐treatment with pertussis toxin (1.0 μg/ml). This indicates that guanine nucleotide binding protein‐mediated regulation of CAMP is involved in modulating the AT2.1 cell response to its AMF. The AT2.1‐AMF belongs to a related family of tumor autocrine motility factors and represents a new model for understanding the role of tumor‐cell migration in the metastatic process of human prostate cancer.
Interleukin 6 is secreted by breast fibroblasts and stimulates 17β‐oestradiol oxidoreductase activity of MCF‐7 cells: Possible paracrine regulation of breast 17β‐oestradiol levels
Authors: Adams Eric F. , Rafferty B. , White M. C. 
Published: February 2007

AbstractPrevious studies have demonstrated that cultured human breast fibroblasts secrete a high‐molecular‐weight polypeptide which stimulates the ability of human breast‐cancer MCF‐7 cells to convert oestrone (E1) to the biologically more active 17β‐oestradiol (E2). This effect is mediated by an increase in reductive E2 oxidoreductase (EOR) activity. We have identified the fibroblast‐derived stimulatory factor as interleukin 6 (IL6) or an immunologically related peptide. Human breast fibroblasts in culture secreted up to 10 ng IL6/ml medium during 24 hr of incubation. The effects of IL6 and breast fibroblast conditioned medium (CM) on reductive EOR activity of MCF‐7 cells were similar; both CM and IL6 potently stimulated enzyme activity in a dose‐dependent manner, and both exerted synergistic stimulatory effects in combination with E2. A polyclonal neutralizing antibody to IL6 completely abolished the reductive EOR‐stimulating activity of CM. These results indicate that breast stromal fibroblasts may have a paracrine role in regulation of breast‐cancer‐tissue levels of E2, and that this effect is mediated by IL6 or a closely related peptide.
TGFβ1 and TGFβ2 are potential growth regulators for low‐grade and malignant gliomas in vitro: Evidence in support of an autocrine hypothesis
Authors: Jennings Mark T. , Maciunas Robert J. , Carver Robert , Bascom Charles C. , Juneau Patrick , Misulis Karl , Moses Harold L. 
Published: February 2007

AbstractLow‐grade astrocytomas, anaplastic astrocytomas and glio‐blastomas in vitro were found to ubiquitously produce the mRNA of transforming growth factor‐β (TGFβ). TGFβ1 and TGFβ2 mRNA were expressed to a lesser degree among the hyperdiploid malignant gliomas. By radioreceptor assay of conditioned medium, TGFβ was secreted predominantly in latent form, in both latent and active form, or only in active form within a panel of low‐grade and malignant gliomas. The TGFβ receptor (types I, II and III) was evident among the glioma lines. Many near‐diploid gliomas were growth‐inhibited by TGFβ1 and TGFβ2. in vitro. Most hyperdiploid glioblastomas showed a positive mitogenic response to exogenous TGFβ1 and TGFβ2. A synergistic or additive mitogenic interaction with epidermal growth factor and insulin was observed among some. Under serum‐free conditions, anti‐TGFβ antibody neutralized the expected growth‐regulatory effect of endogenous TGFβ1 thus establishing the specificity of the response in vitro. TGFβ1 also enhanced the clonogenicity of certain gliomas which had been growth‐stimulated in monolayer. Thus, basic elements in support of an autocrine hypothesis have been demonstrated: TGFβ mRNA was expressed among low‐grade and malignant gliomas, TGFβ was secreted in latent and/or active form into conditioned media and appeared to serve as an endogenous regulator of glioma proliferation in vitro. The mitogenic response, either positive or negative, correlated with the degree of anaplasia and karyotypic divergence.
Mutational activation of c‐Ha‐ras genes in intraductal proliferation induced by N‐nitroso‐N‐methylurea in rat mammary glands
Authors: Sakai Hirotsuka , Ogawa Katsuhiro 
Published: February 2007

AbstractAlthough administration of a single dose of N‐nitroso‐N methylurea (NMU) to young virgin rats induces a high rate of mammary carcinomas, precise histogenesis of the carcinomas has not been well characterized. In this study, we investigated the alterations of H‐ras gene in early focal lesions as well as carcinomas in the mammary glands of F344 rats treated with NMU. At 2 weeks after treatment, intraductal proliferation (IDP) was occasionally observed, and mammary carcinomas emerged at 12 and 36 weeks. The individual lesions of IDP and carcinomas were scooped out from the tissue sections under a stereomicroscope, and the DNA‐sequence‐spanning codon 12 of H‐ras gene was amplified from the tissue sections by polymerase chain reaction (PCR). The analysis of amplified DNA by oligonucleotide hybridization revealed that 65% (11/17) of IDP and 89% (16/18) of carcinomas had a point mutation (G‐to‐A transition) at the 2nd position of H‐ras codon 12. However, the DNA amplified from the areas, which appear histologically normal, never showed such mutation. These results indicate that IDP is a very early change for NMU‐induced mammary carcinogenesis.
Nutritional factors in colorectal cancer risk: A case‐control study in majorca
Authors: Benito E. , Stiggelbout A. , Bosch F. X. , Obrador A. , Kaldor J. , Mulet M. , Muñoz N. 
Published: February 2007

AbstractThe relationship between energy intake, selected nutrients and colorectal cancer was investigated in the population of Majorca, a Spanish island in the Mediterranean basin. A population‐based case‐control study using food frequency questionnaires was conducted during the period 1984‐1988 and included 286 cases of colorectal cancer, 295 population controls and 203 hospital controls. Food composition tables and ad‐hoc estimates of portion sizes were used to derive intake estimates of 29 nutrients and of total calories. Relative risks were calculated for quartiles of consumption of each specific nutrient after adjustment for total calorie intake. Colorectal cancer was found associated with dietary intake of total calories (RRs = 1.0, 1.6, 1.6, 2.6) and cholesterol (RRs = 1.0, 0.9, 1.7, 1.7) and a protective effect was associated with the intake of fibre from legumes (pulses) and folic acid. The associations and the trends were statistically significant. Among the main energy‐supplying nutrients, after adjustment for calories from other sources, increased risks were found for protein (RRs = 1.0, 1.1, 1.7, 2.5), notably animal protein, and carbohydrates (RRs = 1.0, 1.5, 1.4, 2.2), whereas no effects were found for increased consumption of lipids or saturated fats.
Active alpha2 and beta adrenoceptors in lymphocytes from patients with chronic lymphocytic leukemia
Authors: Goin Juan C. , Sterin‐Borda Leonor , Borda Enri S. , Finiasz Marta , Fernandez J. , De Bracco Maria M. E. 
Published: February 2007

AbstractA single population of alpha2 adrenoceptors was characterized in intact B lymphocytes from patients with chronic lymphocytic leukemia (B‐CLL) by binding and saturation studies with 3H labelled yohimbine and by competition studies with alpha adrenergic antagonists. While the affinity of B‐CLL alpha2 adrenoceptors was low (KD: 9.81 nm‐20.98 nm), each cell expressed a large number of receptors. No binding of the alpha1 adrenoceptor antagonist prazosin was observed and the binding properties of beta adrenergic receptors (assayed with 3H‐labelled dihydroalprenolol), were similar to those described for normal lymphocytes. Reaction of B‐CLL with the beta adrenergic agonist isoproterenol raised the levels of cAMP in 11/13 patients tested, and in 8 of these, incubation with the alpha2 adrenergic agonist clonidine prevented the effect and reduced the basal cAMP levels. The presence of active alpha2 adrenoceptors on B‐CLL lymphocytes may be involved in the regulation of metabolic pathways that affect cell functions and favor neoplastic growth.
Depot‐medroxyprogesterone acetate (DMPA) and risk of edometrial cancer
Authors:   THE WHO COLLABORATIVE STUDY OF NEOPLASIA AND STEROID CONTRACEPTIVES, Cuevas Hector Rodriguez , Salazar Socorro Benavides , Palet Antonio , Ontiveros Patricia , Silpisornkosol Suporn , Pardthaisong Tieng , Charoeniam Viruch , Theetranont Shoti , Boosiri Banpot , Chutivongse Supawat , Virutamasen Pramuan , Wongsrichanalai Chansuda , Sindhvananda Sermsri , Koetsawang Suporn , Rachawat Duangdao , Kiriwat Orawan , Koetsawang Amorm , Scully Robert E. , Young Robert H. , Thomas David B. , Stanford Janet L. , Rosenblatt Karin A. , Noonan Elizabeth A. , Ray Roberta M. , Holck Susan , Farley Timothy M. M. , Stanford Janet L. , Thomas David B. 
Published: February 2007

AbstractThe use of depot‐medroxyprogesterone acetate (DMPA), a long‐acting progestational contraceptive, in relation to risk of epithelial ovarian cancer was examined in a hospital‐based case‐control study conducted in Mexico and Thailand. Women with histologically confirmed epithelial ovarian cancer (n = 224) diagnosed between 1979 and 1988 were compared with hospital controls (n = 1,781) matched on age, hospital and year of interview. Overall, 9.8% of cases and 12.9% of controls had ever used DMPA. The relative‐risk (RR) estimate in women who had ever used DMPA, controlling for the confounding effects of number of live births and oral contraceptive use, was 1.07 (95% CI 0.6, 1.8). No consistent patterns of increasing or decreasing risk were noted according to duration of use, time since first or most recent use or age at first use of DMPA. These results suggest that the risk of epithelial ovarian cancer is not altered by the use of DMPA.
Association of ki‐ras mutation with differentiation and tumor‐formation pathways in colorectal carcinoma
Authors: Laurent‐Puig P. , Olschwang S. , Delattre O. , Validire P. , Melot T. , Mosseri V. , Salmon R. J. , Thomas G. 
Published: February 2007

AbstractThe occurrence of a point mutation on the 12th and 13th codons of the Ki‐ras oncogene has been investigated in 99 colorectal carcinomas in relation to 3 histological parameters: extent of differentiation, occurrence of a mucinous component within the tumor, and presence of peripheral adenomatous polyp remnants. The mutation frequency increased with each parameter: from 13% (2/15) to 44% (37/84) with differentiation, from 33% (26/79) to 65% 13/20) with mucinous character, and from 27% (15/56) to 56% (24/43) with the presence of polyp remnants. The frequency was highest in well‐differentiated mucinous tumors with adenomatous remnants 83% (5/6). We suggest that Ki‐ras mutation is preferentially involved in carcinomas that have developed from adenoma and that the mutation preserves differentiation and much secretion in these cancer cells.
Differential susceptibility of balb/c and DBA/2 cells to plasmacytoma induction in reciprocal chimeras
Authors: Silva Santiago , Sugiyama Hiroyuki , Babonits Magdalena , Wiener Francis , Klein George 
Published: February 2007

AbstractReciprocal chimeras were generated between BALB/c and DBA/2 mice by inoculating newborn recipients of either strain with bone‐marrow (BM) cells of the other through the periorbital vein. DBA/2 mice inoculated with the BALB/c with proven chimerism will be referred to as C→D, the reciprocal as D→C. The BALB/c cells carried a Robertsonian 6;15 (Rb6;15) chromosome marker to facilitate identification. The chimeric mice contained between 5% and 70% of donor cells when examined at 4 to 5 weeks of age. Six of 10 C→D developed plasmacytomas (MPC) after 3 × 0.5 ml monthly pristane treatment (incidence 60%) and 8 of 25 (incidence 32%) after 2 to 3 × 0.5 ml pristane followed by Abelson virus (A‐MuLV) infection. Seven of 15 D→C developed MPC after pristane treatment (incidence 47%) and 4 of 17 after pristane + A‐MuLV (incidence 24%). All tumors that have arisen in both reciprocal chimeras originated from BALB/c cells independently of the degree of chimerism. All tumors contained an Ig/myc translocation. Among the C→D chimeras, 5 carried t(12;15) and 1 t(6;15) in the pristane‐treated group, while 4 carried t(12;15), 1 t(6;15) and 3 t(15;16) in the pristane + A‐MuLV. Among the D→C chimeras 6 carried t(12;15) and 1 t(6;15) in the pristane‐treated group, while 3 t(12;15) and 1 t(6;15) in the pristane + A‐MuLV. No tumors developed in 18 pristane‐ and 22 pristane + A‐MuLV‐treated DBA/2 mice nor in 15 pristane‐ and 17 pristane + A‐MuLV‐treated (BALB/c → DBA/2)F1 mice. The data indicate that BALB/c and DBA/2 cells differ in their propensity to transform into plasmacytoma in identical host environments after both pristane and pristane + A‐MuLV treatment. They also show that the oil granuloma can support MPC development in either type of chimeric host.
Invasion by WC5 rat cerebellar cells is independent of RSV‐induced changes in growth and adhesion
Authors: Brady‐Kalnay Susann M. , Boghaert Erwin R. , Zimmer Stephen , Soll David R. , Brackenbury Robert 
Published: February 2007

AbstractThe WC5 rat cerebellar cell line, which is infected with a Rous sarcoma virus that is temperature‐sensitive for pp60src transformation, shows temperature‐dependent expression of the neural‐cell‐adhesion molecule (N‐CAM) and glial fibrillary acidic protein (GFAP). We found that WC5 cells maintained at the non‐permissive temperature in both monolayer cultures and spheroids are subject to density‐dependent inhibition of growth, whereas cells maintained at the permissive temperature continued to grow. The movement of isolated WC5 cells at both temperatures was similar, while the migration of WC5 cells out of 3‐dimensional aggregates was faster at the non‐permissive temperature. We tested whether the RSV‐induced changes affect the invasion of the WC5 cells in 2 in vitro assays: the chorio‐allantoic‐membrane assay and the chick‐heart‐fragment assay. In both assays, WC5 cells grown at either temperature were invasive. These results indicate that growth rate is unrelated to invasion and that loss of N‐CAM‐mediated cell‐cell adhesion is not necessary for invasion.
Establishment of an IL‐2 independent, human T‐cell line possessing only the p70 IL‐2 receptor
Authors: Starkebaum Gordon , Loughran Thomas P. , Waters Cory A. , Ruscetti Francis W. 
Published: February 2007

AbstractA continuous cell line was established from the blood of a patient (HH) with an aggressive cutaneous T‐cell leukemia/lymphoma who lacked antibodies to human T lymphotrophic virus, type 1. The immunophenotype of the cultured cells was CD2+, CD3+, CD4+, CD5+, CD8+, DR+ and CD25− (Tac, IL‐2 receptor α chain). Southern‐blot hybridization analysis of T‐cell‐receptor β chain DNA demonstrated the same rearrangement in freshly isolated blood cells and cultured cells, indicating that the cell line was derived from the patient's malignant clone. Since cultured T‐cells grew in complete medium without added IL‐2, we investigated whether HH cells could be producing and responding to IL‐2 in an autocrine fashion. However, no IL‐2 was detectable in supernatant from the cell line, while antibodies to IL‐2, or to the IL‐2 receptor α or β chains did not inhibit cell growth. In addition, no mRNA message for IL‐2 was detectable in these cells. The results appear to exclude an autocrine IL‐2‐dependent mechanism of cell growth for this T‐cell line. Although cultured HH cells lacked detectable IL‐2 receptor α chain, they did show increased proliferation to exogenous IL‐2. Binding studies with 125I‐IL‐2 demonstrated an intermediate affinity receptor for IL‐2, KD = 1.7nM, with 6400 binding sites per cell, suggesting the presence of an IL‐2 receptor β chain. Consistent with these findings 125I‐IL‐2 cross‐linking studies demonstrated a single receptor calculated to be 75kDa. Also, the β chain of the IL‐2 receptor was detected by immunofluorescence using specific monoclonal antibodies (MAbs). Nanomolar concentrations of an IL‐2‐diphteria toxin fusion protein inhibited cellular protein synthesis, an effect abrogated by native IL‐2. These findings indicate that the IL‐2 receptor β‐chain was functional. This novel mature T‐cell line may be useful in studies of IL‐2 receptor regulation and in analysis of the mechanism of T‐cell leukemogenesis.
Effect of combination treatment with analogs of luteinizing hormone‐releasing hormone (LH‐RH) or somatostatin and 5‐fluorouracil on pancreatic cancer in hamsters
Authors: Szepeshazi Karoly , Lapis Karoly , Schally Andrew V. 
Published: February 2007

AbstractDuctal pancreatic cancers were induced with N‐nitrosobis(2‐oxopropyl)amine (BOP) in female Syrian golden hamsters. The animals were then treated for 2 months with 5‐fluorouracil (5‐FU) and with sustained delivery systems of the LH‐RH agonist D‐Trp‐6‐LH‐RH antagonist (Ac‐D‐Nal(2)1‐D‐Phe(4CI)2‐D‐Pal(3)3‐D‐Cit6, D‐Ala10)LH‐RH(SB:75) and somatostatin analog D‐Phe‐Cys‐Tyr‐D‐Trp‐Lys‐Val‐Cys‐Trp‐NH2, (RC‐160), and with some combinatfon; thereof: In the first experiment, the treatment with D‐Trp‐6‐LH‐RH plus 5‐FU resulted in 52% inhibition of tumorous pancreas weight, a smaller number of tumor nodules on histology, a marked increase of programmed cell death (apoptosis) and a reduced number of AgNOR (argyrophilic nucleolar organizer region) in tumor cells, as compared with controls. The inhibitory effects of this combination were greater than those obtained with 5‐FU and D‐Trp‐6‐LH‐RH treatment alone. In the 2nd experiment, a 76% inhibition of tumorous pancreas weight, a significant decrease in the number of tumor nodules, an increased amount of stroma, enhanced apoptosis and decreased AgNORs were observed after therapy with somatostatin analog RC‐160 plus 5‐FU. Most of these tumor inhibition parameters were superior to those in the group treated with 5‐FU alone, and in some cases slightly better than those treated with RC‐160 alone. Both LH‐RH antagonist SB‐75 and somatostatin analog RC‐160 caused a significant inhibition of tumors, and their combination had the strongest tumor inhibitory effect, with the best survival of animals, the lowest tumorous pancreas weight and the highest apoptosis index among groups. Our results suggest that the combinations of LH‐RH analogs with somatostatin analogs or of either type of analog with 5‐FU may be superior to single agents in the therapy of pancreatic cancer.