bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased prevalence of human papillomaviruses in the lower genital tract of pregnant women
Authors: Schneider Achim , Hotz Marlies , Gissmann Lutz 
Published: February 2007

AbstractIn order to evaluate the influence of pregnancy on the presence of human papillomavirus (HPV) in the lower female genital tract, cervical smears of 92 pregnant and 96 non‐pregnant women, matched by age, were examined for the presence of HPV‐DNA by means of Southern blot hybridization. All patients had negative PAP smears. Twenty‐six (28%) of the pregnant women and 12 (12.5%) of the non‐pregnant women were positive for HPV. HPV 16 accounted for 42% of all positive pregnant cases and only 25% of the positive non‐pregnant cases. Smears of pregnant patients contained more than 10 pg viral DNA in 45% of the cases against 20% in the non‐pregnant group. HPV 16 showed the most active replication in both groups. This study demonstrates an increased prevalence of HPV (preferentially of HPV 16) and a higher replication rate of viral DNA during pregnancy.
Epidermal growth factor stimulates the synthesis of cell‐attachment proteins in the human breast cancer cell line PMC42
Authors: Thorne Heather J. , Jose David G. , Zhang Hui‐Ying , Dempsey Peter J. , Whitehead Robert H. 
Published: February 2007

AbstractThe human breast cancer cell line PMC42 responds to the addition of epidermal growth factor (EGF) by proliferation and increased frequency of attachment of cell‐organoid structures to the culture vessel. Antibodies to fibronectin and laminin reacted strongly, by immunoperoxidase, with the membranes of cells from organoids that became adherent following addition of EGF. This reaction was weak with membranes of cells of non‐adherent organoids in cultures containing EGF and was negative with membranes of cells of free‐floating organoids from cultures without EGF. An increase in biosynthetic labelling with 35S‐methionine was found in cell lysates and supernatants of PMC42 cells cultured in the presence of EGF compared with control cells grown without EGF. One‐dimensional SDS‐polyacrylamide gel electrophoresis and 2‐dimensional NEPHGE‐PAGE of labelled cell proteins showed increased synthesis of several cellular proteins and the appearance in EGF‐treated cells of 2 proteins which were not detected in cells from control cultures lacking EGF. Immunoprecipitation experiments using antibodies to fibronectin and laminin with lysates of 35S‐methionine labelled PMC42 cells cultured with EGF showed strong immunoprecipitation at Mr 200 and 400 with anti‐laminin, and at Mr 200 and 96 with antifibronectin. These immunoprecipitates were blocked specifically by purified laminin or fibronectin, respectively. No immunoprecipitates were detected with these antibodies in lysates from cells grown without EGF. EGF thus stimulates increased adherence of cultured PMC42 cell‐organoid structures together with increased membrane expression of the cell‐adhesive proteins laminin and fibronectin. These effects may play a role in normal development and neoplastic behaviour of breast epithelia.
Tumorigenioty of inorganic arsenic compounds following intratracheal instillations to the lungs of hamsters
Authors: Yamamoto A. , Hisanaga A. , Ishinishi N. 
Published: February 2007

AbstractThe tumorigenicity of arsenic trioxide (As2O3), calcium arsenate (Ca3(AsO4)2) and arsenic trisulfide (As2S3) was studied in male Syrian golden hamsters which received arsenic compounds containing a total dose of 3.75 mg arsenic by means of intratracheal instillations once a week for 15 weeks. As controls, some hamsters were treated with only the vehicle, phosphate buffer solution. During the animals' total life span, one lung adenocarcinoma was seen hi the 17 hamsters in the As2O3 group, one lung adenocarcinoma and 6 lung adenomas in the 25 hamsters in the Ca3(AsO4)2 group, one lung adenoma in the 22 hamsters in the As2S3 group and one lung adenosquamous carcinoma in the 21 hamsters in the control group. From these results, we conclude that calcium arsenate is tumorigenic to the lungs of Syrian golden hamsters. The results concerning the other 2 arsenic compounds were not conclusive.
Tumorigenicity of T24 urinary bladder carcinoma cell sublines
Authors: Flatow Ursula , Rabson Arnold B. , Rabson Alan S. 
Published: February 2007

AbstractTwo sublines of the T24 human urinary bladder carcinoma cell line which differ in tumorigenicity in nude mice have been studied (T24A and T24P). T24A obtained directly from the American Type Culture Collection is non‐tumorigenic while T24P obtained after multiple passages in several NCI laboratories produces tumors in 100% of inoculated mice. T24P cells differ morphologically from T24A, have a higher saturation density, are less serum‐dependent for growth, and are more sensitive to ouabain toxicity. Cytogenetic studies show that the 2 sublines differ significantly in chromosome number, with a modal chromosome range of 76–89 in T24A and a modal chromosome number of 48–51 in T24P. Southern blot analysis of Mspl cleaved T24A and T24P DNAs with the H‐ras Smal probe indicates that both contain only the activated mutant allele originally described in T24. Northern blot analysis shows equal amounts of the l.2kB ras polyadenylated message, and immunoblotting with rasHa antibody demonstrates no significant difference in the amounts of ras proteins. These results indicate that 2 sublines of a ras oncogene‐containing tumor cell line can differ greatly in tumorigenicity and other in vitro characteristics of transformation, and yet have similar expression of the ras oncogene. The fact that the tumorigenic cell line contains fewer chromosomes suggests that tumorigenicity may be related to the loss of some regulatory gene.
Expression of the c‐erbB‐2 protein in normal and transformed cells
Authors: Gullick William J. , Berger Mark S. , Bennett Paul L. P. , Rothbard Jonathan B. , Waterfield Michael D. 
Published: February 2007

AbstractTwo synthetic peptides from the predicted sequence of the human c‐erbB‐2 protein were synthesized and used to raise antisera in rabbits. The sequences chosen were identical to those in the homologous rat c‐neu protein. The antibodies produced reacted with the immunizing peptides in ELISA but showed little or no cross‐reaction with the partly homologous peptides found in equivalent positions in the human EGF receptor. Both antipeptide antibodies, and a monoclonal antibody (MAb) specific for the rat new protein, immuno‐precipitated a 185‐kDa protein from 35S‐methionine‐labelled lysates prepared from a rat cell line known to express high levels of the c‐neu protein. The antipeptide antibodies also recognized a protein of the same size in Western blots. In addition, both antipeptide antibodies immunoprecipitated a 190‐kDa protein from labelled cell lysates prepared from human and monkey cells. Antibodies to one of the peptides, which showed no detectable cross‐reaction with human, rat or monkey EGF receptor, were used to examine the expression of the c‐erbB‐2 protein on a variety of cultured cell types. Eleven transformed, I non‐established and 2 immortalized cell types were examined by immunoprecipitation for their level of expression of the c‐erbB‐2 protein and of the EGF receptor. The numbers of EGF receptors varied widely between different cell lines, whereas the level of the c‐erbB‐2 protein, which was found on all of the cell types examined, was more constant. The number of c‐erbB‐2 molecules present was estimated by autoradiography to be about 100,000 per cell. The antibodies were then used to examine the location and level of expression of the human c‐erbB‐2 and rat c‐neu proteins in normal tissues. Immunohistochemical staining showed that the c‐erbB‐2 protein was highly expressed in rat kidney proximal tubules and loop of Henle. The c‐enbB‐2 protein was also present on normal human epithelial cells but in some cases with a different distribution to that of the EGF receptor.
Establishment and characterization of a human IgA‐κ‐secreting plasma cell line (MT3)
Authors: Donelli Amedea , Narni Franco , Tabilio Antonio , Emilia Giovanni , Selleri Licia , Colo Alessandro , Zucchini Patrizia , Montagnani Giuliano , Torelli Giuseppe , Torelli Umberto 
Published: February 2007

AbstractWe have established a new human plasma cell line from the peripheral blood of a patient with an IgA‐k plasma‐cell leukemia. Morphological, immunological, cytogenetic and molecular studies confirm that the cultured cells are derived from the same clone of leukemic plasma cell in vivo. The established cell line (MT3) grows in suspension, secretes high amounts of IgA k and exhibits morphological and ultrastructural characteristics of plasma cells. Surface marker analysis shows that both primary and cultured cells express the plasmacell‐associated antigens PCA‐1 and T10, while specific B‐and T‐cell determinants and EBV nuclear antigen are undetectable. In the established cell line a few cells express la‐like and CALLA antigens. Cytogenetic analysis of MT3 cells reveals a prevalent hypertriploid karyotype with constant chromosomal aberrations consisting of 14q + 22q‐and marker chromosomes.
Spontaneous mutation rates in cloned murine tumors do not correlate with metastatic potential, whereas the prevalence of karyotypic abnormalities in the parental tumors does
Authors: Kendal Wayne S. , Wang Rui‐Yu , Frost Philip 
Published: February 2007

AbstractWe tested the hypothesis that highly malignant cell lines are genomically more unstable than their less malignant counterparts, and that this instability is more pronounced in clones than in cell lines. We compared MDAY‐D2 to its non‐metastatic variant, D36W25, with regard to (I) the rate of development of ouabain resistance within parallel clones and (2) the prevalence of G‐banded karyotypic abnormalities. We detected no significant difference between the spontaneous mutation rates for ouabain resistance. However, the MDAY‐D2 cell line possessed both a higher prevalence and greater diversity of chromosomal abnormalities. One possible explanation for these seemingly inconsistent results is that genomic instability may remain essentially constant throughout tumor progression, whereas an accumulation of genetic changes may be responsible for the observed increased prevalence of abnormalities and the development of selective survival advantages during progression.
Chemotherapy with estrogenic recruitment and surgery in locally advanced breast cancer: Clinical and cytokinetic results
Authors: Conte P F , Alama A. , Bertelli G. , Canavese G. , Carnino F , Catturich A. , Marco E Di , Gardin G. , Jacomuzzi A. , Monzeglio C. , Mossetti C. , Nicolin A. , Pronzato P. , Rosso R. 
Published: February 2007

AbstractThirty‐nine patients with locally advanced breast cancer (T3b‐4, N13 or inflammatory carcinoma) received 3 cycles of induction chemotherapy with estrogenic recruitment before surgery. The therapeutic regimen consisted of diethylstilbestrol (DES) orally on days 1–3, 5‐Fluorouracil + Doxorubicin + Cyclophosphamide on day 4 q 21 days (DES‐FAC). After surgery 6 additional cycles of chemotherapy (3 DES‐FAC alternating with 3 DES‐CMF with Methotrexate + F and C as in FAC) were administered. The objective response rate was 71.11% with 15.4% CR, and 56.4% PR; after surgery 36/39 (92 3%) patients were rendered disease‐free. So far, 13 of 26 patients in stage 111b have relapsed (9 of 13 with inflammatory carcinomas). Three‐year survival and progression‐free survival are 60% and 53.5%, respectively. Twenty‐three of the 39 patients were subjected to serial tumor biopsies during the first DES‐FAC regimen to allow for tumor‐cell kinetic studies during DES and chemotherapy. A significant estrogenic recruitment occurred in 16 patients (69.6%), irrespective of estrogen‐receptor status. At surgery, 3–4 weeks after induction chemotherapy, tumor proliferate activity was significantly depressed in comparison to basal values. These results indicate that breast cancer cells can be recruited in vivo with DES and that chemotherapy following estrogenic stimulation is effective and feasible with acceptable toxicity.
A cell line from Wilms' tumour with deletion in short arm of chromosome 11
Authors: Kumar S. , Harrison Christine J. , Heighway J. , Marsden H. B. , West D. C. , Jones Pat Morris 
Published: February 2007

AbstractA cell line (T3/73) from a Wilms' tumour has been established from a 9‐month‐old boy with aniridia. The tumour was removed in 1973. On histological examination a diagnosis of Wilms' tumour was made which showed undifferentiated areas, marked tubule formation and abundant striped muscle fibers. The tumour cells, which are fusiform, grew rapidly in culture without the addition of growth factors, and have undergone over 100 passages. Approximately 95% and 5% were positive for desmin and cytokeratin, respectively. The cell doubling time was 28 hr. Cytogenetic studies revealed a karyotype of 46, XY, del(11) (p12::p14). Although the cells stained very intensely with a monoclonal antibody that detects oncogene ras p 21 antigen, Southern blot analysis using c‐Ha‐ras as a probe failed to reveal an obvious deletion or amplification of either Ha‐ras allele.
Regulation of cell‐surface receptors for hematopoietic differentiation‐inducing protein MGI‐2 on normal and leukemic myeloid cells
Authors: Lotem Joseph , Sachs Leo 
Published: February 2007

AbstractThe normal myeloid hematopoietic regulatory proteins include 4 different growth‐inducing proteins (IL‐3, MGI‐1GM = GM‐CSF, MGI‐1G = G‐CSF, and MGI‐1M = M‐CSF = CSF‐1). There is also another type of normal myeloid regulatory protein (MGI‐2) with no MGI‐1 (CSF or IL‐3) activity, which can induce differentiation of normal myeloid precursors and certain clones of myeloid leukemic cells. Studies on the binding of MGI‐2 to differentiation‐competent (D+) and differentiation‐defective (D−) clones of mouse myeloid leukemic cells and to normal cells indicate that: (1) D+ clones of myeloid leukemic cells had about 2,500 high‐affinity surface receptors per cell, like mature normal myeloid cells, and the bound MGI‐2 was rapidly internalized with its cell‐surface receptors at 37°C causing down‐regulation of MGI‐2 receptors in both the normal and leukemic cells; (2) in some D− clones, the number and internalization of MGI‐2 receptors were similar to those of D+ clones whereas other D− clones had only 0–100 MGI‐2 receptors per cell; (3) normal thymus and lymph‐node lymphocytes and T lymphoma cells did not show detectable MGI‐2 receptors; (4) there was an independent expression of receptors for MGI‐2 and for the 4 myeloid growth‐inducing proteins on different clones of myeloid leukemic cells; and (5) none of the 4 myeloid growth‐inducing proteins IL‐3, MGI‐1GM, MGI‐1G, or MGI‐1M, inhibited binding of MGI‐2 to its receptors. The cytotoxic proteins lymphotoxin and tumor necrosis factor did not induce differentiation of the mouse myeloid leukemic cells and also did not inhibit binding of MGI‐2 to its receptors. These results show that the myeloid differentiation‐inducing protein MGI‐2 binds to cell‐surface receptors that are different from the receptors for the 4 myeloid growth‐inducing proteins and these cytotoxic proteins.
Lung cancer among Chinese women
Authors: Gao Yu‐Tang , Blot William J. , Zheng Wei , Ersnow Abby G. , Hsu Cheng Wen , Levin Lynn I. , Zhang Rong , Fraumeni Joseph F. 
Published: February 2007

AbstractA case‐control stud/involving interviews with 672 female lung cancer patients and 735 population‐based controls was conducted to investigate the high rates of lung cancer, notably adenocarcinoma, among women in Shanghai. Cigarette smok‐ ing was a strong risk factor, but accounted for only about one‐ fourth of all newly diagnosed cases of lung cancer. Most patients, particularly with adenocarcinoma, were life‐long non‐smokers. The risks of lung cancer were higher among women reporting tuberculosis and other pre‐existing lung diseases. Hormonal factors were suggested by an increased risk associated with late menopause and by a gradient in the risk of adenocarcinoma with decreasing menstrual cycle length, with a 3‐fold excess among women who had shorter cycles. Perhaps most intriguing were associations found between lung cancer and measures of exposure to cooking oil vapors. Risks increased with the numbers of meals cooked by either stir frying, deep frying or boiling; with the frequency of smokiness during cooking; and with the frequency of eye irritation during cooking. Use of rapeseed oil, whose volatiles following high‐temperature cooking may be mutagenic, was also re‐ ported more often by the cancer patients. The findings thus confirm that factors other than smoking are responsible for the high risk of lung cancer among Chinese women and provide clues for further research, including the assessment of cooking practices.
An estimate of the proportion of colo‐rectal and stomach cancers which might be prevented by certain changes in dietary habits
Authors: Wahrendorf Jürgen 
Published: February 2007

AbstractThe Colo‐rectum and stomach are the 2 sites for which the role of diet in the etiology of cancer is most heavily implicated. Quantitative estimates as to the proportion of cancer deaths attributable to diet vary considerably. This may be partially due to the application of the concept of population attributable risk which has proved a useful yardstick in estimating the public health impact of completely removing an exposure factor under study. This simple concept may well serve in occupational epidemiology, but with more and more risk factors found on a metric scale, or at least characterized on an ordinal scale, extensions should be considered. In this report, a preventable proportion is defined as the excess risk which would be removed if the population exposure distribution were to change in a favorable direction. A simple way of modelling such changes is proposed. This new measure is illustrated with data from 6 case‐control studies on cote‐rectal or stomach cancer. The results Indicate that the proportion of these cancers which may be prevented assuming arbitrary shifts of a single risk factor towards the next lower risk category if populations were to change their dietary habits is in the order of magnitude of 15% to 20%. This figure is much lower, but not necessarily in contradiction to the figures considered for the proportion of cancers attributable to diet.
Characterization of actinomycin‐D‐resistant CHO cell lines exhibiting a multidrug‐resistance phenotype and amplified DNA sequences
Authors: Diddens Heyke , Gekeler Volker , Neumann Manfred , Niethammer Dietrich 
Published: February 2007

AbstractActinomycin D (DACT)‐resistant sublines of the Chinese hamster ovary cell line CHO‐K, were selected in vitro. Sublines were derived which expressed 5.2‐fold (CHO 15DACT) and 35.8‐fold (CHO 100DACT) resistance to DACT. The CHO 100DACT subline displayed marked cross‐resistance to bleomycin, adriamycin, daunomycin, vinblastine, vincristine, VP 16 and VM 26. No cross‐resistance was found to cisplatin or methotrexate. The resistant cells exhibited enhanced (collateral) sensitivity to prednisolone. Combination of prednisolone with vincristine resulted in a pronounced synergistic effect on sensitive cells, whereas in resistant cells the combined effect of both drugs was merely additive. Resistant cells, viably stained with the DNA‐specific dye Hoechst 33342, exhibited decreased fluorescence intensities compared to parental cells. In contrast to sensitive cells the resistant sublines did not accumulate the mitochondria‐specific dye rhodamine 123. Co‐incubation with verapamil, however, effectively enhanced accumulation of the dye. The potential diagnostic value of these fluorescent compounds as marker dyes for the multidrug‐ resistance phenotype is discussed. Non‐toxic doses of verapamil almost completely reversed the resistance to various drugs in CHO 100DACT cells. Specific DNA sequences were amplified in resistant cells, and the increase in resistance was paralleled by a concomitant increase in the copy number of these sequences, suggesting that the corresponding gene may be I functionally linked to the multidrug‐resistance phenotype.
Simultaneous production of IGF‐I and EGF competing growth factors by HT‐29 human colon cancer line
Authors: Culouscou Jean‐Michel , Remacle‐Bonnet Maryse , Garrouste Françoise , Marvaldi Jacques , Pommier Gilbert 
Published: February 2007

AbstractThe conditioned medium from the HT‐29 human colonic adenocarcinoma cell line contains a potent mitogenic activity that can markedly stimulate the proliferation of both rat and human fibroblasts in the absence of serum. Fractionation of conditioned medium on Bio‐Gel P‐100 shows that HT‐29 cells simultaneously produce 2 different types of endogenous growth factors. The first one (molecular mass of 35,8 and 5.5 kDa) exhibits an IGF‐I competing activity which is positively correlated to mitogenic activity. This mitogen is recognized by anti‐IGF‐1 antibodies but Is resistant to reducing agents. It is distinct from IGF‐II, insulin and PDGF. The second one (molecular mass of 40‐and 20‐kDa) is able to displace EGF binding to its receptor. This factor is immunologically recognized by anti‐EGF antibodies but with a lower affinity as compared to EGF. This suggests that this endogenous HT‐29‐growth factor is related to but distinct from native EGF. Although more active in radioreceptor assay than in radioimmunoassay, the EGF‐competing factor is distinct from TGF α or β since it is unable to induce anchorage‐independent growth of NRK or FR3T3 target cells in the presence or absence of exogenous EGF. Moreover, free functional EGF receptors are available at the HT‐29 cell surface.
Invasiveness, proliferative activity and ultrastructural phenotypes of hepatocytes from diethylnitrosamine‐induced neoplastic nodules and hepacarcinomas in vitro
Authors: De Ridder L. , Mosselmans R. , Bernaert D. , Galand P. 
Published: February 2007

AbstractThe invasive behavior of hepatocytes from diethylnitrosamine (DENA) induced neoplastic nodules and hepatocarcinomas was studied in a confronting culture system in vitro. These observations confirm our previous report, demonstrating that hepatocytes from hepatocarcinomas and from neoplastic nodules invaded into embryonic chick precultured heart fragments (PHF), a property associated with malignancy (Mareel, 1979). We now further demonstrate that: (1) Invasiveness was expressed by the hepatocytes in 10 out of 12 samples from hepatocarcinomas, and in 13 out of 36 confronted nodular samples. The hepatocytes from the other two‐thirds of nodule samples died off in the confrontation as did all normal hepatocytes. (2) Invasive hepatocytes from tumors and from nodules showed the same arrangement of invasive liver cells in relation to the heart tissue, and the same ultrastructural phenotypes. The latter did not differ from those in the non‐invading subpopulations, with the exception perhaps of a higher proportion of cells with an indented nucleus. (3) None of the scored ultrastructural alterations was present in all the invasive cells, thus excluding any specific requisite in this respect. (4) When 3H‐TdR was made continuously available to the cultures, starting at the time of confrontation between heart and liver tissues, unlabelled as well as labelled invasive hepatocytes were found inside the PHF in about equal proportions. It is concluded that nodular hepatocytes deviate from normality by at least 2 different properties that may or may not be related to each other and are revealed under in vitro conditions, namely the ability to survive and to proceed through S‐phase and mitosis under such conditions and to actively invade precultured chick heart fragments. The latter property indicates that at least some of the nodules contain hepatocytes that have performed one step in malignant progression.