bluuebunny/crossref_metadata_2025_split huggingface dataset:
Quantification of HPV‐16 E6‐E7 transcription in cervical intraepithelial neoplasia by reverse transcriptase polymerase chain reaction
Authors: Hsu E. M. , McNicol P. J. , Guijon F. B. , Paraskevas M. 
Published: February 2007

AbstractHuman papillomavirus type 16 (HPV‐16) is associated with neoplastic lesions of the uterine cervix. Viral transforming functions have been localized to the E6‐E7 open reading frame (ORF) and this ORF is conserved consistently in cervical intraepithelial neoplasia (CIN). Two mRNAs, generated by alternative splicing, are expressed from the E6‐E7 ORF. These are known as E6*I and E6*II, and potentially encode the viral E7 and E6 proteins, respectively. It is believed that the HPV‐16 transforming ability is mediated by the E6 and E7 proteins. A quantitative RT‐PCR assay, developed by us to characterize the relative expression of E6‐E7 spliced transcripts, was applied to exfoliated cervical cells obtained from patients in varying stages of clinically defined CIN and who were infected with HPV‐16. The relationship between viral expression, disease stage, oral contraceptive use and age was studied. No association was observed between age or oral contraceptive use and HPV‐16 E6‐E7 expression. However, when both E6*I and E6*II were detected, a direct correlation was observed between relative proportions of E6*I/E6*II mRNAs greater than 95%/5% and increased disease severity. This study underscores the importance of the relationship between quantities of viral transforming gene transcript and the course of cervical disease. It also suggests that quantification of HPV‐16 E6‐E7 transcription may be useful as a prognostic tool to identify women who are at increased risk of developing cervical cancer.
Reproductive variables, tobacco, ethanol, coffee and somatometry as risk factors for ovarian cancer
Authors: Polychronopoulou Argy , Tzonou Anastasia , Hsieh Chung‐Cheng , Trichopoulos Dimitrios , Kaprinis George , Rebelakos Apostolos , Toupadaki Nektaria 
Published: February 2007

AbstractA hospital‐based case‐control study of ovarian cancer was conducted in Athens from 1989 to 1991. The cases were 189 women, residents of Greater Athens and less than 75 years old, with histologically confirmed common malignant epithelial tumors of the ovary, operated in the 2 major cancer hospitals of the Greater Athens area. Controls were women residents of Greater Athens, less than 75 years old, who had never had cancer or had an ovary removed and who had visited patients hospitalized in the same wards as the ovarian cancer cases at the same time. The data were analyzed by modeling through multiple logistic regression. Statistically significant associations were found with induced menopause without oophorectomy [relative risk (RR) 0.17; 95% confidence interval (C1) 0.04 to 0.72], age at menopause (for an increment of 5 years RR 1.42; C1 1.00 to 2.01), hormone‐replacement therapy (RR 5.73; C1 1.07 to 30.80), parity (RR 0.48; C1 0.24–0.96) and, marginally, age at first birth (for an increment of 5 years RR 1.30; C1 0.99 to 1.70). Non‐significant but previously suggested or biologically plausible associations were noted with use of oral contraceptives (inverse), weight before onset of the disease (positive), and consumption of more than 2 glasses of alcoholic drinks per day (positive). There were no consistent associations with coffee, tobacco, moderate alcohol intake, broad occupational group, induced abortions, or age at menarche.
Diet and ovarian cancer: A case‐control study in greece
Authors: Tzonou Anastasia , Hsieh Chung‐Cheng , Polychronopoulou Argy , Trichopoulos Dimitrios , Kaprinis George , Toupadaki Nektaria , Karakatsani Anna , Trichopoulou Antonia 
Published: February 2007

AbstractIn a hospital‐based case‐control study of common malignant epithelial tumors of the ovary, conducted in Athens (1989‐1991), 189 cases were compared with 200 hospital visitor controls. Personal interviews were conducted in all cases and diet was ascertained through a semi‐quantitative food frequency questionnaire. Nutrient intakes for individuals were estimated by multiplying the nutrient content of a typical portion size for each specified food item by the frequency at which the food was consumed per month and summing these estimates for all food items. Data were analyzed using logistic regression, controlling for non‐dietary confounding factors, total energy intake and, among nutrients, mutual confounding influences. Adjusted odds ratios (rate ratios) for ovarian cancer, associated with particular nutritional variables, were expressed in terms of increments approximately equal to the standard deviations of (the residual of) the respective nutrients, on a daily basis. The adjusted odds ratios (and 95% confidence intervals) were 0.80 (0.65–0.99) for mono‐unsaturated fat and 0.73 (0.61 – 0.87) for crude fiber. No substantial, statistically significant or consistent independent associations were noted for total energy, total protein, saturated fat, polyunsaturated fat, dietary cholesterol, total carbohydrates, sucrose, vitamin C, vitamin A, riboflavin or calcium. These associations, if causal, could explain to some extent the relatively low incidence of ovarian cancer in Greece and other Mediterranean countries as well as the increasing incidence trends noted in these countries during the last few decades.
Prognostic significance of cathepsin‐D expression in node‐positive breast carcinoma: An immunohistochemical study
Authors: Tětu Bernard , Cǒté Chantal , Brisson Sonia , Roberge Nancy , Brisson Jacques , Potvin Diane 
Published: February 2007

AbstractThe prognostic significance of cathepsin‐D expression was evaluated by immunohistochemistry in 638 node‐positive breast carcinomas diagnosed between 1980 and 1986. A minimum of 2.5 years of follow‐up was available for each patient (maximum: 9.5 years). Cathepsin‐D expression was assessed separately both in cancer and in stromal cells using a commercially available polyclonal antibody. While cancer‐cell immunostaining was not associated with prognosis, positive staining of stromal elements was related to shorter metastasis‐free survival. The difference in distant metastasis‐free survival between positive and negative expressors was greatest in the sub‐group of patients submitted to adjuvant chemotherapy, with a hazard ratio for occurrence of distant metastasis of 1.76 by multivariate analysis, but was lowest for those receiving hormone therapy. Cathepsin‐D expression by stromal cells was related to HER‐2/ neu oncoprotein expression, HSP‐27 expression, poor nuclear grade, aneuploidy, and absence of estrogen and progesterone receptors. No association was found with the number of involved lymph nodes, tumor size, age, histologic grade, S‐phase fraction, or vascular invasion. Our study suggests that cathepsin‐D expression by stromal cells (and not by cancer cells) affects the prognosis of breast cancer, that stromal cells probably play a key role in local invasion and metastatic dissemination of the tumor, and that the prognostic significance of cathepsin‐D expression may vary according to the type of adjuvant therapy.
Contrasting effects of 17 β‐estradiol on the growth of human ovarian carcinoma cells in vitro and in vivo
Authors: Langdon Simon P. , Ritchie Alison , Young Karen , Crew A. Jayne , Smyth John F. , Miller William R. , Sweeting Vicky , Bramley Tony , Hillier Stephen , Hawkins Richard A. , Tesdale Ann L. 
Published: February 2007

AbstractA human ovarian adenocarcinoma cell line (PE04) has been established as a xenograft in nude mice. In vitro, this cell line is estrogen receptor (ER)‐positive and its growth is stimulated by 17 β‐estradiol at concentrations between 10−12 and 10−6 M. When xenografted, PE04 cells remain ER‐positive and also possess progesterone receptors (PR); treatment with 17 β‐estradiol reduces the concentration of ER and increases levels of PR. Growth of the xenograft is reduced in ovariectomized animals while implantation of estrogen pellets also results in growth inhibition. Similar treatment with estrogen does not inhibit the ER‐negative HOX 60 ovarian xenograft, and stimulates growth of the ER‐positive ZR‐75‐1 breast carcinoma xenograft. Serum measurements of 17 β‐estradiol confirm that ovariectomy reduces the level of 17 β‐estradiol while implantation of estrogen pellets results in raised levels of the hormone. Tamoxifen inhibits growth of the PE04 xenograft but not that of the HOX 60 xenograft, consistent with ER status. These results indicate that ER‐positive PE04 ovarian cancer cells are sensitive to 17 β‐estradiol in vivo but that the response may be of a different type from the in vitro response. This lends further support to the concept that ovarian cancer may be hormone‐sensitive and potentially responsive to endocrine therapy.
Involvement of thrombospondin in the adherence of human breast‐adenocarcinoma cells: A possible role in the metastatic process
Authors: Incardona Francesca , Fauvel‐Lafeve Françoise , Legrand Yves , Legrand Chantal , Calvo Fabien 
Published: February 2007

AbstractThe attachment of cancer cells to adhesive molecules, such as laminin (LN) and fibronectin (FN) in the extracellular matrix is a critical step in tumor invasion and metastasis. Recent data have suggested a potential role for thrombospondin (TSP), a 420‐kDa cyto‐adhesive glycoprotein, in the growth and spread of breast cancer. In this study, we have measured the ability of the human breast adenocarcinoma cell line, MDA‐MB‐231, to synthesize TSP and to use this molecule as an adhesion factor. The level of TSP in cells and secreted into the culture medium were determined by an enzyme‐linked immunosorbent assay (ELISA). At pre‐confluence, MDA‐MB‐231 cells were shown to produce a high level of TSP, most of which was retained within the cells. In comparison, FN was almost entirely secreted into the culture medium. An increased secretion of TSP was however measured at low cell density, suggesting that TSP might be required for cell/substratum or cell/cell interactions. As shown by flow cytometry, the cells expressed membrane‐bound TSP as well as unoccupied TSP receptors. 125I‐TSP bound saturably to 1.2 x 106 sites per cell with an apparent dissociation constant of 23 nM. The binding was inhibited by an excess of unlabeled TSP and by heparin, suggesting that the receptor could be a heparian‐sulfate proteoglycan or a sulfatide. TSP promoted attachment but not spreading of MDA‐MB‐231 cells which attached and spread on FN and LN substrates. These results suggest that endogenously synthesized TSP may have a role in the cyto‐adherence of tumor cells during the spread of breast cancer.
Binding properties of monoclonal antibodies recognizing external epitopes of the human MDR1 P‐glycoprotein
Authors: Schinkel Alfred H. , Borst Piet , Smit Jaap J. M. , Wagenaar Els , Dollé Martijn , Arceci Robert J. , Baas Frank , Tsuruo Takashi , Mechetner Eugene B. , Roninson Igor B. 
Published: February 2007

AbstractMonoclonal antibodies (MAbs) recognizing external epitopes of the human MDRI P‐glycoprotein have been used both for the detection of multidrug‐resistant cells and as specific inhibitors of P‐glycoprotein‐mediated multidrug resistance. Using a panel of recently developed transfected or transgenic cell lines containing variants of the human MDRI and MDR3 P‐glycoproteins, we have compared the specificity and binding properties of the previously isolated MAbs MRK16, HYB‐241, UIC2 and 4E3, and of the newly isolated MAb 7G4. The removal of 1, 2 or all 3 of the N‐glycosylation sites present in the first extracellular loop of MDR1 P‐glycoprotein did not significantly affect the binding of these MAbs. In contrast, a 20 amino acid deletion in the first extracellular loop of MDR1 P‐glycoprotein completely abolished binding of UIC2, whereas the binding of all other MAbs was hardly affected. None of the MAbs tested bound detectably to cell lines containing a high level of the human MDR3 P‐glycoprotein. The differences in the binding specificity between UIC2 and the other tested antibodies parallel the reported functional differences in the ability of these antibodies to inhibit P‐glycoprotein‐mediated drug efflux.
Irradiated fibroblasts protect burkitt lymphoma cells from apoptosis by a mechanism independent of BCL‐2
Authors: Falk Martin H. , Bornkamm Georg W. , Hültner Lothar , Milner Anne , Gregory Christopher D. 
Published: February 2007

AbstractWhen cells of fresh Burkitt lymphoma (BL) biopsies are explanted into tissue culture, their survival and growth are greatly dependent on the presence of a feeder layer of irradiated fibroblasts. To investigate the nature of this feeder dependence, we characterized the growth requirements of a panel of Epstein‐Barr Virus (EBV)‐negative and ‐positive BL cell lines in both the absence and the presence of feeder cells in vitro. Four EBV‐negative BL lines and 4 EBV‐positive lines displaying the phenotype of BL cells in vivo required high cell density for proliferation in the absence of feeder cells, but grew out as single‐cell clones when seeded on irradiated human fibroblasts. EBV‐positive BL cell lines which had acquired an activated phenotype similar to that of lymphoblastoid cell lines required much lower cell densities for autonomous proliferation. The EBV‐negative Burkitt lymphoma line BL70 was used as a model to study the feeder‐cell dependence in more detail. BL70 cells grew in the absence of feeder cells only at high cell density and at high FCS concentration. In the presence of feeder cells, BL70 cells became clonogenic even at greatly reduced FCS concentration. A decrease in either cell density or FCS concentration induced apoptosis. Supernatants from feeder cells and from BL70 cells growing autonomously at high cell density were unable to substitute for the survival and growth‐promoting effect of the feeder cells. Protection of Burkitt lymphoma cells from apoptosis by co‐cultivation with irradiated fibroblasts was not mediated by induction of bcl‐2. The system described here may be relevant for the in vivo situation since Burkitt lymphoma cells are protected from c‐MYC induced apoptosis in vivo also by a mechanism which does not involve bcl‐2.
Sodium butyrate induces apoptosis in human colonic tumour cell lines in a p53‐independent pathway: Implications for the possible role of dietary fibre in the prevention of large‐bowel cancer
Authors: Hague A. , Manning A. M. , Hanlon K. A. , Hart D. , Paraskeva C. , Huschtscha L. I. 
Published: February 2007

AbstractThe purpose of this study was to determine whether cultured colonic adenoma and carcinoma cells undergo apoptosis (programmed cell death) in vitro and whether specific growth and dietary factors, thought to be involved in the control of growth and differentiation of human colonic cells, could induce cell death through apoptosis. In cell lines originating from 6 colorectal adenomas and 7 carcinomas, spontaneous apoptosis was observed. Sodium butyrate, a naturally occurring fatty acid, is present in the human large bowel in millimolar amounts as a result of bacterial fermentation of dietary fibre. Sodium butyrate, at physiological concentrations, induced apoptosis in 2 adenoma cell lines, RG/C2 and AA/C1, and in the carcinoma cell line PC/JW/F1. In contrast, transforming growth factor β1, which is thought to have an important role in the control of growth in colonic epithelium, did not induce apoptosis. Neither RG/C2 nor PC/JW/F1 contain wild‐type p53, therefore this tumour‐suppressor gene is not required to mediate signals for the induction of apoptosis in colonic tumour cells. Our studies report the induction of apoptosis in colonic tumour cells by the naturally occurring fatty acid sodium butyrate. Since sodium butyrate is produced by bacterial fermentation of dietary fibre, the observation that this fatty acid can induce apoptosis could, in part, explain why a high‐fibre diet appears to be protective against colon cancer. Escape from the induction of programmed cell death may be an important event in colorectal carcinogenesis.
in vitro effects of recombinant human interferon gamma on human mesothelioma cell lines
Authors: Zeng L. , Buard A. , Saint‐Etienne L. , Jaurand M. C. , Bignon J. , Monnet I. , Brochard P. , Boutin C. , Fleury J. 
Published: February 2007

AbstractMalignant mesothelioma is a tumor arising from serous surfaces and often related to asbestos exposure. Malignant mesothelioma is resistant to various forms of therapy. Radiotherapy, surgery or chemotherapy only slightly improve prognosis. IFN‐γ produces complete or partial responses in stage‐l patients with malignant mesothelioma. The in vitro biological effect of IFN‐γ on malignant mesothelioma cells remains poorly elucidated. In the present study, 32 well‐characterized human mesothelioma cell lines (HMCL) were treated with r‐hu IFN‐‐γ at 4 doses and cell growth was determined by a colorimetric method (MTT assay). Among the 32 HMCLs tested, 11 exhibited significant cell‐growth inhibition; 16 were insensitive to r‐hu IFN‐γ, and 5 were slightly inhibited. The sensitive cell lines were strongly inhibited by r‐hu IFN‐γ. Our results show that HMCL exhibit a large range of responses to r‐hu IFN‐γ, some of which can be compared with those obtained in vivo in humans.
Modulation of sensitivity of human ovarian cancer cells to cis‐diamminedichloroplatinum(II) by 12‐O‐tetradecanoylphorbol‐13‐acetate and D, L‐buthionine‐S, R‐sulphoximine
Authors: Hirata Junko , Kikuchi Yoshihiro , Kita Tsunekazu , Imaizumi Eiji , Tode Takehiko , Ishii Kenji , Kudoh Kazuya , Nagata Ichiro 
Published: February 2007

AbstractThe ability of 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) and D, L‐buthionine‐S, R‐sulphoximine (BSO) to modulate cisdiamminedichloroplatinum(11) (CDDP) sensitivity was investigated in human ovarian cancer cell lines sensitive (KF) or with intrinsic resistance (KK and MH) to CDDP. The KK and MH cell lines were derived from ascites of patients with clear‐cell carcinoma and serous cystadenocarcinoma of the ovary who both showed clinical resistance to CDDP. The CDDP IC50 value of KK and MH cells was about 4.6‐ and 10.2‐fold higher than that of KF cells. PKC activities in the cytosol and membrane of KK and MH cells were also about 4‐ to 5‐fold higher than those of KF cells. Proliferation of KF, KK and MH cells was inhibited in a dose‐dependent manner by TPA. The membrane PKC activities in the KF cells were rapidly activated and down‐regulated 24 hr after exposure to TPA, while those in the KK and MH cells were not down‐regulated even after exposure to TPA for 24 hr, suggesting that the membrane form of PKC may be involved in the intrinsic resistance. Continuous exposure to 10 nM TPA for 5 days significantly reduced the CDDP sensitivity of KF and KK cells, while exposure to 10 nM TPA for I hr significantly elevated that of KK and MH cells. Interestingly, I ‐hr exposure to I m̈M TPA induced CDDP‐resistance in KK cells. Such changes in CDDP sensitivity by TPA seemed to be linked with those of cellular PKC activity, i.e., when the CDDP sensitivity was reduced by TPA, the cellular PKC rose. When the CDDP sensitivity was increased, the cellular PKC decreased. In addition, glutathione (GSH) levels in KK and MH cells, whose proliferation was more markedly inhibited by BSO than the KF‐cell proliferation, were about 7.6‐ and 1.9‐fold higher than those in KF cells. The degree of depletion of GSH by BSO was more marked in the KK and MH cells than in the KF cells, subsequently resulting in a significant elevation of the CDDP sensitivity of KK and MH (but not KF) cells. Our results suggest that intrinsic resistance to CDDP can be reduced by TPA or BSO under some conditions.
Tobacco use and nasopharyngeal carcinoma in a cohort of us veterans
Authors: Chow Wong‐Ho , McLaughlin Joseph K. , Hrubec Zdenek , Nam Jun‐Mo , Blot William J. 
Published: February 2007

AbstractThe risk of nasopharyngeal carcinoma (NPC), a relatively rare neoplasm in the United States, was examined in relation to tobacco use in a cohort of nearly 250,000 US veterans whose mortality experience was followed for 26 years. A total of 48 NPC deaths were identified during the follow‐up period. Current smokers had a nearly 4‐fold increase in risk of NPC compared with non‐users of any tobacco, with risk increasing to 6.4 among those smoking more than 2 packs daily. After adjustment for age and number of cigarettes smoked, risks were inversely associated with age at starting to smoke, with the highest risk observed among those who started smoking before age 15, although no clear trend associated with duration of smoking was observed. Former cigarette smokers had a small excess risk of NPC, but no association was detected for cigar/pipe users. This study adds strong evidence to the increasing literature linking cigarette smoking to NPC.
Abnormalities affecting the APC and MCC tumour suppressor gene loci on chromosome 5q occur frequently in gastric cancer but not in pancreatic cancer
Authors: McKie Arthur B. , Lemoine Nicholas R. , Filipe M. Isabel 
Published: February 2007

AbstractAbnormalities affecting tumour suppressor genes on chromosome 5q21 are increasingly recognised as important in the pathogenesis of a variety of human cancers, particularly of the gastrointestinal tract. We have examined a series of gastric and pancreatic cancers from European patients for loss of heterozygosity (LOH) of markers within and around the APC and MCC genes on chromosome 5q2t using restriction fragment length polymorphism and polymerase chain reaction techniques. We find that LOH of the APC and MCC genes is particularly frequent in gastric cancers of diffuse type, but very infrequent in pancreatic cancers. We have also used single‐strand conformational polymorphism to screen for abnormalities of the sequence of the APC and MCC genes in a panel of pancreatic cancer cell lines. Our results suggest that there are distinct differences in the molecular pathogenesis of gastric and pancreatic cancer and that abnormalities of APC and MCC may be involved particularly in the diffuse type of gastric cancer.
Moloney virus induction of T‐cell lymphomas in a plasmacytomagenic strain of Eμ‐V‐ABL transgenic mice
Authors: Haupt Ygal , Harris Alan W. , Adams Jerry M. 
Published: February 2007

AbstractAlthough the v‐abl gene can provoke several types of lymphoid neoplasm, mice of a transgenic strain (Em̈‐v‐abl 40) in which lymphocytes are targeted for expression of v‐abl by a linked immunoglobulin enhancer (Em̈) spontaneously develop only plasmacytomas. To determine whether other lymphocytes of this strain were susceptible to transformation, and to identify genes that can collaborate with v‐abl in tumorigenesis, Em̈‐v‐abl 40 mice were subjected to insertional mutagenesis by neonatal infection with Moloney murine leukemia virus. Tumorigenesis was accelerated moderately, but nearly all the tumors were T lymphomas. The altered tumor type may reflect both the T‐cell tropism of Moloney virus and the higher level of Em̈‐v‐abl 40 expression found in T lymphocytes than in B lymphocytes. Insertion near the c‐myc, N‐myc or pim‐1 gene was observed in 42% of the induced tumors, indicating that each of these genes may collaborate with v‐abl in lymphomagenesis. Most of the accelerated tumors had a surprisingly low level of transgene expression. Thus, high expression of v‐abl may not be required for Moloney‐induced T lymphomagenesis.