bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prevalence and distribution of human papillomavirus type‐16 DNA in pelvic lymph nodes of patients with cervical cancer and in women with no history of cervical abnormality
Authors: Rose Barbara R. , Thompson Carol H. , Chantrill Lorraine A. , Tattersall Martin H. N. , Cossart Yvonne E. 
Published: February 2007

AbstractThe polymerase chain reaction (PCR) was used to investigate the prevalence and distribution of human papillomavirus (HPV)‐16 DNA in paraffin sections of all pelvic lymph nodes removed from 14 patients with Stage Ib‐cervical cancer at the time of resection of their primary tumours. The results were compared with those obtained from 8 women with no known history of cervical abnormality. In all, 22 cervical biopsies and 401 lymph nodes (296 paraffin blocks) were examined. Nine of the 14 cervical cancer patients had primary tumours that were positive for HPV‐16 DNA: only 3 of these had lymph nodes with histological evidence of metastasis, and HPV 16 DNA was detected in each of the corresponding paraffin blocks. HPV 16 DNA was also detected in varying proportions (8%‐92%) of the histologically‐negative lymph nodes from these women. There was no correlation between the HPV DNA‐positive lymph nodes and their proximity to the primary tumour. HPV‐16 DNA was not identified in any of the lymph nodes from the 5 women whose cancers were not HPV‐16‐related, or in those of women with no evidence of cervical abnormality. This preliminary survey suggests that HPV DNA is frequently transported from HPV‐16‐related cervical tumours to regional lymph nodes. However, its practical significance will not be clear until sufficient time has elapsed for correlation of the results with the clinical outcome. © 1992 Wiley‐Liss, Inc.
Determination of placental ferritin (PLF)‐positive lymphocytes in women in early stages of breast cancer
Authors: Rosen Harald R. , Stierer Michael , Göttlicher Josef , Wolf Hermann , Weber Renate , Vogl Erich , Eibl Martha 
Published: February 2007

AbstractPrevious studies have proved that a certain acidic isoform of ferritin is specifically synthesized by the placenta and breast‐cancer tissue. In this context it has been further reported that the determination of this so‐called placental isoferritin (PLF) on the surface of a subset of peripheral lymphocytes is highly specific and sensitive for early stage breast cancer. By use of the monoclonal antibody CM‐H‐9 and flow cytometry, the levels of placental ferritin (PLF)‐positive cells were determined in 133 female patients undergoing surgical excision of a controversial or highly suspicious lesion of the breast detected by mammography. In addition, 61 healthy blood donors served as controls. Values of PLF‐positive cells in breast cancer patients differed significantly from those found in women with benign diseases and healthy controls (3.87% vs. 1.55% and 2.02, respectively; p < 0.00001). Analysis of prognostic factors in breast cancer patients (tumor size, lymph‐node status, menopausal status, estrogen receptor status, histologic grading and grading subfactors) revealed significantly higher levels of PLF‐positive cells in lymph‐node‐negative patients compared with node‐positive patients (p < 0.00001). Furthermore, levels of PLF‐positive cells s lowed a significantly negative correlation with tumor size and nuclear polymorphism. In 15 patients who underwent a guidewire‐directed surgical biopsy for a non‐palpable, mammographically suspect lesion, 4 cases of cancer correlated with high values of PLF‐positive lymphocytes while only I patient with a enign histologic result exhibited more than 4% positive cells. © 1992 Wiley‐Liss, Inc.
Matrigel promotes retinoblastoma cell growth in vitro and in vivo
Authors: Albini Adriana , Melchiori Antonella , Garofalo Angela , Noonan Douglas M. , Basolo Fulvio , Taraboletti Giulia , Chader Gerald J. , Giavazzi Raffaella 
Published: February 2007

AbstractCells derived from retinoblastomas grow slowly in vitro and only very rarely form tumors in nude mice. Matrigel, a mixture of components normally found in basement membranes, promotes the growth of Y‐79 and WERI‐Rbl retinoblastoma (Rb) cells when added to suspension cultures of the 2 Rb cell lines. It also substantially increases cell adhesion in vitro. Y‐79 cells, seeded into a Matrigel matrix, form round colonies over a 3‐week period similar to those of control, weakly metastatic murine melanoma cells. In vivo, s.c. co‐injection of Matrigel with either Y‐79 or WERI‐Rbl cells into nude mice promotes retino‐lastoma tumor formation. Transplantation of as few as 1,000 cells allows for xenografting under these conditions, while no tumors were observed in the absence of Matrigel, even at 10 × 106 cells/inoculum. The tumors produced have the expected morphology and express an mRNA for a highly specific retina/retinoblastoma marker protein, the interphotoreceptor retinoid‐binding protein. Thus, the xenografts obtained maintain the original morphological and molecular characteristics of the injected cells and represent a useful model for in vivo studies of retinoblastoma growth and treatment. © 1992 Wiley‐Liss, Inc.
Over‐expression of P‐glycoprotein and glutathione S‐transferase PI in MCF‐7 cells selected for vincristine resistance in vitro
Authors: Whelan Richard D. H. , Waring Clare J. , Wolf C. Roland , Hayes John D. , Hosking Louise K. , Hill Bridget T. 
Published: February 2007

AbstractThis study has provided evidence that exposure of the wild‐type MCF‐7 human breast carcinoma cell line to the mutagen ethyl methane sulphonate (EMS), followed by selection in vincristine (VCR), resulted in a stably‐resistant subline, designated VCREMS, which expressed an approximately 14‐fold level of resistance to VCR. This VCREMS subline showed cross‐resistance (3‐fold) to adriamycin (ADR) and to etoposide (3‐fold), but not to cisplatin. The addition of a non‐toxic concentration of verapamil (6.6 μM) significantly enhanced VCR cytotoxicity only in the resistant subline. This resistance was associated with over‐expression of P‐glycoprotein (Pgp), but without a concomitant increase in Pgp mRNA or gene amplification. In addition, activities of total glutathione S‐transferases (GST) and glutathione peroxidase were elevated in this resistant subline, with over‐expression of the GST‐pi isozyme and its associated mRNA being identified, without gene applification. This VCR‐selected resistant MCF‐7 cell line therefore provides another example of a breast carcinoma subline in which there is co‐ordinate over‐expression of both Pgp and GST‐pi, without attributing a causal relationship to either event, and extends the range of anti‐tumour drugs known to elicit modifications in glutathione metabolism. © 1992 Wiley‐Liss, Inc.
The human squamous cervical carcinoma cell line, HOG‐1, is responsive to steroid hormones
Authors: White J. O. , Jones R. N. , Croxtall J. D. , Gleeson R. P. , Krausz T. , Pervez S. , Jamil A. , Guida L. , Beesley J. E. , Soutter W. P. 
Published: February 2007

AbstractGrowth of the human squamous cervical carcinoma cell line, HOG‐1, was stimulated in response to oestradiol in serum‐containing and chemically defined medium. The oestradiol‐stimulated growth could be inhibited by 4‐OH tamoxifen, progesterone and medroxyprogesterone acetate; the last 2 compounds also inhibited basal cell growth in serum‐containing and chemically defined media. The data are consistent with the sensitivity of human squamous cervical cancer to sex‐steroid hormones and suggest that endocrine therapies may be of benefit in this disease. © 1992 Wiley‐Liss, Inc.
Two new human cholangiocarcinoma cell lines and their cytogenetics and responses to growth factors, hormones, cytokines or immunologic effector cells
Authors: Shimizu Yukihiro , Demetris Anthony J. , Gollin Susanne M. , Storto Patrick D. , Bedford H. Melanic , Altarac Silvio , Iwatsuki Shunzaburo , Herberman Ronald B. , Whiteside Theresa L. 
Published: February 2007

AbstractTwo new human cholangiocarcinoma (CC) cell lines (CC‐SW‐1 and CC‐LP‐1) were established and maintained in culture for 2 years. Histologically, both original liver tumors were adenocarcinomas, and the cell lines exhibited morphologic eatures of moderately differentiated adenocarcinoma. Immunohistochemistry showed that both cell lines were strongly positive for cytokeratin AEI but negative for carbohydrate tumor‐associated antigen, CA19–9. Ultrastructural analysis of both cell lines showed the presence of tight junctional complexes and focally formed microvilli. Both CC cell lines were tumorigenic in nude mice. Cytogenetic analysis showed that both cell lines expressed highly aneuploid karyotypes with numerous structural and numerical deviations. CC‐SW‐1 was hypodiploid with numerous chromosome losses and structural rearrangements, while CC‐LP‐1 was hyperdiploid and displayed multiple additional chromosomes. Doubling times for the CC‐SW‐1 and CC‐LP‐1 cell lines in the presence of 15% fetal bovine serum were 72 hr and 180 hr, respectively. Growth of the CC‐SW‐1 cell line was significantly stimulated in the presence of insulin, while that of the CC‐LP‐1 cell line was significantly augmented by epidermal growth factor (EGF). In contrast, dexamethasone strongly inhibited proliferation of both cell lines in a dose‐dependent manner. Among various recombinant cytokines examined for effects on growth or surface antigen expression on CC cell lines, only interleukin 1‐β (ILI‐β) strongly inhibited growth of the CC‐LP‐1 cell line, while interferons (IFNs) or tumor necrosis factor‐alpha (TNF‐α) were mildly inhibitory. Both tumor cell lines were resistant to natural killer (NK) cells but sensitive to lymphokine‐activated killer (LAK) cells. Preincubation of tumor cells with IFN‐γ, IFN‐α or TNF‐α significantly decreased the susceptibility of each tumor cell line to lysis by LAK cells, and the change in sensitivity did not correlate with the expression of HLA antigens or intercellular adhesion molecule‐1 (ICAM‐1) on the surface of tumor cells. These 2 CC cell lines are expected to provide valuable information about cell biology of human CC. © 1992 Wiley‐Liss, Inc.
Biodistribution of lymphokine‐activated killer (LAK) cells in WAG rats after hepatic‐artery or jugular‐vein infusion
Authors: Kuppen Peter J. K. , Marinelli Andreas , Camps Jan A. J. , Pauwels Ernest K. J. , van de Velde Cornells J. H. , Fleuren Gert Jan , Eggermont Alexander M. M. 
Published: February 2007

AbstractThis study deals with the biodistribution of syngeneic radiolabeled lymphokine‐activated killer (LAK) cells in Wag rats after infusion via the hepatic artery or the jugular vein. The biodistribution of IIIIndium‐labeled LAK cells was evaluated using serial whole‐body gamma camera imaging. Furthermore, we investigated 2 factors that might influence the biodistribution of these effector cells: purity of LAK cells and administration of interleukin‐2 (IL‐2). After injection of IIIIndium‐labeled LAK cells via the hepatic artery or via the jugular vein we could detect important differences in the biodistribution pattern up to 5 hr after injection. LAK cells administered via the jugular vein were all found in the lungs up to 2 hr after injection and then redistributed to the liver and to the spleen. LAK cells administered via the hepatic artery were all found in the liver after injection and redistributed after 2 hr mainly to the spleen. About 8 hr after injection we could no longer detect any differences in the biodistribution pattern according to the route of administration. Biodistribution was followed for up to 72 hr after injection but the pattern showed no change after 8 hr, whichever the route of administration. A purified adherent‐LAK population, a large granular lymphocyte culture with only 6% T cells, showed the same distribution pattern as standard LAK cells (40% T cells). Infusion of 40,000 units of IL‐2 per day, starting 3 days before and continuing after administration of radio‐labeled LAK cells, accelerated the redistribution of these cells by both routes of administration. We conclude that up to 2 hr after local infusion, a high concentration of LAK cells in the first capillary bed can be obtained. Therefore, local administration of LAK cells may be more effective against tumors. © 1992 Wiley‐Liss, Inc.
Derivation of tumorigenic and non‐tumorigenic mouse alveolar type‐II cell lines from fetal type‐II cells after a combined in vivo/in vitro carcinogen treatment
Authors: Oomen L. C. J. M. , Calafat J. , Have‐Opbroek A. A. W. Ten , Egberts J. , Demant P. 
Published: February 2007

AbstractAlveolar type‐II cells wens isolated from the lungs of fetuses (day 18 of gestation) of the A/WySnAf (A/Sn) mouse strain, which were treated in utero at day 15 with the directly‐acting carcinogen N‐ethyl‐N‐nitrosourea (ENU). The isolated type‐II cells were again treated with ENU during their initial growth in vitro. After a prolonged culture period, 5 cell lines were obtained, which were identified as type‐II cell lines. Differences between cell lines were found with respect to contact‐inhibited growth, cell doubling time and ability to grow in a serum‐free medium. Two out of the 5 cell lines produced highly invasive type‐II cell carcinomas after s.c. injection of 5 × 106 cells into nude nice. Thus, both tumorigenic and non‐tumorigenic mouse alveolar type‐II cell lines were derived after this combined in vivo and in vitro carcinogen treatment of fetal mouse alveolar type‐ll cells. This offers the possibility of studying in vitro the factors thought to influence lung tumorigenesis in vivo. In addition, our findings strongly suggest that alveolar type‐II cells are the progenitor cells of malignant mouse lung tumors. © 1992 Wiley‐Liss, Inc.
Epidermal growth factor reduces HER‐2 protein level in human ovarian carcinoma cells
Authors: Marth Christian , Lang Thomas , Cronauer Marcus V. , Doppler Wolfgang , Zeimet Alain G. , Bachmair Franz , Ullrich Axel , Daxenbichler Günter 
Published: February 2007

AbstractOver‐expression of the proto‐oncogene HER‐2 (c‐erbB‐2/neu) in ovarian, endometrial, and mammary carcinoma is an indicator of poor prognosis. Interactions between the epidermal growth factor (EGF) receptor and the HER‐2 protein have been described. The aim of this study was to elucidate the effects of EGF on HER‐2 expression. In the human ovarian carcinoma cell lines HTB‐77, OVCAR‐3, 2780, SKOV‐6, SKOV‐8 and 2774, and the human mammary tumor cell line SKBR‐3, total cellular p185HER‐2 was determined by an ELISA, whereas the surface p185HER‐2 was measured with a living‐cell RIA. Stimulation of these cell lines with either EGF (0.1–30 nM) or TGF‐α (0.1–30 nM) led to a significant reduction in p185HER‐2 expression. The effect was more pronounced in cells with normal HER‐2 expression. A reduction of mRNA levels for p185HER‐2 by EGF was observed in OVCAR‐3 cells but not in the over‐expressing lines HTB‐77 and SKBR‐3. Interestingly, the EGF‐induced effect was not always associated with growth stimulation and was not correlated with the number of EGF binding sites detected by a radioligand assay. Our data indicate that EGF treatment results in a down‐regulation of p185HER‐2. © 1992 Wiley‐Liss, Inc.
Lipoprotein(a) and CA125 levels in the plasma of patients with benign and malignant ovarian disease
Authors: Kuesel Annette C. , Kroft Thérèse , Préfontaine Michel , Smith Ian C. P. 
Published: February 2007

AbstractElevated plasma levels of apolipoprotein (a) have been reported earlier in cancer patients. In order to investigate the potential of apolipoprotein(a) as an ovarian tumour marker, plasma apolipoprotein(a) and CA125 levels were measured in healthy women and women with benign or malignant pelvic masses. Among women younger than 49 years, 80% of healthy controls and ovarian cancer patients had apolipoprotein(a) levels below 350 U/I. Among women aged 49 years or older, 46% of healthy controls but 73% of ovarian cancer patients and 77% of women with successfully treated ovarian cancer, had low apolipoprotein(a) levels. For both age groups, apolipoprotei‐n(a) is not a suitable marker for ovarian cancer. No correlation was found between apolipoprotein(a), triglyceride or cholesterol in plasma. Healthy women younger than 49 years had significantly higher CA125 levels than women 49 years or older (20 × 14 U/ml vs. 13 × 12 U/ml, p < 0.005). Levels of CA125 above 35 U/ml were found in 12% of the younger and 4% of the older healthy women, 73% of the younger and 61 % of the older patients with untreated or residual tumours, and in 33% of the younger and 31 % of older patients with no evidence of disease, as well as in 58% of women of both age groups with benign pelvic masses. The sensitivity and specificity of CA125 levels for the detection of cancer were 73% and 74% respectively for women younger than 49 years, and 62% and 78% respectively for women 49 years or older. © 1992 Wiley‐Liss, Inc.
Isolation of exfoliated colonic epithelial cells, a novel, non‐invasive approach to the study of cellular markers
Authors: Albaugh George P. , Iyengar Vasantha , Lohani Althaf , Malayeri Mehran , Bala Shukal , Nair P. P. 
Published: February 2007

AbstractHuman stool is a heterogeneous mixture of non‐digestible food residues, bacteria, cells exfoliated from the gastrointestinal mucosa and other secretory products. We have demonstrated that fresh human stools dispersed in a buffered saline solution can be fractionated over Percoll/BSA gradients to yield 9 discrete bands of cells in the density range of p 1.033 to 1. 139 and which could be further purified over Histopaque 1077. Enzyme‐linked immunoassays (ELISA) for colon‐specific antigen (CSA) and cytokeratins (CK) were positive. Western blot analysis showed the presence of 3 cytokeratin bands in the 40‐kDa to 60‐kDa range suggestive of cytokeratins 8, 18, and 19. Fluorescence flow‐cytometric analysis of these cells using antibodies against CSA, CK, the blood‐group antigens, carcinoem‐bryonic antigen (CEA), non‐mucus‐secreting columnar‐epithelium‐specific MAb PRIA3, and to mucus‐secreting colonic‐epithelium‐specific MAb PR5D5 showed varying degrees of reactivity. Expression of the blood‐group phenotype suggests that cells from the proximal half of the colon had survived the transit, since in the adult the expression of this marker is limited to cells from the proximal region of the colon. In this report we demonstrate the feasibility of studying, non‐invasiveLy, cell‐specific markers on exfoliated cells isolated from stools. The evidence strongly suggests that almost all the cells are of colonic origin. © 1992 Wiley‐Liss, Inc.
Glucose depletion enhances the anti‐tumor effect of TNF
Authors: Volland Sabine , Amtmann Eberhard , Sauer Gerhard 
Published: February 2007

AbstractTreatment of human carcinoma xenotransplants in athymic mice with recombinant human tumor necrosis factor (rh TNF) causes necrosis mainly in the central parts of the tumors, while peripheral sections remain mitotically active. As tumors are known to be supplied with adequate glucose exclusively in their periphery, the influence of the lack of glucose on the cytotoxic activity of rh TNF was studied. The absence of glucose enhanced the killing of tumor cell lines by rh TNF in tissue culture. Meth‐A, a cell line known to be resistant to TNF in vitro but highly sensitive to it in vivo, was readily killed in tissue‐culture medium lacking glucose. All non‐transformed cell lines tested were found to be resistant to rh TNF, regardless of the presence or absence of glucose. In tumor‐bearing mice a reduction of the blood glucose content augmented by insulin led to increased anti‐tumor efficiency of rh TNF. The enhanced anti‐tumor activity was reflected both in histological sections of the tumor xenotransplants, by extensive central necroses, and by reduction of the tumor volumes. © 1992 Wiley‐Liss, Inc.
Induction of protein kinase C down‐regulation by the phorbol ester TPA in a calpain/protein kinase C complex
Authors: Savart Michel , Letard Pascale , Bultel Sandrine , Ducastaing Andre 
Published: February 2007

AbstractUsing a calpain/protein kinase C (PKC) complex, we were able to reproduce, in vitro, the induction of PKC down‐regulation by the phorbol ester 12‐O‐tetradecanoyl‐phorbol‐13‐acetate (TPA) which had been previously observed in cells. We show that TPA initiates this phenomenon by promoting a calpain‐dependent conversion of PKC to the Ca2+ phospholipid‐independent protein kinase M (PKM), at physiological calcium concentrations. This effect of TPA was dependent upon the presence of phosphatidylserine and was observed only when PKC was the substrate for the protease, inactivation of calpain by autolysis not being modified by the presence of TPA. Moreover, PKM generated from the calpain‐PKC complex was resistant to calpain, even after addition of TPA. These results suggest that TPA induces a conformational change in PKC, increasing the affinity of the kinase for calpain and consequently permitting its proteolysis for the basal level of calcium in cells. © 1992 Wiley‐Liss, Inc.
Production of stable phenotypes from 9L rat brain tumor multicellular spheroids treated with 1,3‐bis(2‐chloroethyl)‐1‐nitrosourea
Authors: Barcellos‐Hoff Mary‐Helen , Linfoot Peter A. , Marton Laurence J. , Deen Dennis F. 
Published: February 2007

AbstractDuring chemotherapy and regrowth of brain tumors, tumor‐cell heterogeneity, and possibly tumor progression, may change as a result of both the selective forces and mutagenic effects of treatment. We have isolated and characterized drug‐response variants of multicellular rat 9L brain‐tumor spheroids exposed to 1,3‐bis(2‐chloroethyl)‐1‐nitrosourea (BCNU). Ten colonies were isolated from spheroids disaggregated immediately after treatment, and 10 colonies were isolated from treated spheroids disaggregated after 1 week in suspension culture. The sensitivity to BCNU was determined by assays of sister chromatid exchange and colony‐forming efficiency in monolayer cultures of each subline after a 1‐hr exposure to graded doses of BCNU. Three classes of response were found: BCNU sensitivity increased, decreased, or was comparable to that of uncloned, parent 9L cells. Resistant phenotypes were predominant (8/10) in sublines from spheroids disaggregated immediately after treatment, whereas hypersensitive phenotypes (4/8) were isolated only from spheroids disaggregated after 1 week of re‐growth. Since subpopulations isolated immediately after treatment do not have the same biological characteristics as those isolated after a period of regrowth, these data suggest that tumor‐cell heterogeneity may be generated by distinct processes at various times during therapy. The predominance of hypersensitive sublines obtained by the regrowth protocol may have resulted from the recovery of cells that would have died if isolated but were instead able to repair the drug‐induced damage when left in contact with neighboring, possibly resistant cells. Two resistant and two hypersensitive sublines were studied further. © 1992 Wiley‐Liss, Inc.