bluuebunny/crossref_metadata_2025_split huggingface dataset:
Androgen receptors in endocrine‐therapy‐resistant human prostate cancer
Authors: van der Kwast Theodorus H. , Schalken Jack , de Winter Jacobus A. Ruizeveld , van Vroonhoven J. Cor C. , Mulder Eppo , Boersma Wim , Trapman Jan 
Published: February 2007

AbstractDespite the initial androgen‐dependent growth of most human prostate cancers, eventually all prostate cancers become androgen‐independent at varying intervals after androgen ablation or anti‐androgen therapy. In order to gain more insight into the role of the androgen receptor (AR) in this process, AR and prostate‐specific antigen (PA) expression was evaluated immunohistochemically in prostatic tumour tissues from patients who developed urinary flow obstruction between 4 and 107 months after onset of treatment. AR expression was evaluated with a monoclonal antibody (MAb) specific for the N‐ terminal domain of the human AR. To substantiate the progressive tumour growth, proliferative activity was assessed immunohistochemically by staining with MAb Ki‐67. Ki‐67‐defined tumour‐growth fractions varied from 0.8–64.7%. In 13 of the 17 examined tumours over 80% of the tumour cells were AR‐positive, 3 tumours showed a considerable heterogeneity in AR expression and in I tumour almost all tumour cells seemed to be AR‐negative. Two‐thirds of the examined tumours contained variable proportions of PA‐positive tumour areas. These observations contrast with the view that androgen ablation induces a preferential outgrowth of receptor‐negative tumour cells.
Prognostic significance of argyrophilic nucleolar organizer staining in soft‐tissue sarcomas
Authors: Kuratsu S. , Aozasa K. , Myoui A. , Tsujimoto M. , Ueda T. , Uchida A. , Hamada H. , Ono K. , Matsumoto K. 
Published: February 2007

AbstractThe utility of argyrophilic stain for nucleolar organizer region (AgNOR) for estimating proliferative activity and prognosis of soft‐tissue sarcomas (STS) was examined. Formalin‐fixed and paraffin‐embedded sections of 38 cases with STS were used; the reaction product of AgNOR stain was observed as dots mainly in the nucleoli. The mean number of AgNOR dots per nucleus of tumor cells was calculated in 200 cells (AgNOR count). The AgNOR count, ranging from 1.4 to 16.1 (mean, 7.5), showed a good correlation with cellularity (r = 0.483, p < 0.003) and histologic grade (r = 0.626, p < 0.00005), but less shown with mitotic counts (r = 0.350, p < 0.04). The prognosis of cases with AgNOR low‐count group (5‐year survival rate was 74.6%) was much better than those in high count group (33.3%) (p < 0.0005). The AgNOR count correlated well with reactivity of tumor cells for Ki‐67 staining, which was available only in freshly prepared sections. These findings suggested that the AgNOR staining is a simple and useful method for estimating tumor‐cell proliferation and prognosis of patients with STS.
Transglutaminase activity and Nϵ(γ‐glutamyl) lysine isopeptide levels during cell growth: An enzymic and immunological study
Authors: Alaoui Said El , Legastelois Stéphane , Roch Anne‐Marie , Chantepie Jacqueline , Quash Gérard 
Published: February 2007

AbstractA monoclonal antibody (MAb) 81D1c2, which recognizes the Nϵ(γ‐glutamyl) lysine isopeptide produced by the action of transglutaminase activity was prepared. Its reactivity towards the homologous isopeptide was about 3‐fold greater than that with either Nα (α glutamyl) lysine (a naturally occuring heterologous dipeptide) or Nϵ(γ glutamyl) lysine, another heterologous peptide not described so far in naturally occuring proteins. When used in an immunohistochemical study on cells in culture derived from human carcinoma of the larynx (HEp2) and from chicken embryo cells (CEC), both fixed in acetone, this MAb detected Nϵ(γ glutamyl) lysine residues In the nucleus. The amount of Nϵ(γ glutamyl) lysine isopeptides follows closely transglutaminase activity during the lag phase of growth of both CEC and HEp2 cells. However, during exponential growth, the 2 parameters decrease concomitantly in HEp2 cells, whereas in CEC, transglutaminase activity increases but isopeptide bond levels drop. Compared with other reported methods for measuring isopeptides, this immunohistological approach permits the localization and at least the semi‐quantitative determination of Nϵ(γ glutamyl) lysine in cells in situ.
V‐ABL does not abolish IL‐6 requirement by murine plasmacytoma cells
Authors: Sugiyama Hiroyuki , Wiener Francis , Babonits Magda , Silva Santiago , Hirano Toshio , Kishimoto Tadamitsu , Klein George 
Published: February 2007

AbstractActivation of c‐myc by juxtaposition to an immunoglobulin locus and introduction of the v‐ab/ oncogene act synergistically in generating a mouse plasmacytoma (PC). The question arose whether the effect of v‐ab/ could be attributed to a deregulation of interleukin‐6 (IL‐6) production or responsiveness, in view of the fact that IL‐6 exerts potent growth‐stimulatory activity on PC cells. We studied the effect of IL‐6 on the in vitro growth of primary PCs induced by pristane alone (TEPCs) or by pristane + A‐MuLV (ABPCs). Five of 13 TEPCs and 3 of 7 ABPCs responded to IL‐6. Macrophage supernatants prepared from both TEPCs and ABPCs had similar stimulatory effects on PC cells. From 30 primary PCs (including both TEPCs and ABPCs), we established 9 in vitro lines, 2 of which expressed v‐abJ. All were able to grow on macrophage feeder layers. Three types of behavior could be distinguished on the basis of growth in feeder‐free cultures in the presence and absence of IL‐6. Group I contained 4 IL‐6‐dependent lines. Group II contained 2 IL‐6‐independent lines (one v‐abl expressor) that grew faster In the presence of IL‐6. Group III consisted of 3 feeder‐dependent lines (one v‐ab/ expressor) that were not significantly stimulated by IL‐6. These findings indicate that v‐ab/ expression does not Influence IL‐6 dependence or responsiveness by itself. The supernatant of one line in group II was able to stimulate PC cells. All 6 lines of Groups I and II carried a typical (12; 15) translation, while all 3 lines in group III had a variant (6;15) or (15;16) translocation.
Retinoic acid suppression of squamous differentiation in human head‐and‐neck squamous carcinoma cells
Authors: Poddar Susmita , Hong Waun K. , Thacher Scott M. , Lotan Reuben 
Published: February 2007

AbstractRetinoids (vitamin A analogues) inhibit the squamous differentiation of normal and malignant epithelial cells. This Study investigated the ability of the head‐and‐neck squamous‐cell carcinoma (HNSCC) cell line 1483 to undergo squamous differentiation in the absence and presence of β‐all‐trans retinoic acid (RA). The growth of these cells in culture is accompanied by an increase in keratinocyte trans‐glutaminase, involucrin and keratin KI, 3 established markers of squamous cell differentiation. Higher levels of these differentiation markers were detected in cells cultured in delipidized serum (DLS), from which endogenous retinoids have been extracted, than in cells cultured in fetal bovine serum (FBS), which contains retinoids. Treatment with I μM RA decreased the levels of the various differentiation markers in cells cultured in either FBS or DLS as revealed by labelling of permeabilized cells and by immunoblotting of cell extracts using specific monoclonal or polyclonal antibodies. The cells' ability to cross‐link proteins to form envelopes under the plasma membrane was stimulated in the presence of calcium ionophore but Inhibited by RA. These results indicate that the malignant 1483 HNSCC cells recapitulate the main characteristics of normal squamous‐cell differentiation in culture and that RA suppresses this differentiation as it does in normal keratinizing epithelial cells.
Comparative cytotoxicity of CI‐973, cisplatin, carboplatin and tetraplatin in human ovarian carcinoma cell lines
Authors: Perez R. P. , O'Dwyer P. J. , Handel L. M. , Ozols R. F. , Hamilton T. C. 
Published: February 2007

AbstractThe clinical efficacy of cisplatin‐based chemotherapy for ovarian cancer is frequently compromised by drug resistance or dose‐limiting renal and neurologic toxicities. CI‐973 (NK‐121), a 2‐methyl‐1, 4‐butanediamine analogue of carboplatin, has shown little nephro‐and neuro‐toxicity in pre‐clinical model systems and in phase‐I trials. Its in vitro spectrum of activity against ovarian cancer cell lines has not been previously characterized. The in vitro activities of CI‐973, cisplatin, carboplatin and tetraplatin were compared in several platinum‐sensitive and‐resistant human ovarian carcinoma cell lines. Cytotoxicity was assessed by inhibition of clonogenic survival in soft agar with continuous drug exposure. On a molar basis, cisplatin and tetraplatin were the most potent analogues, while carboplatin was consistently less potent. Cisplatin, carboplatin and CI‐973 elicited a very similar response pattern by Spearman rank correlation, distinct from that seen with tetraplatin. The magnitude of resistance to CI‐973 was comparable to cisplatin in 5 cell lines but was substantially lower in the highly cisplatin‐resistant 2780‐CP70 and OVCAR‐10 cell lines. These results suggest that CI‐973 and teatraplatin may have potential utility in some cases of cisplatin‐resistant ovarian cancer. In addition, our data are consistent with the existence of at least 2 platinum‐resistance phenotypes—one with moderate levels of resistance to cisplatin, carboplatin and CI‐973 but highly resistant to tetraplatin, the other highly resistant to cisplatin and carboplatin but only partially cross‐resistant with tetraplatin and CI‐973. The recognition of different resistance phenotypes may facilitate the study of cellular resistance mechanisms to cisplatin and newer platinum analogues.
Immunological and non‐immunological influence of H‐2Kb gene transfection on the metastatic ability of B16 melanoma cells
Authors: De Giovanni C. , Palmieri G. , Nicoletti G. , Landuzzi L. , Scotlandi K. , Bontadini A. , Tazzari P.‐L. , Sensi M. , Santoni A. , Nanni P. , Lollini P.‐L. 
Published: February 2007

AbstractThe H‐2b‐negative B78HI clone (derived from B16 melanoma) was transfected with the H‐2Kb gene; 4 cell clones expressing membrane H‐2Kb antigens and 2 control clones (transfected with pSV2neo alone) were used for studies of metastatic ability, immunogenicity, NK sensitivity and homo‐typic adhesion. The experimental metastatic capacity of H‐2Kb transfectants In syngeneic mice was greatly diminished in comparison with control and parent cells. Both immune‐mediated and Intrinsic properties of transfectants correlated with their lower metastatic ability. A cell‐mediated cytotoxic response was induced by repeated in vivo immunizations of syngeneic mice followed by in vitro restimulation of effectors when transfectants (but not controls) were used as immunizers and as targets. Moreover, homotypic adhesion of H‐2Kbtransfectants was significantly lower than that of controls. Sensitivity to NK ceils of transfectants was not decreased in comparison to H‐2‐negative controls. It is known that In vitro treatment with IFN‐γ of H‐2‐positive B16 melanoma cells induces a simultaneous increase in H‐2 expression and in experimental metastasis; treatment of H‐2Kb transfectants with IFN‐γ induced a higher Kb expression, but no increase in metastatic ability, thus suggesting that the IFN‐sensitive component that mediates enhancement of metastasis is not H‐2Kb.
Use of combination of monoclonal antibodies directed against three distinct epitopes of a tumor‐associated antigen: Analysis of cell binding and internalization
Authors: Casalini Patrizia , Mezzanzanica Delia , Canevari Silvana , Della Torre Gabriella , Miorn Silvia , Colnaghi Maria Ines , Matzku Siegfried 
Published: February 2007

AbstractThree monoclonal antibodies (MAbs), MOv17, MOv 18 and MOv19 with tumor‐restricted specificity for human ovarian carcinoma, were tested alone or in double combination with the aim of analyzing their binding and internalization behavior on different In vitro cell lines. Biochemical studies indicated that the 3 MAbs were directed against 3 epitopes of the same 38 kDa surface molecule. By immuno‐electron‐microscopy they exhibited a different internalization behavior since MOv17 Induced evident endocytosis through coated vesicles, whereas MOv18 gave rise to occasional uncoated vesicles and MOv19 was completely unable to promote internalization of the relevant molecule. When tested 2 by 2 there was a binding synergy in one of the 9 possible combinations (125I‐labelled MOv18 and unlabelled MOv19), but no change in the internalization behavior. The binding synergy, which was highly reproducible, was temperature‐dependent and was also evident on glutaraldehyde‐fixed cells. A metabolism involvement is therefore unlikely. This could be attributed to an easier accessibility of the CaMOv18 due to a conformational change of the molecule after MOv19 MAb binding.
Liver cancer in Thailand. I. A case‐control study of cholangiocarcinoma
Authors: Parkin D. Maxwell , Srivatanakul Petcharin , Khlat Myriam , Chenvidhya Dhiraphol , Chotiwan Pornarong , Insiripong Somchai , L'abbé Kristan A. , Wild Christopher P. 
Published: February 2007

AbstractPotential risk factors for cholangiocarcinoma were investigated in a case‐control study among inhabitants of north‐east Thailand, which included 103 cases from 3 hospitals, with age‐and sex‐matched controls. A clear association with past or present infection with Opisthorchis viverrini, as indicated by raised serum antibodies, was found (o.r. 5.0), and at least two‐thirds of cases can be attributed to this cause. The results suggest that males may be at higher risk than females. There was no association with hepatitis B infection, with aflatoxin Intake as estimated from albumin adducts in serum or with any particular dietary patterns. Alcohol consumption was very low in the population, and the risk associated with regular drinking was non‐significant. Regular users of betel nut—predominantly female—had a high risk (o.r. 6.4), a possible mechanism being through their increased exposure to nitro‐samines.
Liver cancer in Thailand. II. A case‐control study of hepatocellular carcinoma
Authors: Srivatanakul Petcharin , Parkin D. Maxwell , Khlat Myriam , Chenvidhya Dhirapol , Chotiwan Pornarong , Insiripong Somchai , L'Abbé Kristan A. , Wild Christopher P. 
Published: February 2007

AbstractPotential risk factors for hepatocellular carcinoma were investigated in a case‐control study among inhabitants of north east Thailand. Sixty‐five cases from 3 hospitals, with matched controls, were included. Infection with hepatitis‐B virus was the major risk factor—chronic carriers of HB surface antigen had an estimated relative risk of 15.2. Infection with hepatltis‐C virus appeared to be rare. No increase In risk was found with recent aflatoxin intake, as estimated by consumption of possibly contaminated foods, or by measuring aflatoxin‐albumln adducts in serum. Regular use of alcohol (2 or more glasses of spirits per week) was associated with a nonsignificant elevation in risk (o.r. = 3.4, 95% c.i. 0.8–14.6), but the number of regular drinkers in the population was small. The meaning of an apparent protection conferred by certain food items is uncertain, but a possible role of betel nut in the aetiology deserves further investigation.
Prevalence of antibody against the core protein of hepatitis C virus in patients with hepatocellular carcinoma
Authors: Watanabe Yushiro , Harada Shizuko , Saito Izumu , Miyamura Tatsuo 
Published: February 2007

AbstractWe have cloned the whole structural region of the hepatitis C virus (HCV) genome and transiently expressed the nucleocapsid protein in animal cells. Since the nucleotide sequences of this region of the HCV genome has been shown to be highly conserved among different HCV isolates, the assay detecting the antibody to this expressed protein is useful for studying the pathogenicity of HCV. in this work, we investigated the presence of antibodies to HCV nucleocapsid protein (p22) in patients with hepatocellular carcinoma (HCC) and compared it* frequency with that of antibody to HCV non‐structural protein (C‐100), which is presently applied for blood screening for transfusion and diagnosis for chronic hepatitis C. By a sensitive Western blot analysis, 85 of 102 (83.3%) sera of hepatitis B virus surface antigen (HBsAg)‐negative HCC patients were positive for the antibody to p22 (anti‐p22), whereas 68 of the same 102 cases (66.7%) were positive for the anti‐C100 by ELISA. The prevalence of anti‐p22 in 23 HBV carrier HCC patients, 56 patients with non‐HCC cancer and 100 healthy blood donors were 4.3, 12.5 and 1.0%, respectively. Thus, high prevalence of anti‐p22 in non‐B HCC confirmed that HCV infection is closely related to the development of HCC. Furthermore, the anti‐p22 assay can detect HCV‐infected patients who could not previously be identified as such by the present anti‐C100 assay.
Vegetable and fruit consumption and cancer risk
Authors: Negri Eva , La Vecchia Carlo , Franceschi Silvia , D'Avanzo Barbara , Parazzini Fabio 
Published: February 2007

AbstractThe relationship between cancer risk and frequency of consumption of green vegetables and fruit has been analyzed using data from an integrated series of case‐control studies conducted in northern Italy between 1983 and 1990. The overall dataset included the following histologically confirmed cancers: oral cavity and pharynx, 119; oesophagus, 294; stomach, 564; colon, 673; rectum, 406; liver, 258; gall‐bladder, 41; pancreas, 303; larynx, 149; breast, 2,860; endometrium, 567; ovary, 742; prostate, 107; bladder, 365; kidney, 147; thyroid, 120; Hodgkin's disease, 72; non‐Hodgkin lymphomas, 173; myelomas, 117; and a total of 6,147 controls admitted to hospital for acute non‐neoplastic conditions, unrelated to long‐term dietary modifications. Multivariate relative risks (RR) for subsequent tertiles of vegetable and fruit consumption were derived after allowance for age, sex, area of residence, education and smoking. For vegetables, there was a consistent pattern of protection for all epithelial cancers, with RRs in the upper tertile ranging from 0.2 for oesophagus, liver and larynx to 0.7 for breast. All the trends in risk were in the same direction and significant for all carcinomas except gallbladder. In contrast, no protection was afforded by high vegetable consumption against non‐epithelial lymphoid neoplasms. With reference to fruit, strong Inverse relationships were observed for cancers of the upper digestive and respiratory tract, with RRs in the upper tertile between 0.2 and 0.3 for oral cavity and pharynx, oesophagus and larynx relative to the lowest tertile. The lower the location of the tumour in the digestive tract, the weaker appeared to be the protection afforded. Significant inverse relationships were observed for liver, pancreas, prostate and urinary sites, but not for rectum, breast and female genital cancers or thyroid. No relationship emerged for lymphomas and myelomas. Even in the absence of a clear biological interpretation, the consistency and strength of the patterns observed indicate that, in this population, frequent green vegetable intake is associated with a substantial reduction of risk for several common epithelial cancers, and that fruit intake has a favourable effect, especially on upper digestive cancers and, probably, also on urinary tract neoplasms.
Nutritional factors and pancreatic cancer: A case‐control study from South‐West Poland
Authors: Zatonski W. , Przewozniak K. , Howe G. R. , Maisonneuve P. , Walker A. M. , Boyle P. 
Published: February 2007

AbstractA population‐based case‐control study of diet and pancreatic cancer has been conducted in the Opole Voivodeship region in Poland, using 110 cases and 195 controls. A full diet history was used to estimate the daily intake of calories, fat, protein, carbohydrate, cholesterol, retinol, vitamin C, and fibre. There Is a strong positive association with the intake of cholesterol with relative risks of 1.90, 3.77, and 4.31 for the 3 upper quartiles compared with the lowest (p, trend = < 0.01). An inverse association was seen with vitamin C intake, with corresponding relative risks of 1.10, 0.30, and 0.37 (p, trend = < 0.01). Weak Inverse associations were seen with the Intake of retinol and fibre. There is evidence of an inverse association with fat intake, particularly unsaturated fats, and of a positive association with the intake of carbohydrate and to a lesser extent, protein. These results further support the potential importance of dietary factors in the aetiology of cancer of the pancreas.
Proteinase‐alpha2 macroglobulin complexes are not increased in plasma of patients with cancer
Authors: Zucker Stanley , Lysik Rita M. , Zarrabi Mohamed H. , Fiore John J. , Strickland Dudley K. 
Published: February 2007

Abstractα2‐macroglobulin, a major glycoprotein component of plasma, is unique in its capacity to bind and inhibit the proteolytic activities of all classes of proteinases. Since proteinases implicated in cancer dissemination (type‐IV collagenase, plasminogen activator, cathepsins B) are normal constituents of blood, we have explored the hypothesis that elevated tissue levels of activated proteinases bound to α2M might be detected in plasma of patients with cancer. To test this premise, blood was collected from 149 subjects (33 healthy controls, 31 patients with infections and non‐malignant diseases, 16 with myeloproliferative disease, 10 with gastrointestinal cancer, 7 with genito‐urinary cancer, 16 with lung cancer, 14 with lymphoma, 11 with miscellaneous cancers and 11 with chronic lymphocytic leukemia and myeloma). Plasma was assayed for α2M‐proteinase complexes using a sandwich ELISA which employs a mouse monoclonal antibody (MAb) that binds to a neo‐antigenic determinant on complexed α2M and a rabbit polyclonal anti‐native human α2M antibody. The concentration of complexed α2M in healthy controls was 14.2 ± 9.8 μg/ml (mean ± standard deviation). No significant differences in complexed α2M were noted between normal and cancer groups (range 7.4–14.6 μg/ml). On the basis of these data, we propose that, in patients with cancer, activated proteinases are bound locally to inhibitors in the tissues and are not available to form complexes with plasma α2M. An alternative explanation is that proteinases are not secreted in excess by cancer cells in vivo.