bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of cell lines established from human hepatocellular carcinoma
Authors: Park Jae‐Gahb , Lee Jae‐Ho , Kang Myung‐Soo , Park Kyu‐Joo , Jeon You‐Me , Lee Hyun‐Ju , Kwon Hae‐Sung , Park Hyun‐Sook , Yeo Kyong‐Sook , Lee Kuhn‐Uk , Kim Soo‐Tae , Chung June‐Key , Hwang You‐Jin , Lee Hyo‐Suk , Kim Chung Yong , Lee Young Ik , Chen Tchaw‐Ren , Hay Robert J. , Song Sang‐Yong , Kim Woo‐Ho , Kim Chul‐Woo , Kim Yong‐Il 
Published: February 2007

AbstractWe characterized 8 human hepatocellular‐carcinoma cell lines established from the primary tumors of Korean patients. All lines showed substrate adherence and one line from anaplastic tumor also grew as floating aggregates. Most cultured cells maintained many morphological characteristics of the original tumors from which they were derived. Doubling times varied from 34 to 72 hr. All lines showed relatively high viability and were not contaminated with Mycoplasma or bacteria. All lines showed aneuploidy and were proven to be unique by DNA fingerprinting analysis. Hepatitis‐B‐virus (HBV) DNA was integrated in the genomes of all lines. Two of the cell lines (SNU‐354, SNU‐368) showed expression of HBV and HBVx (HBx) transcripts. SNU‐354 strongly expressed albumin, and SNU‐368 expressed transferrin and insulin‐like growth factor II. No lines produced alpha‐fetoprotein at the RNA and protein level. These cell lines represent useful tools for in vitro studies related to hepatocellular carcinoma. © 1995 Wiley‐Liss Inc.
An in vivo model of intratumoural aromatase using aromatase‐transfected MCF7 human breast cancer cells
Authors: Lee Kathryn , Macaulay Valentine M. , Nicholls Joanne E. , Detre Simone , Ashworth Alan , Dowsett Mitchell 
Published: February 2007

AbstractAbout two‐thirds of human breast carcinomas contain detectable levels of aromatase, the enzyme which converts androgens to oestrogens. Assessment of the importance of this enzyme to breast cancer growth has been hampered by the absence of an adequate model system. We have previously reported that MCF7 human hormone‐dependent breast cancer cells transfected with human aromatase cDNA (Aram I cells) showed a growth response in vitro to exogenous androgens and this effect was blocked by aromatase inhibitors. We report here our use of these cells to develop a xenograft model in athymic nude mice. Neither MCF7 cells nor Aram 1 cells formed tumours in oophorectomised (ovx) nude mice unless provided with oestradiol (E2) support. Once established, Aram 1, but not MCF7, tumours could be grown in ovx females supplemented with androstenedione (Δ4A). The mean plasma level of Δ4A was 14 nmol/L in supplemented animals and < 0.5 nmol/L in unsupplemented animals. Similarly, unsupplemented male nude mice were able to support the growth of Aram 1 tumours but not MCF7 tumours. The potent and highly specific aromatase inhibitor CGS20267 (letrozole) significantly decreased tumour growth at 2 mg/kg/day and completely inhibited growth at 20 mg/kg/day in Δ4A‐supplemented but not E2‐supplemented animals. Our results indicate that Δ4A‐dependent growth of Arom 1 tumours in vivo is mediated through the action of intratumoural aromatase. This model should allow an assessment of the critical levels of aromatase required for tumour growth support. © 1995 Wiley‐Liss Inc.
Increased experimental pulmonary metastasis in pregnant mice
Authors: Tanaka Hajime , Tanigaki Yumiko , Saeki Yoshiko , Ishibashi Hiroko , Matsuhisa Tadao , Mori Yoichi , Ogawa Mutsuko , Akedo Hitoshi 
Published: February 2007

AbstractThe effect of pregnancy on experimental pulmonary metastasis was studied. Compared to the incidence of pulmonary metastasis induced by G6 cells in non‐pregnant mice, the incidence of such metastasis was found to be greatly enhanced when the cells were injected i.v. in the latter half of pregnancy. The maximum enhancement was seen on the 15th day of pregnancy. The incidence of pulmonary metastasis returned to the level observed in non‐pregnant mice when the cells were injected 4 days after parturition. Pregnancy also significantly increased the incidence of pulmonary metastasis of 2 other cell lines (3LL and Colon 26). Injection of G6 cells after hysterectomy performed on the 15th day of pregnancy resulted in decreased lung colonization, similar to that seen after parturition. Quantificative analysis of the arrest of G6 cells labeled with [1251]‐5‐iodo‐2′‐deoxyuridine in the lungs showed that the tumor‐cell clearance from the lungs during the 24–72 hr after tumor‐cell injection was much slower in pregnant than in non‐pregnant mice. The continuous administration of β‐estradiol and/or progesterone, which maintained serum levels of the hormones equivalent to those prevailing on the 15th day of pregnancy, did not affect the lung colonization of G6 cells. Tumor‐cell‐platelet aggregation was more extensive with platelets obtained from mice at the 15th day of pregnancy than with those from non‐pregnant mice. When platelets isolated from pregnant mice were injected into normal mice 5 min before G6 injection, lung metastasis was also enhanced. These findings suggest that a pregnant host is handicapped with regard to pulmonary metastasis, this being partly due to increased platelet‐aggregating activity in response to tumor cells. © 1995 Wiley‐Liss Inc.
Inflammatory carcinomas of the breast: A clinical, pathological, or a clinical and pathological definition?
Authors: Bonnier Pascal , Charpin Colette , Lejeune Christiane , Romain Sylvie , Tubiana Nicole , Beedassy Bassodeo , Martin Pierre Marie , Serment Henri , Piana Lucien 
Published: February 2007

AbstractSome controversy remains about the clinical or pathological definition of the different types of inflammatory breast cancer (IBC) and especially the diagnostic and prognostic value of dermal lymphatic involvement. Our purpose was to classify the different types of IBC for which diagnosis was confirmed intraoperatively and ascertain features allowing reliable diagnosis. We studied clinical findings, biological data, and treatment outcome in a series of 144 successive patients. Our results suggest that there are 2 biologically different entities i.e., true IBC and pseudo‐IBC. True IBC, whose course is currently fatal in all cases, can be divided into 2 sub‐categories i.e., common true IBC (75.7% of cases), in which inflammatory signs occur primarily or secondarily, and occult true IBC (13.2% of cases). Dermal emboli have been observed in 61% of common true IBC, but their absence did not alter the rapidly unfavourable outcome. Extensive lymph‐node involvement, other biological features and survival were the same in the 2 sub‐categories. Pseudo‐IBC (11.1% of cases) can easily be confused with common true IBC. The biological characteristics of pseudo‐IBC differ from those of true IBC: no dermal lymphatic involvement and little or no lymph‐node involvement. Despite large tumour size, outcome was particularly favourable. It is of great importance to differentiate true and pseudo‐IBC, for which the treatments are different. Confirmation of true IBC requires pathological demonstration of dermal lymphatic emboli or extensive lymph‐node involvement. Occult IBC must be identified for patients presenting rapidly growing tumours. © 1995 Wiley‐Liss, Inc.
Overall and site‐specific risk of malignant melanoma associated with nevus counts at different body sites: A multicenter case‐control study of the german central malignant‐melanoma registry
Authors: Rieger Edgar , Soyer H. Peter , Garbe Claus , Büttner Petra , Kofler Regina , Weiss Jürgen , Stocker Ulrich , Krüger Sabine , Roser Marianne , Weckbecker Jörg , Panizzon Renato , Bahmer Friedrich , Tilgen Wolfgang , Kerl Helmut , Orfanos Constantin E. 
Published: February 2007

AbstractA large number of benign melanocytic nevi is the major risk factor for malignant melanoma (MM). In a multicenter case‐control study, the number of common (CN) and clinically atypical (AN) nevi were counted separately at individual sites in 278 melanoma patients and 278 age‐and gender‐matched non‐melanoma controls. Relative risk (RR) adjusted for age and sex was calculated. In men as well as women, the number of CN on the legs was the best predictor of overall melanoma risk. In men, RR for developing MM when ≥1 AN were present on the trunk was 4‐fold (vs. none). In women, presence of AN on the arms increased RR 9.5‐fold. For men and women combined, after adjusting for age and gender, the RR for developing MM on the trunk and on the legs was best predicted by counts of CN at the respective body region. However, high counts of CN on the arms were associated with high melanoma risk on the legs (somewhat lower on the trunk). For AN, no site‐specificity of melanoma risk was found. Our data suggest that nevus counts of the legs are the best predictor of overall melanoma risk if total body nevus counts are not feasible. Although high counts of CN on the trunk and legs are associated with a higher risk of developing MM at the respective site than at another site, our data do not unequivocally support a direct site‐specific melanoma risk. © 1995 Wiley‐Liss, Inc.
Insulin resistance, insulin‐like growth factor I and breast cancer: A hypothesis
Authors: Kazer Ralph R. 
Published: February 2007

AbstractConsideration of existing data regarding clinical and biochemical risk factors for the development of breast cancer leads to the hypothesis that enhanced insulin‐like growth factor 1 (IGF‐1) activity plays a significant role in the development of this disease. Abnormal IGF‐1 activity may be related to events occurring prenatally, during puberty, or during adult life. Insulin resistance, a common feature in populations characterized by high caloric intake, may result in the amplification of IGF‐1 action at the tissue level by altering serum concentrations of IGF‐1 binding proteins. Several approaches toward testing the hypothesis are proposed, and potential opportunities for clinical application are described. © 1995 Wiley‐Liss, Inc.
Expression and in‐situ localization of genes coding for extracellular matrix proteins and extracellular matrix degrading proteases in pancreatic cancer
Authors: Gress T. M. , Müller‐Pillasch F. , Lerch M. M. , Friess H. , Büchler M. , Adler G. 
Published: February 2007

AbstractPancreatic cancer shows a strong desmoplastic reaction characterized by a remarkable proliferation of interstitial connective tissue (collagens type I and III, fibronectin). In this study we have analyzed the balance of expression of mRNAs encoding extracellular matrix components (collagens I, III and IV, laminin, fibronectin), extracellular matrix‐degrading metalloproteinases (MMP‐1,‐2,‐3 and‐9) and tissue inhibitors of metalloproteinases (TIMP‐1 and‐2) in pancreatic cancer and control pancreatic tissue by Northern‐blot analysis and mRNA in situ hybridization. Transcripts for MMP‐1 (interstitial collagenase) and MMP‐3 (stromelysin‐1) were not detectable in pancreatic cancer and control tissues. Steady‐state levels of transcripts encoding extracellular matrix proteins, MMP‐2 (72‐kDa collagenase IV), MMP‐9 (92‐kDa collagenase type IV), TIMP‐1 and TIMP‐2 were elevated in the majority of pancreatic‐cancer tissue samples as compared to control pancreatic tissue. A good correlation was seen between overexpression of these MMPs and TIMPs and the steady‐state levels of transcripts coding for extracellular matrix proteins, the amount of collagen protein and the severity of the desmoplastic reaction. In situ hybridization studies localized transcripts coding for collagens type I and III to spindle‐shaped stromal cells, whereas transcripts for MMP‐2, MMP‐9, TIMP‐1 and TIMP‐2 were found in both stromal and tumor cells. However, MMP‐2 transcripts appeared to be more abundant in stromal cells, TIMP‐1 and TIMP‐2 transcripts were evenly distributed over tumor and stromal cells and relatively more MMP‐9 transcripts were found in tumor cells. We conclude that, in human pancreatic cancer, MMP‐2, MMP‐9, TIMP‐1 and TIMP‐2 may be involved in processes leading to the strong desmoplastic reaction observed in these tumors. Both stromal and tumor cells appear to be the source of MMPs and TIMPs in human pancreatic cancer. © 1995 Wiley‐Liss, Inc.
Apoptosis in human lymphoblastoid cells induced by acivicin, a specific γ glutamyltransferase inhibitor
Authors: Graber Riccardo , Losa Gabriele A. 
Published: February 2007

AbstractWe examined the effects of acivicin, a specific inhibitor of the ectoenzyme γ‐glutamyltransferase (γ‐GT), on γGT activity and apoptosis in 2 human T‐lymphoblastoid CEM cell lines, CCRF and VBL‐100. In both cell lines, acivicin was found to cause morphological and biochemical changes of apoptosis in a dose‐ dependent manner. There was a close correlation between inhibition of γ‐GT activity and the emergence of apoptotic cells. However, VBL‐100 cells had a 50% higher γ‐GT basal activity than CCRF‐CEM cells, their enzyme activity was more inhibited, and, they had a greater apoptotic response to acivicin. The γ‐GT‐specific activity in apoptotic/dead cells was also almost totally inhibited, while that of cells that remained alive after 5 days of acivicin treatment was not. These findings confirm that γ‐GT is implicated in the process of apoptosis of CEM cells. © 1995 Wiley‐Liss, Inc.
Patterns of splice variant CD44 expression by normal human urothelium in situ and in vitro and by bladder‐carcinoma cell lines
Authors: Southgate Jennifer , Trejdosiewicz Ludwik K. , Smith Barbara , Selby Peter J. 
Published: February 2007

AbstractCD44 core and splice variant exon expression was investigated in the stratified transitional epithelium of the urinary tract and in normal and malignant bladder epithelial cell lines in vitro. Antibodies against core CD44 epitopes and splice exon variants v3, v4/5, v5 and v6 showed an intense reaction in the basal and lower intermediate urothelial cell layers, which was consistently lost from the upper intermediate and superficial cell layers. Seven independent cell lines established from normal human urothelium expressed complex multiple‐spliced CD44 mRNA transcripts when tested by RT‐PCR and were positive with antibodies against CD44 core epitopes and splice variants v3, v4/5, v5 and v6. Of the 13 bladder‐carcinoma cell lines, all were positive for CO44 core. The more differentiated cell lines had retained some splice‐variant antibody reactivity and showed multiple but less complex CD44 mRNA transcript patterns, compared with normal cells. Anaplastic cell lines did not react with variant antibodies and did not contain multiple‐spliced CD44 transcripts. These data suggest that loss of alternatively‐spliced CD44 may reflect a selection pressure in the evolution of anaplastic bladder cancers. © 1995 Wiley‐Liss, Inc.
Tumor‐reactive superantigens suppress tumor growth in humanized scid mice
Authors: Lando Peter A. , Dohlsten Mikael , Ohlsson Lennart , Kalland Terje 
Published: February 2007

AbstractSuperantigens are extremely potent activators of T lymphocytes. To develop a tumor‐reactive superantigen for cancer therapy, we made a recombinant fusion protein of the superantigen staphylococcal enterotoxin A (SEA) and the Fab region of the C242 monoclonal antibody (C242Fab‐SEA), which recognize human colon carcinoma cells. The therapeutic effect of C242Fab‐SEA on colon‐cancer growth was examined in lymphocyte‐engrafted humanized SCID mice bearing intraperitoneally growing Colo205 colon carcinomas. I.V. injections of C242Fab‐SEA significantly inhibited tumor growth. The anti‐tumor effect required the presence of human T cells in the SCID mice. Optimal therapeutic effects were seen with C242Fab‐SEA, but not with C242Fab fragment or SEA alone, demonstrating that both entities of the fusion protein were required. C242Fab‐SEA‐treated tumors showed a massive infiltration of T cells in the tumor parenchyme, and was accompanied by enhanced expression of ICAM‐I and HLA‐DR on the tumor cells. The results demonstrate that Fab‐SEA fusion proteins convey superantigenicity on tumor cells which evoke T‐cell‐dependent suppression of tumor growth. © 1995 Wiley‐Liss, Inc.
The pure antiestrogen ICI 182,780 binds to a high‐affinity site distinct from the estrogen receptor
Authors: Parisot John P. , Hu Xiu F. , Sutherland Robert L. , Wakeling Alan , Zalcberg John R. , Deluise Mario 
Published: February 2007

AbstractBoth estrogen receptor‐positive (ER+), tamoxifen‐sensitive (5–21) and tamoxifen‐resistant (5–23) subclones of the parental MCF‐7 breast cancer cell line were used in competitive ligand binding studies involving either [3H]ICI 182,780 or 4‐OH‐[3H]tamoxifen (4OHT) displacement by unlabelled estradiol (E2) or the antiestrogens (AE) 4OHT and ICI 182,780. Neither radioligand was displaced significantly by E2 over a range of concentrations; binding was predominantly inhibited by the corresponding radio‐inert ligand. Scatchard analysis of the data revealed that the binding capacities of both cell lines for ICI 182,780 were approximately 7‐fold greater than the previously determined number of ER sites per cell, with the affinity being an order of magnitude less than that of E2 for ER. No difference was found between the TAM‐sensitive and ‐resistant cells in their binding of either AE. When cells were preincubated with either E2, TAM or 4OHT at a high, fixed concentration to block the ER or AE binding sites (AEBS), respectively, displaceable binding of [3H]ICI 182,780 was still observed, indicating binding at a site other than the classical ER or previously described AEBS. Our results suggest that there is a specific, saturable and relatively high‐affinity binding site for ICI 182,780 in MCF 5–21 and MCF 5–23 breast cancer cells. However, the physiological relevance of this binding site requires further clarification because in cell growth assays, E2 (at the dose of ICI 182,780) overcame the inhibitory effect of the antiestrogen in both of the cell lines. © 1995 Wiley‐Liss, Inc.
Pro‐transforming growth factor‐alpha processing in human colon carcinoma cells: Role of protein kinase C
Authors: Ramesh Gadiraju , Levine Alan E. 
Published: February 2007

AbstractThe human colon cancer cell lines HCT 116 (poorly differentiated) and CEO (well differentiated) express the mitogenic peptide transforming growth factor alpha (TGF‐α). The secretion of TGF‐α was enhanced by phorbol 12‐myristate 13‐acetate (PMA), indicating the possible role of protein kinase C (PKC) in the formation of mature TGF‐α. Cells were metabolically labeled with 3SS‐cysteine and the formation of the mature 6 kDa TGF‐α polypeptide from the 17 kDa pro‐TGF‐α precursor was determined. The conversion of pro‐TGF‐α was complete in 2–4 hr with the HCT 116 cells showing faster kinetics of TGF‐α formation than GEO cells. HCT 116 cells secreted more TGF‐α than GEO cells and the rate and extent of formation of TGF‐α was enhanced by PMA in both cell lines. The expression of several PKC isozymes by HCT 116 and GEO cells was examined by immunoblotting. The expression of all isozymes examined was higher in HCT 116 cells compared with GEO cells. Calphostin C, an inhibitor of PKC, reduced the enzyme activity and significantly inhibited the PMA‐induced secretion of TGF‐α by both cell lines. Two agonists of PKC that act on specific PKC isozymes, thymeleatoxin and 12‐deoxyphorbol 13‐phenylac‐etate 20‐acetate (dPPA), stimulated the release of TGF‐α into the medium to the same extent as PMA. Since dPPA has been reported to stimulate PKC‐4bT1 specifically, our results suggest a potential role for PKC‐β in the processing of pro‐TGF‐α by these 2 human colon carcinoma cell lines. © 1995 Wiley‐Liss, Inc.
Low‐dose IL‐2 treatment: Activation of discrete T‐ and NK‐cell sub‐populations in vivo
Authors: Farace Franchise , Angevin Eric , Dietrich Pierre‐Yves , Leboullaire Christophe , Vanderplancke Josy , Escudier Bernard , Triebel Frédéric 
Published: February 2007

AbstractThe activation of T‐ and NK‐cell sub‐populations in vivo was evaluated in a phase‐l study (18 patients) with a 3‐month course of low‐dose s.c. IL‐2, 1,3 and 6±10* IU/day once daily, 6 days a week. At the higher doses, we observed early on (day 15) an increase in CD3+ CD56−, CD3− CD56+ and CD56+ DR+ cell counts, as well as an increase in circulating slL‐2R and non‐MHC‐restricted cytotoxicity against K562 and Daudi cells. In contrast, at the lowest dose, T‐ and NK‐cell counts were not appreciably altered, while a substantial increase in NK cytotoxic activity was still observed. In addition, thyroid dysfunction resembling that described in auto‐immune thyroiditis, was documented in 6 out of the 14 patients studied. Using a high‐resolution method analyzing CDR3 sizes of TCRp transcripts, we observed the appearance of dominant T‐cell clonotypes in I patient out of 2 analyzed, corresponding to the clonal expansion of T cells primed in vivo. Overall, these results show that long courses of low‐dose s.c. IL‐2 treatment lead to the activation of discrete T‐and NK‐cell sub‐populations. © 1995 Wiley‐Liss, Inc.
Plasma endothelin‐1 As a marker for doxorubicin cardiotoxicity
Authors: Yamashita Jun‐Ichi , Ogawa Michio , Shirakusa Takayuki 
Published: February 2007

AbstractThe use of doxorubicin is often limited by cardiotoxicity that can lead to congestive heart failure (CHF). Although various techniques have been used to predict its cardiotoxicity, none has proven useful. We reported 2 patients in whom the level of plasma endothelin (ET)‐ I rose progressively during doxorubicin treatment of breast cancer, and who subsequently developed CHF. Accordingly, we conducted a prospective study of 30 consecutive patients, 23 with breast cancer and 7 with small‐cell lung cancer, who were treated with doxorubicin. Serial changes in plasma ET‐I during doxorubicin treatment were measured by a specific radioimmunoassay, and plasma levels of atrial natriuretic peptide (ANP) were determined by a sensitive immunoradiometric assay. M‐mode echocardiography was performed serially to monitor the fractional shortening (FS) and the left ventricular ejection fraction (LVEF). The plasma concentrations of ET‐I rose progressively in 5 of the 30 patients during doxorubicin treatment. Two of the 5 patients developed clinically overt CHF after developing cumulative doses of doxorubicin of 500 and 480 mg/m2. Serial measurement of plasma levels of ANP, FS and LVEF showed no abnormalities until the development of CHF. Another 25 patients who had received doxorubicin (cumulative doses ranging from 400 to 660 mg/m2) and had not developed CHF showed no appreciable change in plasma ET‐I or other, markers. This prospective study suggests that plasma ET‐I may be useful for predicting the risk of doxorubicin‐induced cardiotoxicity. © 1995 Wiley‐Liss, Inc.