bluuebunny/crossref_metadata_2025_split huggingface dataset:
Human T‐cell‐leukemia virus type I in post‐transfusional spastic paraparesis: Complete proviral sequence from uncultured blood cells
Authors: Bazarbachi Ali , Huang Menger , Gessain Antoine , Saal Fortuna , Saib Ali , Peries Jorge , De The Hugues , Galibert Francis 
Published: February 2007

AbstractHhdman‐T‐cell‐leukemia virus type I (HTLV‐I) is the causative agent of adult T‐cell leukemia/lymphomhd (ATL) and tropical spastic paraparesis/HTLV‐I‐associated myelopathy (TSP/HAM). The different disease outcome may be attributable to subtle mutations leading to modification of viral tropism or infectivity. Initial attempts found a very high level of sequence conservation among all HTLV‐I strains. However, only one complete proviral DNA sequence is reported from a TSP/HAM patient, with a provirus derived from immortalized lymphocytes, which might be expected to be a leukemogenic variant rather than a neutrotropic one. We cloned and sequenced a complete HTLV‐I provirus (HTLV‐Iboi) derived from the uncultured lymphocytes of a sub‐acute post‐transfusional TSP/HAM patient with clonal integration of HTLV‐I. HTLV‐Iboi proviral genome is 9033 bp long, and its overall genetic organization is similar to that of the prototype HTLV‐I(ATK), without major deletions or insertions. No premature termination codon was found in the 4 open reading frames of the pX region. Divergence at the nucleotide level of HTLV‐lBoi from the reported full‐length HTLV‐I varies from 1 to 9.4%, and indicates that it corresponds to a cosmopolitan genotype. This study did not identify specific sequences associated with neurotropic strains.
Trisomy 20 is a primary chromosome aberration in desmoid tumors
Authors: Mertens Fredrik , Willén Helena , Rydholm Anders , Brosjö Otte , Carlén Birgitta , Mitelman Felix , Mandahl Nils 
Published: February 2007

AbstractChdtogenetic analysis revealed trisomy 20 in 4 desmoid tumors: in 2 cases as the sole aberration, in hd together with +X, ‐Y and −13 and in I with +8 and a supernumerary marker chromosome. Our findings indicate that gain of chromosome 20 is an early event in the development of a large subset of desmoid tumors and that it is as frequent as +8, the only consistent chromosomal change previously reported in this tumor type. The non‐random occurrence of trisomies 8 and 20 in desmoid tumors indicates shared pathogenetic mechanisms with infantile fibrosarcoma, a fibrous tissue tumor characterized by various combinations of trisomies for chromosomes 8, 11, 17 and 20.
Implication of the αvβ3 integrin in the adhesion of the ovarian‐adenocarcinoma cell line IGROV1
Authors: Carreiras Franck , Lehmann Maxime , Sichel François , Marvaldi Jacques , Gauduchon Pascal , Le Talaer Jean‐Yves 
Published: February 2007

AbstractAccumulating evidence suggests that integrins, which participate in many complex cellular processes, are important for tumor progression and metastasis. In order to understand the role of these cell‐surface receptors and of their ligands in the biological behavior of ovarian tumor cells, we have examined the expression of integrins in the human ovarian‐adenocarcinoma cell line IGROVI. These cells expressed the αv sub‐unit and used it to attach on vitronectin (Vn). A monoclonal antibody (MAb) (69‐6‐5) specific to αv blocked the attachment of IGROVI cells on Vn and fibrinogen (Fg), but not on fibronectin (FN) and other adhesive ligands. Immunoprecipitation of surface biotinylated cells followed by Western blotting showed that the αv sub‐unit was associated with β3, but not with β1, β5 or β6. When cells were cultivated on glass coverslips or on Vn sub‐stratum in serum‐free medium, immunofluorescence staining with MAb 69‐6‐5 revealed the presence of αv at cell‐cell contacts and at focal contacts, supporting its active participation in adhesion as part of a functional heterodimer. Furthermore, immunofluorescence data showed the presence of Vn as a fibrillar network in IGROVI cells cultivated on FN‐coated slides. These results suggest that αvβ3 and its Vn ligand may play a important role in the behavior of ovarian epithelial tumors.
Bidirectional interactions between the estrogen receptor and the c‐erbB‐2 signaling pathways: Heregulin inhibits estrogenic effects in breast cancer cells
Authors: Grunt Thomas W. , Saceda Miguel , Martin Mary Beth , Lupu Ruth , Dittrich Evelyn , Krupitza Georg , Harant Hanna , Huber Heinz , Dittrich Christian 
Published: February 2007

AbstractThde responsiveness of estrogen receptor (ER)‐positive breast cancer to endocrine therapy is frequently reduced ihd cells over‐expressing c‐erbB‐2. Stimulation of ER suppresses c‐erbB‐2, indicating that estrogen controls the activity of c‐erbB‐2. Heregulin (HRG) has been described to bind to c‐erbB‐3/c‐erbB‐4 and to stimulate c‐erbB‐2. Here we describe the effects of HRG on cell growth and on ER and c‐erbB‐2 expression in breast cancer cell lines containing distinct levels of c‐erbB‐2 and ER (BT‐474: c‐erbB‐2 + + +, ER +; MDA‐MB‐361: c‐erbB‐2 + +, ER ++; MCF‐7: c‐erbB‐2 +, ER + + +). Proliferation of estrogen‐stimulated, c‐erbB‐2 and ER‐positive cells is inhibited by HRG in a dose‐dependent manner. In addition, HRG dose‐dependently inhibits ER expression. Estrogen, however, inhibits c‐erbB‐2. Estrogen‐mediated down‐regulation of c‐erbB‐2 is most pronounced in MCF‐7 but weaker in BT‐474. In the latter cells HRG efficiently blocks the estrogenic effect on c‐erbB‐2. In MCF‐7 cells, however, the inhibition of c‐erbB‐2 cannot be completely reverted by HRG. This modulation occurs in all 3 cell lines at protein, RNA and transcriptional levels, suggesting that the activity of the c‐erbB‐2 promoter, which contains an estrogen‐responsive region, is affected by HRG. The intensity of the mutual inhibition between the HRG/c‐erbB‐2 and the estrogen/ER system depends on the relative levels of ER and c‐erbB‐2 expression in the respective cell lines.
Dominant‐negative p53 can restore tumorigenicity of L‐929 cells in immunocompetent mice
Authors: Appleman Leonard J. , Frey Alan B. 
Published: February 2007

AbstractThd study the effect of a transforming allele of the tumor suppressor p53 upon the anti‐tumor immunhd response, anti‐genic L‐929 cells were transfected with the dominant‐negative valine135 mutant of murine p53. Several p53val135‐expressing transfectants formed non‐regressing tumors in immunocompetent hosts. The growth rates of tumorigenic and non‐tumorigenic clones were equivalent in vitro in sublethally irradiated C3H/HeN mice and in nude mice. Tumorigenic and non‐tumorigenic p53val 135‐expressing L‐929 clones expressed equivalent levels of cell surface class I major histocompatibility complex (MHC) glycoproteins. Immunization with a tumorigenic Lp53val135 clone protected mice from subsequent challenge and primed MHC class I‐restricted cytotoxic T‐lymphocytic precursors. Secretion of an immunosuppressive cytokine, transforming growth factor β‐1 and sensitivity to tumor necrosis factor‐α were equivalent from tumorigenic and non‐tumorigenic cell lines. These data suggest that expression of a transforming allele of p53 can allow L‐929 cells to escape the host immune system.
Expression of the cyclin‐dependent kinase inhibitors p16INK4, p15INK4B and p21Waf1/cip1 in human breast cancer
Authors: Musgrove Elizabeth A. , Liuschkis Richard , Cornish Ann L. , Lee Christine S. L. , Setlur Vittal , Seshadri Ram , Sutherland Robert L. 
Published: February 2007

AbstractAhderrant cyclin expression has been implicated in oncogenesis in a number of human cancers. Since alterehd function of regulators of cyclin‐dependent kinase (CDK) activity other than cyclins, in particular CDK inhibitors, might play a similar role in oncogenesis, we examined the expression and regulation of the CDK inhibitors p16INk4 p15INK4B and p21WAF1/CIP1 in human breast cancer cell lines. Both the INK4 and INK4B genes were homozygously deleted in 3 cell lines, while INK4 alone was deleted in 2 cell lines. A further 2 cell lines displayed loss of an allele at this locus, and in 1 of these the remaining allele contained a mis‐sense mutation within the coding region of the p16INK4 protein. The majority of cell lines examined, including 2 normal mammary epithelial cell strains, expressed low levels of INK4 mRNA and low or undetectable levels of INK4B mRNA. However, INK4 mRNA was expressed at high levels in 5 cell lines, and this was associated with deletion or inactivation of the retinoblastoma susceptibility gene product pRB but not with mutation of TP53. No deletions of the WAF1/CIP1 gene were observed, but WAF1/CIP1 mRNA levels were reduced in cell lines with TP53 mutation. Transfection of a p16INK4 expression vector into MDA‐MB‐231 cells lacking the INK4 gene failed to produce any p16INK4‐expressing cell lines, suggesting that such cells were selected against in continuous culture. Despite the frequent deletion of INK4 in breast cancer cell lines, no evidence was obtained for INK4 deletions in DNA from 45 primary breast carcinomas. Thus, homozygous deletion of the INK4 gene appears to be a rare event in primary breast cancer.
Influence of hepatic artery occlusion and desferrioxamine on liver‐tumour growth
Authors: Lindnér Per , Naredi Peter , Peterson Anders , Hafström Larsolof 
Published: February 2007

AbstractThde mechanisms behind tumour regression during ischaemic therapy of liver malignancy are not thoroughlhd elucidated. Ischaemia‐reperfusion injury and release of free radicals is one mechanism suggested. The aim of the present study was to explore whether inhibition of hydroxyl radicals, by complex binding Fe+++ with desferrioxamine (DFO), counteracted the retardation in tumour growth rate after HAL and whether DFO in itself had an effect on tumour growth in 2 experimental rat liver tumours. Rats with a hepatoma or an adenocarcinoma were subjected to HAL or to a sham procedure with or without additional injections of DFO daily for 2 or 7 days. HAL had an inhibitory effect on tumour growth rate. The effect of HAL was not counteracted by DFO, while DFO alone caused a decrease in tumour volume. There was an additive effect of DFO and HAL on tumour growth rate in both tumour systems. In vitro there was a growth inhibitory effect of DFO in both tumours, more pronounced in the hepatoma than in the adenocarcinoma. Our findings indicate that the effect of HAL is not mediated by release of oxygen free radicals. In the adenocarcinoma system, an additive effect of DFO and HAL was seen. As a rate‐limiting enzyme for DNA synthesis is dependent on iron, depletion of iron can decrease mitotic activity, a mechanism that could explain the effect of DFO on tumour growth.
c‐erbB‐2 anti‐sense phosphorothioate oligodeoxynucleotides inhibit growth and serum‐induced cell spreading of p185c‐erbB‐2‐overexpressing ovarian carcinoma cells
Authors: Wiechen Kai , Dietel Manfred 
Published: February 2007

AbstractOverexpression of the c‐erbB‐2 proto‐oncogene product (p185c‐erbB‐2) occurs frequently ihd different types of human cancer and is correlated with a significantly decreased survival in ovarian cancer patients. The effect of c‐erbB‐2 anti‐sense phosphorothioate oligodeoxynucleotides (S‐ODNs) was examined on the ovarian cancer cell line SK‐OV‐3. p185c‐erbB‐2 levels were specifically reduced by a single‐dose application of 5 μM c‐erbB‐2 anti‐sense S‐ODNs. This was accompanied by a 60% inhibition of anchorage‐dependent cell growth. More strikingly, c‐erbB‐2 anti‐sense S‐ODNs almost completely abrogated serum‐induced cell spreading. A control of complementary sense oligodeoxynucleotides did not show significant inhibitory effects on cell growth or on cell spreading. The inhibition of cell spreading was imitated by a monoclonal antibody (9G6) targeting the extracellular domain of p185c‐erbB‐2 and by the tyrosine kinase inhibitor erbstatin. The inhibitory activity of these 2 compounds was lost after a few hours, while the inhibition of serum‐induced cell spreading by anti‐sense S‐ODNs was still present after 24 hr. Our results show that c‐erbB‐2 anti‐sense S‐ODNs effectively inhibit the mitogenic and spreading activity of p 185c‐erbB‐2 in ovarian cancer cells. Thus, anti‐sense strategies have the potential of providing new strategies for the therapy of ovarian cancer.
Expression of p21WAF1/CIP1 is heterogeneous and unrelated to proliferation index in human ovarian carcinoma
Authors: Barboule N. , Mazars P. , Baldin V. , Vidal S. , Jozan S. , Martel P. , Valette A. 
Published: February 2007

AbstractThe growth‐inhibitory protein p21WAF1/CIP1 is a potent inhibitor of various cyclin‐dependent kinases, the expression of which is regulated at the transcriptional level by p53‐dependent and ‐independent mechanisms. We examined p21WAF1/CIP1 mRNA and protein expression in 5 human ovarian‐adenocarcinoma cell lines, I primary culture of normal surface epithelium and 17 human ovarian‐tumor specimens. In culture cells, the p21 WAF1/CIP1 protein was expressed in normal ovarian epithelial cells and at a high level in the adenocarcinoma 2008 and IGROV‐I cell lines. p21WAF1/CIP1 expression was undetectable at the mRNA and protein levels in the NIH‐OVCAR‐3 and SKOV‐3 ovarian‐adenocarcinoma cell lines which are respectively mutated and deleted in the p53 gene. Heterogeneous expression of p21 WAF1/CIP1 observed in ovarian‐cancer cell lines in culture was also found in vivo on tumor specimens. p21WAF1/CIP1 expression is undetectable in 25% of the ovarian biopsies examined. Since it has been found that the p53 gene is mutated in 79% of ovarian cancer, the absence of p21WAF1/CIP1 expression in 25% of these ovarian cancer could not be correlated with p53 mutation. The proliferation index of the 17 tumors showed great variation from one tumor to another. However, no significant correlation was found between p21 WAF1/CIP1 expression and the proliferation rate of the tumors. © 1995 Wiley‐Liss, Inc.
Loss of heterozygosity at 9p21 loci and mutations of the MTS1 and MTS2 genes in human lung cancers
Authors: Shimizu Tatsunori , Sekiya Takao 
Published: February 2007

AbstractTo elucidate the involvement of abnormalities of the MTS1/p16 and MTS2/p15 genes located at chromosomal region 9p21 in human lung cancers, we analyzed DNA from 30 primary lung cancers and detected loss of heterozygosity at the 9p21‐p23 region in 15 tumors. Single‐strand‐conformation‐polymorphism analysis of polymerase‐chain‐reaction products from the MTS1 and MTS2 genes and determination of the nucleotide sequences revealed the presence of a mutated MTS1 gene in 2 of 15 tumors with a loss of corresponding loci. No mutations of the MTS2 gene were found. These results suggested that mutations of the MTS1 gene are associated with at least some human lung cancers. © 1995 Wiley‐Liss, Inc.
Cell kinetics of CD34‐positive hematopoietic cells following chemotherapy plus colony‐stimulating factors in advanced breast cancer
Authors: Danova Marco , Rosti Vittorio , Mazzini Giuliano , De Renzis Maria R. , Locatelli Franco , Cazzola Mario , Riccardi Alberto , Ascari Edoardo 
Published: February 2007

AbstractBone‐marrow (BM) hematopoietic precursors are recruited into proliferative activity when colony‐stimulating factors (CSF) are sequenced with chemotherapy (CT). Previous studies suggested that further CT can be safely administered only when the increased proliferative activity of these cells has subsided, because most cytostatic drugs selectively damage cycling cells. The safest interval between CSF discontinuation and the start of the next CT course needs to be ascertained in vivo. Thirty patients with advanced breast cancer were treated with an intensified FEC regimen, planned at 21‐day intervals, sequenced with granulocyte‐macrophage (GM)‐CSF (15 patients) or granulocyte (G)‐CSF (15 patients). Using flow cytometry (FCM) we evaluated the proliferation kinetics of CD34+ BM hematopoietic progenitors before CT + CSF and at different times after CSF administration was stopped. FEC + GM‐ and FEC + G‐CSF sequences both induced a rapid and sustained increase in the percentage of BM myeloid precursors (BMMP%) and in the cycling status of CD34+ BM cells. However, while the BMMP% remained elevated in both cases after CSF were stopped, the enhanced proliferative activity of CD34+ cells decreased more rapidly after GM‐ than after G‐CSF. Using FCM, CD34+ BM‐derived hematopoietic presursor cell kinetics is readily evaluated in the clinical setting. The administration of CSF following CT increases both the proliferative activity of CD34+ BM cells and the BMMP%. After CSF were discontinued a kinetic refractoriness of hematopoietic progenitors was more evident after GM‐CSF than after G‐CSF. These data may be of value in designing clinical trials to avoid cytostatic damage to the BM hematopoietic stem‐cell compartment. © 1995 Wiley‐Liss, Inc.
Over‐expression of tissue inhibitor of matrix metalloproteinases (TIMP1 and TIMP2) suppresses extravasation of pulmonary metastasis of a rat bladder carcinoma
Authors: Kawamata Hitoshi , Kawai Koji , Kameyama Shuji , Johnson Mark D. , Stetler‐Stevenson William G. , Oyasu Ryoichi 
Published: February 2007

AbstractThe balance between matrix metalloproteinases and their inhibitors is a critical factor which affects tumor invasion and metastasis. We have established a rat bladder carcinoma cell line, LMC19, which is tumorigenic, invasive and metastatic to the retroperitoneal lymph nodes and to the lungs in nude mice. LMC19 cells secrete pro‐gelatinases A and B as well as tissue inhibitors of matrix metalloproteinase (TIMP1 and TIMP2). We conducted the present study to determine whether or not over‐expression of TIMP1 and TIMP2 can affect the metastatic potential of LMC19 cells. We transfected the cells with an expression vector containing TIMP1 or TIMP2 cDNA, isolated several clones over‐expressing TIMP1 or TIMP2 and assessed their invasive and metastatic potential by inoculation at an orthotopic site (urinary bladder) in nude mice. Our results show that the transfectants over‐expressing TIMP1 and TIMP2 marginally affect primary tumor growth, local invasion or metastasis to the retroperitoneal lymph nodes but significantly inhibit extravascular growth of pulmonary tumor emboli. Our results suggest that the net activity of matrix metalloproteinases of tumor cells may be a critical factor that controls extravasation at this distant metastatic site. © 1995 Wiley‐Liss, Inc.
A novel human B‐cell line (U‐2904) bearing t(8;14) and t(14;18) translocations
Authors: Sambade Clara , Sállström Jan , Wiklund Helena J. , Enblad Gunilla , Kivi Syrje , Gartner Fátima , Zech Lore , Glimelius Bengt , Sundström Christer 
Published: February 2007

AbstractSequential activation of bcl‐2 and c‐myc appears to be involved in the pathogenesis of rare de novo acute lymphoid leukemias bearing both t(8; 14) and t(14;18). Acquisition of t(8;14) by follicular‐lymphoma cells with t(14;18) has also been related to the clinical transformation into an overt acute lymphoid leukemia in rare cases reported, and a role for c‐myc involvement in the progression of some follicular lymphomas with t(14;18) has been suggested by the detection of c‐myc rearrangements in association with histologic transformation. However, c‐myc abnormalities different from those observed in Burkitt's lymphoma have been reported in diffuse large‐cell lymphomas with breakpoints in 8q24, and a t(8;14) molecularly different from the classical one has been found in follicular lymphomas without t(14;18). We report the preliminary characterization of the EBV‐negative cell line U 2904 established from a transformed follicular lymphoma that carries both t(8;14) (q24;q32) and t(14;18) (q32;q21) translocations. U 2904 cells have a mature B‐cell phenotype, grow in agarose and are tumorigenic in nude mice. Rearrangements of both c‐myc and bcl‐2 confirmed the involvement of both oncogenes in the translocations which lead to abundant c‐myc and bcl‐2 transcripts. Two JH rearrangements and one Cα rearrangement were observed which did not co‐migrate with either c‐myc or bcl‐2 rearrangements. This is the first report of a cell line bearing both t(8;14) and t(14;18) derived from a follicular lymphoma after documented transformation into a centroblas‐tic lymphoma without leukemic features. U 2904 provides further evidence for the involvement of c‐myc in the progression of follicular lymphomas. © 1995 Wiley‐Liss, Inc.
Suppression by amiloride of bombesin‐enhanced peritoneal metastasis of intestinal adenocarcinomas induced by azoxymethane
Authors: Iishi Hiroyasu , Tatsuta Masaharu , Baba Miyako , Yano Hiroyuki , Uehara Hiroyuki , Nakaizumi Akihiko 
Published: February 2007

AbstractThe effects of concomitant administration of bombesin and of the diuretic drug amiloride on the development of large and small intestinal tumors induced by azoxymethane (AOM), the incidence of their metastasis to the peritoneum and the labeling index of intestinal adenocarcinomas were investigated in inbred Wistar rats. From the start of the experiment, rats were given weekly s.c. injections of AOM for 10 weeks and s.c. injections of bombesin and/or a higher or lower dose of amiloride hydrochloride (amiloride) every other day until the end of the experiment in week 45. Administration of bombesin significantly increased the incidence of intestinal tumors and cancer metastasis to the peritoneum in week 45. It also significantly increased the labeling index of intestinal adenocarcinomas. Although administration of both doses of amiloride with bombesin had little or no influence on the enhancement of intestinal tumorigenesis by bombesin, the location, histological type, depth of involvement or labeling index of intestinal adenocarcinomas, a higher dose of amiloride significantly reduced the incidence of cancer metastasis to the peritoneum. Our findings indicate that amiloride possesses an anti‐metastatic activity. © 1995 Wiley‐Liss, Inc.
A zinc metalloproteinase is responsible for the release of cd30 on human tumor cell lines
Authors: Hansen Hinrich P. , Kisseleva Tatiana , Kobarg JÖRg , Horn‐Lohrens Ottmar , Havsteen Bent , Lemke Hilmar 
Published: February 2007

AbstractThe activation marker CD30 is expressed on the cell surface of the malignant cells in Hodgkin's disease and a few non‐Hodgkin lymphomas. We have analyzed the regulation of membrane‐bound CD30 and found that the binding of a variety of anti‐CD30 antibodies induced down‐regulation of CD30 on cell lines. In addition, such down‐modulation was also observed after treatment of the cell surface proteins with the sulfhydryl reagent iodoacetamide or after stimulation of the second messenger pathway with phorbol ester or calcium ionophore. This modulation was abolished at 4°C and strongly inhibited by chelators like EDTA or 1, 10‐phenanthroline, whereas EGTA, a selective inhibitor of Ca2+‐dependent proteinases and other inhibitors of serine, thiol and acid proteinases, showed no effect. The down‐modulation was strengthened by Zn2+ or Cd2+, but not by other divalent cations such as Fe2+, Mn2+, Mg2+, Ca2+ or Co2+, thus indicating the involvement of a zinc metalloproteinase in CD30 modulation which can be activated by protein kinase C and by alkylation of sulfhydryl groups. Pulse‐chase experiments, analysis of the CD30 glycosylation and specific measurement of the 90‐kDa soluble form of CD30 (sCD30) with a sandwich radioimmunoassay revealed that CD30 down‐modulation results from enhanced release of 90‐kDa sCD30 by the site‐specific cleavage of CD30 accomplished by a zinc metalloproteinase. This release occurs at the cell membrane without prior endocytosis. © 1995 Wiley‐Liss, Inc.