bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tenascin and fibronectin isoforms in human renal cell carcinomas, renal cell carcinoma cell lines and xenografts in nude mice
Authors: Lorn Jouni , Tani Taneli , Laitinen Liisa , Kangas Lauri , Lehto Veli‐Pekka , Virtanen Ismo 
Published: February 2007

AbstractWe studied the expression of tenascin (Tn) and isoforms of fibronectin (Fn) in human renal cell carcinomas (RCC) and oncocytomas, in RCC cell lines and in their s.c. implanted xenografts in nude mice. In well‐differentiated RCCs and oncocytomas extra‐domain A (EDA)‐Fn and Tn immunoreactivities were confined to the basement membranes and blood vessels, while in less‐differentiated RCCs they were also widely seen in the stroma, correlating with the morphological differentiation of the tumor. Expression of EDB‐Fn and oncofetal (onc)‐Fn was very scarce in most of the RCCs and oncocytomas. Western blotting results demonstrated the predominance of the Mr 190,000 Tn subunit in most RCCs. Among the 4 RCC cell lines, 3 showed Tn in the extracellular matrix. As xenografts, they formed moderately or poorly differentiated tumors, with abundant Tn. Three of the RCC cell lines also showed secretion of EDA‐Fn and 2 of them secretion of onc‐Fn and EDB‐Fn into the culture medium, while in xenografts there was a strong expression of all Fn isoforms. In xenografts, the expression of Tn closely recapitulated that seen in clinical tumors and in the cell lines in vitro, while the expression of Fn isoforms in cultured cells and their xenografts was highly discordant.
Hyaluronic acid/CD44H interaction induces cell detachment and stimulates migration and invasion of human glioma cells in vitro
Authors: Koochekpour Shahriar , Pilkington Geoffrey J. , Merzak Abderrahim 
Published: February 2007

AbstractThe mechanisms underlying the invasive properties of glio‐mas, the major form of intrinsic brain tumours in humans, are poorly understood. We have reported that CD44 plays an important role in this behaviour in vitro. In the present work, we investigated the role of its ligand, hyaluronic acid (HA), in invasion in 8 human glioma cell lines. We found that HA mediates cell detachment via its interaction with its high affinity receptor, CD44H. Using 8 μm porosity polycarbonate filter transwells, we demonstrate that HA strongly stimulates migration in all 8 cell lines. This effect was found to be partially counteracted by a CD44H monoclonal antibody (MAb), suggesting the involvement of CD44H, as well as other HA receptors, in this process. Furthermore, incorporation of increasing concentrations of HA in Matrigel in an in vitro invasion assay resulted in a substantial increase in the invasive propensity of the glioma cell lines. Moreover, blocking experiments with the CD44H MAb suggest that CD44H and other receptors interact with HA to promote cell invasion in vitro. Our results show that HA induces cell detachment, stimulates migration and promotes invasion via its interaction with CD44H and other HA receptors in vrtro. These effects could be prevented by use of specific HA receptor antibodies.
Inhibition of metastasis of lewis lung carcinoma by urinary trypsin inhibitor in experimental and spontaneous metastasis models
Authors: Kobayashi Hiroshi , Shinohara Hiromitsu , Fujie Michio , Gotoh Junko , Itoh Mariko , Takeuchi Kinya , Terao Toshihiko 
Published: February 2007

AbstractA purified human urinary trypsin inhibitor (UTI) and its related synthetic peptides were examined to determine whether they could inhibit production of experimental and spontaneous lung metastases by murine Lewis lung carcinoma (3LL) cells. Three peptides, peptide 1, peptide 2 and peptide 3, representing the amino acid sequences within the UTI molecule, were synthesized. UTI and peptide 2 inhibited human leukocyte elastase (HLE). UTI and peptide 3 specifically inhibited human and murine plasmin activity. Peptide 1 had essentially no inhibitory activity. In an in vivo spontaneous metastasis model, multiple s.c. injections of UTI or peptide 3 for 7 days immediately after s.c. tumor cell inoculation significantly inhibited the formation of lung metastasis in CS7BL/6 mice in a dose‐dependent manner. UTI reduced lung tumor colonization more effectively than peptide 3. Peptides 1 and 2, however, did not affect the formation of lung metastasis. Inhibition of lung metastasis was not due to direct anti‐tumor effects of UTI and peptide 3. In an in vivo experimental metastasis assay, multiple s.c. injections of UTI for 7 days after i.v. tumor cell inoculation inhibited metastatic lung tumor colonization, while peptide 3 did not affect metastasis. Peptides 1 and 2 did not affect the formation of lung metastasis. When examined with an in vitro assay system using a modified Boyden chamber, UTI and peptide 3 suppressed the invasion of tumor cells through Matrigel. UTI and peptide 3 inhibited neither cell proliferation nor the binding of tumor cells to Matrigel and showed no significant suppression of chemotactic migration of tumor cells to fibronectin. Our results suggest that UTI efficiently regulates the mechanism involved in not only the entry into vascular circulation of tumor cells (intravasation, though, at least in part, inhibition of the proteolytic enzyme plasmin) but also the extravasation step of the metastatic process.
Epstein barr virus (EBV)‐carrying cells of a chronic lymphocytic leukemia (CLL) subpopulation express EBNA1 and LMPS but not EBNA2 in vivo
Authors: Laytragoon‐Lewin Nongnit , Chen Fu , Avila‐Cariño Javier , Zou Jie‐Zhi , Mellstedt Håkan , Ernberg Ingemar , Klein George 
Published: February 2007

AbstractWe have previously described an exceptional CLL patient, P.G., whose leukemic cell population contained a small fraction of Epstein‐Barr virus (EBV)‐carrying cells. These cells grow directly into permanent cell lines in vitro. Using RT‐PCR analysis, we now show that the in vivo EBV‐carrying CLL cells expressed EBNAI, LMPI, LMP2a and 2b, but not EBNA2, in 4 of 4 blood samples obtained during the last 3 years of the patient's life. Our data also show that the CLL cells used a promoter in the F/Q, but not the W or C, region. This is consistent with the fact that CLL cells resemble resting lymphocytes rather than immunoblasts. Expression of LMPI and LMP2b differs from the exclusive EBNAI and LMP2a expression of normal resting B cells, however, and corresponds to the state defined as latency II. This form of latency was until now detected only in EBV‐carrying non‐B cells in vivo. Our data show that a B‐cell subtype can also show this expression pattern in vivo.
A cohort study of serum testosterone and hepatocellular carcinoma in Shanghai, China
Authors: Yuan Jian‐Min , Ross Ronald K. , Stanczyk Frank Z. , Govindarajan Sugantha , Gao Yu‐Tang , Henderson Brian E. , Yu Mimi C. 
Published: February 2007

AbstractAhdnested case‐control study of HCC based on a cohort of 18,244 middle‐aged men in Shanghai, Chinahd who had been followed for an average of 5.3 years, was conducted. Our hypothesis dealt with the possible role of testosterone in the etiology of HCC, which shows a minimum of a 2‐ to 3‐fold male excess in all populations world‐wide. Seventy‐six incident cases of HCC and 410 control subjects drawn from the cohort and individually matched to the cases by age (within 1 year), time of blood sample collection (within 1 month) and neighborhood of residence were assessed for serum HBsAg, anti‐HBc, anti‐HBs, anti‐HCV and testosterone. Among controls, serum testosterone levels were similar between those who had no markers of HBV infection, those who were positive for anti‐HBs only and those who were positive for anti‐HBc but negative for HBsAg. However, the geometric mean level of testosterone in HBsAg‐positive controls was 21% higher relative to HBsAg‐negative controls and the difference was statistically significant (2‐sided p = 0.0006). Relative to controls, HCC cases had a significantly higher mean level of testosterone at the time of recruitment (570 vs. 485 ng/dl, 2‐sided p = 0.0005), but the difference was explicable on the basis of a higher proportion of HBsAg‐positive individuals among cases than controls (p = 0.42 after adjustment for HBsAg status).
Human papillomavirus type 18 DNA in gestational trophoblastic tissues and choriocarcinomas
Authors: Pao Chia C. , Hor Jyu Jen , Wu Chi‐Jung , Shi Yi‐Fu , Xm Xing , Lu Shi‐Ming 
Published: February 2007

AbstractThde objectives of our study were to better understand carcinogenesis of gestational trophoblastihd tumors and to investigate the possible presence of human papillomavirus types 16 and 18 DNA sequences in these tumors. Amplification‐based DNA methodology was used on 11 hydatidiform moles, 5 invasive moles, 8 choriocarcinomas and 9 normal early placental tissues. Human papillomavirus type 16 DNA was not found in any of these tissues. Although human papillomavirus type 18 DNA was also not found in the 9 normal placentas and 5 invasive moles, it was present in 2 of the 11 (18%) hydatidiform moles and in 4 of the 8 (50%) choriocarcinomas.
Expression and function of α2,3‐sialyl‐ and α,3/l,4‐fucosyltransferases in colon adenocarcinoma cell lines: Role in synthesis of E‐selectin counter‐receptors
Authors: Majuri Marja‐Leena , Niemelä Ritva , Tiisala Sinikka , Renkonen Ossi , Renkonen Risto 
Published: February 2007

AbstractWe show here that colon‐carcinoma cell lines adhere to E‐selectin via sialyl Lewis x and sialyl Lewis a (sLex and sLea) oligosaccharides and that this adhesion can be enhanced by TNF stimulation. To study in greater detail this endothelial binding, we analysed the mRNA expression and function of the enzymes participating in the generation of sLex and sLea on cancer cells. These oligosaccharides are synthesized by sequential action of α2,3 sialyl (α2,3‐ST) and α1,3/1,4 fucosyltransferases (α1,3/1,4‐FT) on existing (poly)N‐acetyllactosamine chains. We report here that mRNAs of 2 recently cloned α2,3‐STs and 4 α1,3/l,4‐FTs are expressed in adenocarcinoma cells. In functional assays α2,3‐ST and α1,3‐ or 1,4‐FT activities were observed in adenocarcinoma cell lysates to exogenous N‐acetyllactosamine and lacto‐N‐biose acceptors and to their sialytated derivatives, leading to the synthesis of the sialyl‐N‐acetyllactosamine and sLex or the sialyllacto‐N‐biose and sLea, respectively. Furthermore, the inflammatory cytokine TNF could enhance some α2,3‐ST and α1,3/1,4‐FT activities capable of generating E‐selectin counter‐receptors. Taken together, these data show that COLO 205 and HT‐29 adenocarcinoma cell lines adhere to E‐selectin in a TNF‐inducible manner via their cell‐surface sLex and sLea. These cells also express mRNA as well as inducible enzyme activities of several α2,3‐STs and α,3/1,4‐FTs responsible for the final steps in the synthesis of sLex and sLea. We show here that the TNF‐induced adhesion to E‐selectin might be due to the increased synthesis of sLex and sLea in colon‐carcinoma cells.
Marked acceleration of the metastatic phenotype of a rat bladder carcinoma cell line by the expression of human gelatinase a
Authors: Kawamata Hitoshi , Kameyama Shuji , Kawai Koji , Tanaka Yoshinori , Nan Li , Barch David H. , Stetler‐Stevenson William G. , Oyasu Ryoichi 
Published: February 2007

AbstractNhdmerous studies have reported a correlation between the production of gelatinases A and B by cancer cells anhd invasive and metastatic potential. It has been suggested that the expression of gelatinase A (72‐kDa type IV collagenase) is associated more closely with the metastatic phenotype of malignant cells in vitro and in vivo than that of gelatinase B (92‐kDa type IV collagenase). We have established a rat bladder carcinoma cell line, MYU3L, which is tumorigenic and locally invasive but is not metastatic to the distal organs in nude mice. The MYU3L cell line secretes pro‐gelatinase B but not any detectable level of pro‐gelatinase A. We undertook the present study to determine whether over‐expression of gelatinase A can affect the metastatic potential of MYU3L cells. We transfected MYU3L cells with an expression vector containing human pro‐gelotinase A cDNA under the transcriptional control of the SRα promoter. Two stable transfectants over‐expressing gelatinase A activity were isolated. We assessed the biological behavior of the transfectants by an orthotopic site (urinary bladder) inoculation and an i.v. injection in nude mice. Our results demonstrate that the induced expression of human gelatinase A enzyme markedly accelerates the metastatic phenotype of the rat bladder carcinoma cell Vine MYU3L. Our results suggest that gelatinase A produced by tumor cells plays a major role in the metastatic process.
Reaction of peripheral‐blood lymphocytes to the human chorionic gonadotropin β sub‐unit in patients with productive tumors
Authors: Housseau Frank , Rouas‐Freiss Nathalie , Benifla Jean‐Louis , Marcillac Isabelle , Roy Maguy , Troalen Frédéric , Fernandez Hervé , Prapotnich Dominique , Valencien Guy , Bougaran Joelle , Cottu Paul , Culine Stéphane , Droz Jean‐Pierre , Bidart Jean‐Michel , Bellet Dominique 
Published: February 2007

AbstractHuman chorionic gonadotropin (hCG) and its β sub‐unit (hCGβ) are secreted by trophoblast cells during pregnancy, and by tumoral cells of trophoblastic and non‐trophoblastic origin. In contrast to hCG, the free hCGβ sub‐unit is consistently undetectable in healthy non‐pregnant subjects. With this in mind, we sought to determine whether an immune response to hCGβ can be detected in patients with bladder or germ‐cell testis cancers. Peripheral‐blood mononuclear cells (PBMC) from 31% of patients with hCGβ‐productive bladder cancers and 33% of testis‐tumor‐bearing patients displayed an hCGβ‐specific proliferative response, whereas no patients with non‐hCGβ‐productive cancers had a proliferative response. PBMC from pregnant women and healthy controls did not elicit significant reactivity. By the use of overlapping synthetic peptides, the immunogenic regions of hCGβ were delineated within the central 20–65 portion. Moreover, in 2 bladder‐cancer patients with the HLA DR7, DQ2 haplotype, the T‐cell response to hCGβ was focused on the hCGβ(20–47) peptide. Taken together, these results indicate that hCGβ is a tumor‐associated antigen capable of inducing a cell‐mediated immune response in patients with productive tumors. © 1995 Wiley‐Liss, Inc.
Presence and persistence of HPV infection and p53 mutation in cancer of the cervix uteri and the vulva
Authors: Milde‐Langosch Karin , Albrecht Kathrin , Joram Simone , Schlechte Horst , Giessing Markus , Löning Thomas 
Published: February 2007

AbstractWe studied 51 cervical carcinomas, among them 25 squamous‐cell carcinomas (SCC) and 26 cervical adenocarcinomas (AdCa), and 40 vulvar SCC for the presence of HPV and mutant p53. HPV was detected by PCR, and p53 alterations by temperature‐gradient gel electrophoresis/direct sequencing and immunohistochemistry. HPV, mostly type 16/18, was found in 80.4% of the cervical tumors (92.0% of the SCC and 69.2% of the AdCa), but in only 27.5% of vulvar carcinomas. In contrast, p53 mutations were found in 7.8% and 52.5% of cervical and vulvar tumors respectively. Mutant p53 occurred in pre‐invasive vulvar lesions, indicating that this oncogenic factor is involved early in carcino‐genesis. Further analysis of recurrent/metastatic lesions of 9 cervical and 14 vulvar tumors also showed remarkable differences: in cervical cancer, HPV was persistent, and p53 mutations absent, whereas in vulvar tumors, HPV was mostly absent or not persistent, and the p53 mutation rate was very high (78.6%). These observations suggest that HPV persistence is an important event for the evolution and maintenance of cervical cancer, whereas for vulvar cancers p53 mutation and not HPV activity is a central oncogenic event. © 1995 Wiley‐Liss, Inc.
Characteristics of EBV‐infected cells in HIV‐related lymphadenopathy: Implications for the pathogenesis of EBV‐associated and EBV‐unrelated lymphomas of HIV‐seropositive individuals
Authors: Dolcetti Riccardo , Gloghini Annunziata , De Vita Salvatore , Vaccher Emanuela , De Re Valli , Tirelli Umberto , Carbone Antonino , Boiocchi Mauro 
Published: February 2007

AbstractThe present study was performed with the aim of better defining the possible role of Epstein‐Barr‐virus(EBV)‐infected cells in the pathogenesis of HIV‐related lymphadenopathy syndrome (LAS). In addition, since LAS has been considered as a pre‐lymphomatous lesion, we also wished to elucidate the possible contribution of EBV‐carrying cells present in LAS tissues to the development of HIV‐associated malignant lymphomas. To this end, we have characterized EBV‐infected cells in LAS lymph nodes in terms of EBV DNA prevalence, tissue distribution in relation to HlV‐carrying cells, virus sub‐type, expression of latent and replicative antigens, and presence of clonal EBV episomes. When compared with HIV‐unrelated lymphadenopathies (4/10, 40%), LAS showed a higher prevalence of EBV DNA (14/20, 70%). Comparable values of EBV prevalence were detected in LAS with follicular hyperplasia (12/16, 75%) and with follicular involution (4/4, 100%). All EBV+ non‐neoplastic lymph nodes from HIV‐seronegative patients carried type‐1 EBV, whereas LAS specimens showed almost equivalent distribution of the 2 EBV sub‐types. Of the 14 EBV‐carrying LAS, 4 (29%) were positive by Southern‐blot analysis for the BamHI‐W region of the virus genome but negative for the presence of monoclonal EBV episomes. In situ hybridization revealed a remarkably higher load of EBV‐infected cells in LAS than in HIV‐unrelated lymphadenopathies. In LAS lymph nodes, EBV‐carrying cells were identified as isolated, cytologically normal elements, sometimes with immunoblastic morphology, usually scattered throughout the interfollicular areas. By contrast, the expression of HIV p24 was restricted to germinal center cells. All the EBV+ LAS samples were negative for the expression of EBV‐encoded latent (LMP‐1 and EBNA‐2) and replicative proteins (BZLF‐1, BHLF‐1, EA‐D, EA‐R and VCA). In addition, amplification of the immunoglobulin heavy‐chain genes using 2 different polymerase‐chain‐reaction protocols showed evidence of B‐cell clonal expansion in 2/20 (10%) LAS, one EBV− case, and one sample with low numbers of EBV‐infected cells. These results suggest that: (i) EBV‐carrying cells are probably not involved in the development of LAS, either directly or indirectly; (ii) type‐2‐EBV‐infected cells are present in LAS lymph nodes from the early phases of HIV infection; (iii) EBV‐carrying LAS per se probably does not constitute a lesion at high risk for subsequent development of EBV+ lymphomas; (iv) it is unlikely that a high viral load or strong EBV‐mediated antigenic stimulation plays a contributory role in the development of EBV‐unrelated lymphomas of HIV‐seropositive individuals. © 1995 Wiley‐Liss, Inc.
Rapid increase in plasma tenascin‐C concentration after isolated limb perfusion with high‐dose tumor necrosis factor (TNF), interferon gamma (IFNγ) and melphalan for regionally advanced tumors
Authors: Schenk Susanne , Liénard Danielle , Gérain Jean , Baumgartner Murielle , Lejeune Ferdy J. , Chiquet‐Ehrismann Ruth , Rüegg Curzio 
Published: February 2007

AbstractThe matrix protein tenascin‐C (TN‐C) is present in the blood of healthy individuals at concentrations around 1 mg/1. Elevated serum levels have been reported in cancer patients. In this study we have measured the concentration of circulating TN‐C in 40 patients with melanoma, soft‐tissue sarcoma (STS) or squamous‐cell carcinoma (SCC) of the limbs, and have found a minor increase in the mean concentration compared with healthy subjects. Only 10 patients had TN‐C levels above the normal range. No correlation was observed between TN‐C levels and tumor burden. Nineteen patients were treated by isolation limb perfusion (ILP) with TNF, IFNγ, melphalan (11 melanoma, 2 SCC and 1 STS), melphalan alone (3 melanoma) or hyperthermia at 41.5°C (2 melanoma). ILP with TNF, IFNγ and melphalan induced a rapid increase in plasma TN‐C levels, peaking in most patients between 24 to 48 hr after ILP. Two patients treated with hyperthermia only had a slow increase in TN‐C concentration peaking at day 4, while the patients treated with melphalan alone had no significant change. In some cases elevated TN‐C levels persisted for over 8 weeks after ILP. The early rise in TN‐C concentration correlates with the increase in circulating C‐reactive protein. Our findings suggest that circulating TN‐C behaves, at least in part, as an acute‐phase protein and that it may play a role in the inflammatory response. © 1995 Wiley‐Liss, Inc.
Adenovirus‐mediated gene transfer of wild‐type p53 results in melanoma cell apoptosis in vitro and in vivo
Authors: Cirielli Corrado , Riccioni Teresa , Yang Chunlin , Pili Roberto , Gloe Torsten , Chang Joan , Inyaku Kyosuke , Passaniti Antonino , Capogrossi Maurizio C. 
Published: February 2007

AbstractGene transfer techniques may provide efficient treatment for a variety of malignant neoplasms. A replication‐deficient adeno‐virus (Ad) vector which carries the cDNA for wild‐type p53 (AdCMV.p53) was tested for its in vitro and in vivo effects on the growth of murine melanoma cell line B16‐G3.26 and human melanoma cell line SK‐MEL‐24. The growth of B16‐G3.26 cells infected with AdCMV.p53 was inhibited when compared to the uninfected cells or cells infected with the control vector AdCMV.NLSβgal. Similarly, the growth of SK‐MEL‐24 cells infected with AdCMV.p53 was also below that of AdCMV.NLSβgal‐infected and uninfected controls. DNA laddering using agarose gel electrophoresis and in situ labeling of DNA fragmentation (TUNEL) showed that AdCMV.p53‐infected murine and human melanoma cells underwent apoptosis. Nude mice injected s.c. either with B16‐G3.26 cells or with SK‐MEL‐24 cells developed localized tumors. These tumors were subsequently infiltrated with either AdCMV.p53, AdCMV.NLSβgal or saline alone. One week after infection, B16‐G3.26 tumors exposed to AdCMV.p53 were 2.5 times smaller than control tumors and exhibited DNA fragmentation. A similar growth‐inhibitory effect of AdCMV.p53 was observed with SK‐MEL‐24 tumors. Thus, Ad‐mediated wild‐type p53 overexpression resulted in melanoma cell apoptosis and inhibition of melanoma growth in vitro and in vivo. These gene therapy approaches may be useful in targeting rapidly growing, malignant melanomas in a clinical setting. © 1995 Wiley‐Liss, Inc.