bluuebunny/crossref_metadata_2025_split huggingface dataset:
Correlation of myc expression with the growth‐arrested and transformed phenotypes in hybrids between A T lymphoma and an antigen‐responsive T‐cell line
Authors: Kubota Koichi , Imreh Stephan , Katoh Hideki , Babonits Magdalena , Wiener Francis 
Published: February 2007

AbstractFusion of the YACUT lymphoma cell line with the Mls‐Ia‐antigen‐specific non‐tumorigenic T‐cell line G4 produced growth‐arrested hybrids that could be induced to proliferate in the presence of Mls‐Ia antigen. Prolonged growth of such hybrids by repeated antigenic stimulation resulted in the appearance of autonomously growing hybrid lines. Of the 4 antigen‐independent hybrid clones, I was weakly tumorigenic (25% incidence) while the other 3 were highly tumorigenic (100% incidence). In the growth‐arrested hybrids the de‐regulated c‐myc expression characteristic of the YACUT cells was suppressed. In the autonomously growing clones, however, c‐myc expression had reverted to the levels of the lymphoma parent and 1 to 2 extra copies of chromosome 15 were consistently present. These results indicate that repeated antigenic stimulation somehow abrogated the down‐regulation of c‐myc in the growth‐arrested hybrid lines. The increase in the number of copies of chromosome 15, however, suggests that genes located on this chromosome may abolish the effect of the negative regulatory functions of the non‐malignant parent in a gene‐dosage‐dependent manner.
Expression of the epstein‐barr virus (EBV)‐encoded membrane protein LMP1 impairs the In vitro growth, clonability and tumorigenicity of an EBV‐negative burkitt lymphoma line
Authors: Cuomo Laura , Ramquist Torbjörn , Trivedi Pankaj , Wang Fred , Klein George , Masucci Maria G. 
Published: February 2007

AbstractIn a previous study on several independently established Epstein‐Barr virus (EBV)‐converted sublines of the EBV‐negative Burkitt lymphoma (BL) line BL41, we found that expression of the virally encoded membrane protein LMP I was accompanied by reduced agarose clonability and tumorigenicity. In order to investigate whether LMPI can induce these phenotypic changes by itself, we have now studied the growth in suspension culture, the clonability in agarose and the tumorigenicity in immunosuppressed and SCID mice of 4 LMPItransfected sublines of BL4I that carry the gene under the control of the ZnSO4‐inducible metallothionein promoter. Expression of LMPI at levels comparable to those detected in EBV‐transformed lymphoblastoid cell lines (LCL) correlated with impairment of growth in suspension and reduction of clonability and tumorigenicity. Only minor changes were observed in transfectants expressing low LMPI levels. Upregulation of LMPI by ZnSO4 treatment of the low LMPI clone MTLM5 was accompanied by a slowing down of proliferation, increased cell clumping and decreased clonability. The results suggest that expression of LMP I at levels which are compatible with immortalization of normal B‐cells antagonizes the ability of BL cells to grow in vitro and in vivo, and illustrate a possible mechanism by which down‐regulation of this viral antigen may favor tumorigenicity in EBV‐carrying BLs. © 1992 Wiley‐Liss, Inc.
MHC class‐I‐restricted auto‐tumor‐specific CD4+CD8 −T‐cell clones established from autologous mixed lymphocyte‐tumor‐cell culture (MLTC)
Authors: Wang P. , Vànky F. , Klein E. 
Published: February 2007

AbstractAutologous mixed lymphocyte‐tumor cell cultures (MLTC) were initiated with cytokine (IFNγ and TNFα)‐treated ex‐vivo tumor cells of lung, ovarian, breast and stomach carcinomas. The cytokine‐treated tumors expressed class‐l but not class‐M molecules. Although the proportion of CD8+ lymphocytes increased in the bulk culture of MLTCs, in 5/7 experiments the majority of the established T‐cell clones were CD4+. Among the CD8+ clones a high proportion (77%) was cytotoxic, while the proliferative response was more frequent among the CD4+clones (70%). In 4/26 cytotoxic T‐lymphocyte (CTL) clones (3/17 CD4+ and I /9 CD8+), derived from a patient with class l+class II− stomach carcinoma, lysis was restricted to the autologous tumor cells. These auto‐tumor‐specific clones did not lyse the autologous ConA blasts, the 5 allogeneic ex‐vivo tumors, the NK‐sensitive K562 or the relatively sensitive Daudi cells. The cytotoxicity of these clones was inhibited by pre‐incubation of the tumor cells with W6/32 (α‐class I) MAb, or by preincubation of the lymphocytes with OKT3 (α‐CD3) MAb. The α‐CD4 (OKT4) MAb had only a marginal effect on the CD4+clones, while the lytic function of the CD8+ clone was inhibited by the α‐CD8 (OKT8) MAb. The 3 CD4+CTL clones also responded with proliferation to the autologous tumor cells. This proliferative response was inhibited by the presence of W6/32 MAb. Our results indicate that the auto‐tumor lysis exerted by CD4+ CTL clones was restricted by the class‐l antigens, and that the CD4 molecules of the clones were not essential for the lytic interaction. © 1992 Wiley‐Liss. Inc.
Growth in serum‐free medium of NIH3T3 cells transformed by the EJ‐H‐ras oncogene: Evidence for multiple autocrine growth factors
Authors: Pironin Martine , Clément Gilles , Benzakour Omar , Barritault Denis , Lawrence' David , Vigier Philippe 
Published: February 2007

AbstractRodent fibroblastic cells transformed by ras oncogenes can grow in serum‐free (S−) medium. We have studied clonal lines of mouse NIH3T3 fibroblasts transfected with the EJ‐H‐ras oncogene, and observed that practically all become independent of exogenous growth and attachment factors shortly after transfection. Moreover, all the clones tested soon form anchorage‐independent (Al) colonies in S− medium, and most give rise to spheroids able to grow in suspension. The cell‐conditioned S−medium of the transformed (TR) cells stimulates autocrinally the Al and anchored growth of these cells, in the absence of serum, and it contains growth factors related to TGF‐α (or EGF), PDGF and bFGF, and other uncharacterized factors. Some of these factors are not found, or are found only in very small amounts, in the S− medium of non‐transformed NIH3T3 cells, which also stimulates the growth of the TR cells, in the absence of serum. In addition, the TR cells contain 4‐6 times more cell‐associated bFGF than the non‐transformed cells and release more latent TGF‐β activatable by acid treatments. However, no active TGF‐β is secreted by either cell type. Activated TGF‐β and pure TGF‐β I stimulate the growth of the anchored TR and NIH3T3 cells, but inhibit the Al growth of the TR cells. Another inhibitor of this growth is also found in the concentrated medium of the NIH3T3 cells. © 1992 Wiley‐Liss, Inc.
Hyaluronan (hyaluronic acid) and hyaluronectin in the extracellular matrix of human breast carcinomas: Comparison between invasive and non‐invasive areas
Authors: Bertrand P. , Girard N. , Delpech B. , Duval C. , D'Anjou J. , Dauce J. P. 
Published: February 2007

AbstractWe performed quantitative determination of the distribution of hyaluronan (hyaluronic acid, HA) and the HA‐binding protein, hyaluronectin (HN), 2 components of the extracellular matrix of tumor desmoplasia, within 71 human breast carcinomas. Results showed that HA and HN were more elevated in tumoral than in non‐tumoral adjacent tissue, and that the peripheral invasive area of tumors contained increased levels of HA and HN as compared with the central non‐invasive area (p < 10–3 and p < 10–5 respectively). HN and HA levels of 61 ductal carcinomas were related to the histological grade of tumors; no significant difference was found between grades for HA; HN was found to be significantly lower in grade III than in grade II tumors (p < 0.01). HA and HN rates were correlated in grade I and grade II tumors and were not correlated in grade III. Mean percentage of HA saturation level by HN for whole tumors was found to be less than 4%, indicating that HA is essentially free of proteins and could be used as a target for cancer diagnosis or therapy. © 1992 Wiley‐Liss, Inc.
Breast cancer in a low‐risk population. The influence of age and menstrual status on disease pattern and survival in Saudi Arabia
Authors: Al‐Idrissi Hassan Y. , Ibrahim Ezzelin M. , Kurashi Nabil Y. , Sowayan Saleh A. 
Published: February 2007

AbstractData on 130 women with invasive breast cancer, seen at our institution between April 1981 and November 1990, were retrospectively reviewed to assess the influence of age and menstrual status on the pattern and prognosis of their disease. Patients were mostly young (median age 40 years) and in 21 patients (16%) the diagnosis was established at the age of 30 years or younger. Eighty‐six patients (66%) were under 50 and 82 patients (63%) were pre‐menopausal. Pre‐menopausal patients were more numerous than expected in stage III and less numerous in stage II. On the other hand, the differences between observed and expected values for both stage I and stage IV in the 2 menopausal groups were not significant. Comparedwithpost‐menopausal patients, pre‐menopausal patients with 1–3 or > 3 positive lymph nodes were more numerous than expected. Differences between pre‐menopausal and post‐menopausal patients have persisted after categorizing patients into 2 age‐groups with a cut‐off point at 50 years. Comparable initial assessment and therapeutic modalities were offered to the 2 menopausal groups. At the time of analysis (January, 1991) all patients had a complete follow‐up. Over a median follow‐up of 46 months, the overall median survival (±SE) was 85.7 (±4.4) months with a survival probability (±SE) at 5 years of 62% (±5%). The proportional hazard model of Cox has identified advanced stage (stages III and IV) and involvement of lymph nodes as the only independent adverse predictors of survival with estimated hazard rates of 2.9 and 2.8, respectively. Unadjusted analysis, adjusted analysis and stratified survival functions failed to reveal any survival difference based on age or menstrual status. We conclude that, in a low‐risk population and despite apparent baseline differences in demographic and disease characteristics between pre‐menopausal and post‐menopausal breast cancer patients, neither age nor menopausal status had a significant influence on survival. Our results should guide future cancer‐care programs in Saudi Arabia. © 1992 Wiley‐Liss, Inc.
The role of mucin in colon‐cancer metastasis
Authors: Schwartz Bertha , Bresalier Robert S. , Kim Young S. 
Published: February 2007

AbstractMucinous colorectal cancer often presents at an advanced stage. We have previously observed that mucin production by human colon‐cancer cells correlates with their ability to colonize the liver in experimental animal models. The present study was undeitaken in order to further elucidate the mechanisms by which production of mucin by colon‐cancer cells affects metastasis. Cell lines showing high mucin production (HMP) (HM 7, HM 3 and LS LiM 6) demonstrated increased adherence to basement membrane proteins and invaded a reconstituted basement membrane to a greater extent than their counterpart cell lines showing low mucin production (LMP) (LS174T and LM 12). Adherence of the LMP parental cell line LS 174T to various matrix proteins was potentiated by the addition of purified human colon‐cancer mucin in a dose‐dependent fashion. HMP cell lines secreted more proteolytically active type‐IV collagenase than LMP lines, and collagenase activity was further stimulated by purified mucin in a dose‐dependent manner. Specific inhibition of mucin O‐glycosylation by benzyl‐α‐N‐ acetylgalactosamine significantly affected each of the metastasis‐ related events, with the greatest effect on the HMP cell lines. The present data further indicate that cumin may play an important role in the metastutic process. © 1992 Wiley‐Liss, Inc.
Morphological, immunohistochemical and biochemical characterization of 6 newly established human ovarian carcinoma cell lines
Authors: Möbus V. , Gerharz C. D. , Press U. , Moll R. , Beck T. , Mellin W. , Pollow K. , Knapstein P. O. , Kreienberg R. 
Published: February 2007

AbstractSix permanent human tumor cell lines (OV‐MZ‐1 to 6) were established from 6 patients with serous adenocarcinomas of the ovary. These cell lines were derived from both solid tumors and ascites, from pre‐treated and untreated patients, and are available over a range of in vitro passage numbers. The tumor cells grow its monolayers and develop foci of “piled‐up” cells in confluent cultures. Flow cytophotometry showed that all the lines exhibited DNA hyperdiploidy with DNA tetraploidy in one cell line and DNA aneuploidy in the other cell lines. The mean population doubling time ranged from 24 to 52 hr. Transmission electron microscopy demonstrated that the tumor cells of all cell lines exhibited features of epithelial differentiation such as desmosomes and intracellular gland‐like lumina. Immunocy‐ tochemical analysis showed that the co‐expression of cytokeratins and vimentin, which is a feature of ovarian serous cystadeno‐ carcinomas; in situ, was fully preserved in the majority of cell lines. The main cytokeratin polypeptides expressed were numbers 7, 8, 17, 18 and 19. The tumor‐associated antigen CA‐125, but not CEA, was shed in the culture supernatant. This was in accordance with FACScan analysis of the cell lines and the level of CA‐125 and CEA in the patients' serum. The estrogen and progesterone receptors were negative both in the cell lines and in the original tumors. These new ovarian carcinoma cell lines will be valuable models for further investigations into a variety of biological properties. © 1992 Wiley‐Liss, Inc.
Establishment and characterization of human uterine leiomyosarcoma heterotransplanted into nude mice
Authors: Sawada Masumi , Terada Nobuyuki , Yamamoto Reiko , Nishizawa Yasuko , Wada Akira , Mori Yoichi , Sakamoto Hiromi , Tanizawa Osamu 
Published: February 2007

AbstractHuman uterine leiomyosarcoma is a rare gynecological malignancy with a generally poor prognosis. We have established a human uterine leiomyosarcoma tumor line in nude mice, designated UTS‐1, and describe the characteristics of this tumor. The UTS‐1 tumor doubled in 12.1 days and retained the histological characteristics of leiomyosarcoma, even after 14 serial generations. Ultrastructurally, the tumor is characterized by nuclear pleomorphism typical of smooth muscle, intracyto‐plasmic filaments with dense bodies, a relative paucity of micropinocvtotic vesicles, and an incomplete external lamina. Immunohistochemically, the UTS‐1 cells reacted with antibodies against vimentin, desmin, smooth‐muscle actin and myosin, but not with antibodies against keratin, CEA and S‐100 protein. Serum levels of AFP, CAI25, CEA and SCC ranged within normal limits in tumor‐bearing mice. The serum level of immu‐nosuppressive acidic protein correlated well with an activity of the tumor. Estrogen and progesterone receptors were not detected in the tumor. Chromosomal analysis showed a human karyotype with some marker chromosomes and a modal number of 85 chromosomes. The UTS‐1 tumor should prove a useful model to explore the biological characteristics and treatment of human uterine leiomyosarcoma. © 1992 Wiley‐Liss, Inc.
Protein‐kinase‐C inhibitor calphostin C reduces B16 amelanotic melanoma cell adhesion to endothelium and lung colonization
Authors: Liu Bin , Renaud Colette , Nelson Kevin K. , Chen Yong Q. , Bazaz Rajesh , Kowynia Julie , Timar Jozsef , Diglio Clement A. , Honn Kenneth V. 
Published: February 2007

AbstractWe recently reported that the Ca2+‐and phospholipids‐dependent protein kinase, protein kinase C (PKC), was involved in rat Walker carcinosarcoma cell adhesion to large‐vessel endothelium. We extended our studies to explore the role of this kinase in the adhesion to small‐vessel endothelium and lung colonization of murine B16 amelanotic melanoma (B16a). Sub‐populations of B16a cells, which differ in lung‐colonization potentials, were isolated by centrifugal elutriation from solid tumors. In this study, we demonstrate that cells from a high metastatic sub‐population (HM340), when compared with cells from a low metastatic sub‐population (LM180), exhibit elevated levels of total cellular as well as membrane‐bound PKC. The increase in PKC in cells from the HM340 correlates positively to their increased ability to adhere to murine pulmonary‐microvessel endothelial‐cell monolayer, and to form pulmonary colonies in syngeneic mice. Calphostin C, a potent and selective PKC inhibitor, decreases in a dose‐dependent manner the adhesion to endothelium and the lung colonization of cells from both the low and the high metastatic sub‐populations with IC50 at sub‐micromolar concentrations. In conclusion, our results suggest that PKC may be a key element in regulating tumor‐cell metastasis and that PKC inhibitors may be anti‐metastatic agents. © 1992 Wiley‐Liss, Inc.
Receptors for hormones and growth factors and (ONCO)‐gene amplification in human ovarian cancer
Authors: Berns Els M. J. J. , Klijn Jan G. M. , Henzen‐Logmans Sonja C. , Rodenburg Cees J. , van der Burg Maria E. L. , Foekens John A. 
Published: February 2007

AbstractReceptor status and gene amplification were studied in advanced human ovarian adenocarcinoma tissues, borderline and benign ovarian tumours and normal ovarian tissues. Sixty‐five percent (53/82) of ovarian adenocarcinomas, 57% (8/14) of benign/borderline tumours and only 31% (5/16) of normal ovarian tissues studied showed specific 125I‐EGF (epidermal growth factor) binding (median: 17; 10; and 0 fmol EGF‐R/mg protein, respectively) and a significant increase in progesterone receptor (PgR) levels was observed in these groups (median: 5; 33; and 152 fmol/mg protein, respectively). No correlations were observed between the levels of EGF‐R and the levels of either oestrogen receptors (ER) or PgR. All membrane samples of 25 adenocarcinomas studied by Scatchard analysis were positive for insulin‐like growth‐factor‐1 receptors (IGF‐1 ‐R) and contained higher IGF‐I‐R levels than membranes of 10 normal ovarian tissues, of which 9 were positive (median: 64 and 26 fmol IGF‐I‐R/mg membrane protein, respectively). Also, as measured by autoradiography, 37 adenocarcinoma tissues showed a higher expression of IGF‐I‐R (1.5+ to 4+) than sections derived from 10 normal ovarian tissues (I +). 125I‐IGF‐I binding was predominantly associated with epithelial tumour cells, the surrounding connective tissue was negative and in several samples high expression of IGF‐I‐R was found in areas of tumour necrosis. Southern blot analysis of DNAs isolated from 25 ovarian adenocarcinomas revealed no amplification of the IGF‐I ‐R or the EGF‐R gene. The HER2/neu gene was amplified only in 2 out of 3 histologically confirmed endometrioid adenocarcinomas studied but not in 22 other tumours. An amplification of the c‐myc gene was observed in 28% (7/25) of the tumours. All c‐myc‐amplified tumours were PgR‐negative. No rearrangement was observed for any of the genes studied. In conclusion, ovarian adenocarcinoma tissues show a decrease in PgR levels and an increased expression of IGF‐I‐R and EGF‐R, in the absence of gene amplification, when compared to benign/borderline ovarian tumours and normal ovarian tissues. In addition, amplification of the c‐myc and HER2/neu genes, without rearrangement of these genes, occurs in a minority of these tumours. © 1992 Wiley‐Liss, Inc.
Influence of recombinant human interleukin (IL)‐7 on disease progression in mice infected with friend virus complex
Authors: Lu Li , Zhou Zhen , Wu Bo , Xiao Mang , Shen Rong‐Nian , Williams Douglas E. , Kim Young‐Junc , Kwon Byoung S. , Ruscetti Sandra , Broxmeyer Hal E. 
Published: February 2007

AbstractRecombinant human (rhu) IL‐7 was evaluated for its influence on disease progression in mice infected with the polycythemia‐inducing strain of the Friend virus complex (FVC). DBA/2 mice were injected i.v. with FVC, and then treated s.c. with rhuIL‐7. IL‐7 significantly prolonged survival time and decreased spleen focus‐forming virus (SFFV) levels, expression of SFFV mRNA and SFFV protein production in FVC‐infected mice. IL‐7 did not appear to directly inactivate SFFV. Although both splenic weight and cellularity in FVC‐infected mice treated with IL‐7 were higher than those of normal mice, they were respectively 58% and 66% lower than those of the untreated FVC‐infected mice. NK‐cell activity was substantially lower in FVC‐infected mice than in normal mice, while IL‐7 restored NK‐cell activity to normal levels. IL‐6 and IFN‐γ levels were markedly reduced in FVC‐infected mice compared to normal mice, but treatment of FVC‐infected mice with IL‐7 restored these cytokine levels. While the actual mechanisms of these effects are not yet known, the results suggest the potential therapeutic efficacy of IL‐7 for certain hematopoietic and viral disorders, possibly mediated through an action on accessory cells and cytokine production. © 1992 Wiley‐Liss, Inc.
Phenotype‐specific “tissue” transglutaminase regulation in human neuroblastoma cells in response to retinoic acid: Correlation with cell death by apoptosis
Authors: Piacentini Mauro , Annicchiarico‐Petruzzelli Margherita , Oliverio Serafina , Piredda Lucia , Biedler June L. , Melino Gennaro 
Published: February 2007

AbstractNeuroblastomas in culture are characterized by the presence of 2 morphologically and biochemically distinct phenotypes (i.e., neural “N‐type” and flat substrate‐adherent “S‐type”) which undergo transdifferentiation. Human neuroblastoma SK‐N‐BE(2) cells differentiate toward a neural phenotype upon retinoic acid (RA) treatment. However, we recently showed that, during the RA treatment, a subset of SK‐N‐BE(2) cells undergo apoptosis; these cells specifically express a high “tissue” transglutaminase (tTG) level. This study was undertaken to investigate the cellular and molecular basis of the action of retinoic acid on apoptosis in human neuroblastoma cells. As a biochemical marker of the phenomenon we studied the tTG gene expression in the parental line SK‐N‐BE(2) and in 2 clones which stably express neuroblastic [BE(2)‐M17] and substrate‐adherent [BE(2)‐C] features, respectively. Data showed a differential phenotype‐specific regulation of tTG gene expression. In fact, RA treatment enhanced tTG expression and apoptotic index in the flat substrate‐adherent variant, whereas, in cells expressing the neural phenotype, very low tTG expression and apoptosis were found. Northern‐blotting analysis revealed that the substrate‐adherent cells had a basal 3‐fold higher level of tTG mRNA. An increase in tTG mRNA major transcript levels (3.7 kb) occurred within a few hours of exposure to RA in both the phenotypic variants. By contrast, tTG protein level was very low in the cell expressing the neuronal phenotype, even after prolonged exposure to RA. Immunohistochemical analysis indicated that tTG protein, in addition to mature apoptotic cells, was specifically localized in the flat substrate‐adherent variant both in the wild‐type and in the BE(2)‐C clone. These findings suggest that the ability to undergo apoptosis in the neuroblastoma cells is associated with the expression of a non‐neuronal neuroectodermal (substrate‐adherent cells) immature phenotype. © 1992 Wiley‐Liss, Inc.