bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cytotoxic T lymphocytes recognize tumor antigens of a murine colonic carcinoma by using different T‐cell receptors
Authors: Rodolfo Monica , Castelli Chiara , Bassi Cinzia , Accornero Paola , Sensi Marialuisa , Parmiani Giorgio 
Published: February 2007

AbstractTo see whether different antigens expressed by the same tumor are recognized by distinct T ‐cell receptors (TCR), we used cytotoxic T‐lymphocyte (CTL) lines known to lyse in vitro the syngeneic BALB/c adenocarcinoma C‐26. Four of these CD3+ CD8+ lines showed 4 different patterns of lysis on a panel of MHC‐class‐I‐compatible targets. The activity was H‐2d‐restricted and could be blocked by anti‐CD3 and anti‐TCR‐α/β monoclonal antibodies (MAbs). The CTL lines were also effective, although to a different extent, in adoptive immunotherapy of mice bearing lung metastases. Phenotypic analysis revealed in all the lines a high frequency of cells positive for CD45, asialo GMI (ASGMI), lymphocyte‐function‐associated antigen‐I (LFA‐I), intercellular adhesion molecule‐I (ICAM‐I) and CD44, but negligible expression of L‐selectin (LAM‐I) and very late antigen‐4 (VLA‐4); 2 lines expressed the vitronectin‐receptor (VNR). Analysis of TCR Vβ‐chains used by the 4 lines showed selective presence of Vβ6, Vβ8.2, Vβ8.3 and of Vβ13 chains. MAbs directed to these Vβ chains blocked their lytic activity in vitro. Vα‐chain transcripts of the lines were identified by polymerase chain reaction (PCR) as VαITTII and Vα52 in 2 lines, while one could not be identified. Analysis of Vβs in mixed lymphocyte‐tumor‐cell cultres (MLTC) of T cells deriving from tumor‐infiltrating lymphocytes (TIL) or from spleen of C‐26 tumor‐bearing or immune animals indicated that the TCR of the CTL lines were representatives of the TCR repertoire recognizing C‐26 tumor, since their Vβ were shown to be selectively expanded in MLTC. © 1994 Wiley‐Liss, Inc.
Ki‐67 staining in benign, borderline, malignant primary and metastatic ovarian tumors: Correlation with steroid receptors, epidermal‐growth‐factor receptor and cathepsin D
Authors: Henzen‐Logmans Sonja C. , Fieret Elly J. H. , Berns Els M. J. J. , van der Burg Maria E. L. , Klijn Jan G. M. , Foekens John A. 
Published: February 2007

AbstractKi‐67 immunoreactivity was studied in relation to immunohistochemically assessed expression of epidermal‐growth‐factor receptor (EGFR), estrogen receptor (ER) progesterone receptor (PgR) and cytosolic levels of cathepsin D in advanced human ovarian adenocarcinomas, borderline and benign cystadenomas and normal ovaries. A significantly higher number of Ki‐67‐positive cells were found in metastatic tumors vs. primary adenocarcinomas and in the total group of adenocarcinomas vs. benign/borderline cystadenomas. Cathepsin‐D levels were also significantly higher in metastatic tumors than in primary adenocarcinomas, which in turn presented higher levels than were found in normal ovaries. However, no significant difference was observed between cathepsin‐D levels in malignant adenocarcinomas and borderline/benign cystadenomas. Immunohistochemically assessed expression of ER and PgR was detected in variable percentages of epithelial tumor cells, and stromal cells were occasionally positive as well. In the group of primary adenocarcinomas, 46% were ER‐positive and 34% were PgR‐positive, although there was no significant difference between primary and metastatic lesions with respect to ER or PgR expression. Concordance between immunohistochemically assessed ER or PgR data and cytosolic ER and PgR levels measured with enzyme immunoassay was relatively low. EGFR, immunohistochemically assessed with MAb‐EGFRI, was positive in 76% of the primary and in 78% of the metastatic adenocarcinomas. A strong positive association was detected between ER and PgR, and EGFR was observed to present a weak positive correlation with Ki‐67 and ER. Cathepsin‐D levels were not found to be significantly correlated with the expression of ER, PgR, EGFR or Ki‐67. © 1994 Wiley‐Liss, Inc.
Distinct pattern of HSP72 and monomeric laminin receptor expression in human lung cancers infiltrated by γ/δ T lymphocytes
Authors: Ferrarini Marina , Pupa Serenella M. , Zocchi M. Ratfaella , Rugarli Claudio , Ménard Sylvie 
Published: February 2007

AbstractWe have previously demonstrated that γ/δ T lymphocytes may participate in the host immune response against lung adenocarcinomas. Here we show that, in about one‐fourth of human lung cancers, γ/δ T cells represented a significant proportion of freshly isolated tumor‐infiltrating lymphocytes. Moreover, these cells selectively expand in vitro upon culture in the presence of IL‐2, thus suggesting a prior activation in vivo. Finally, when we evaluated the expression of heat shock proteins and of a panel of tumor‐associated antigens in lung cancers infiltrated by γ.δ vs. α/β T cells, we found that the former displayed a distinct antigenic pattern, characterized by over‐expression of HSP72 and of the 67‐kDa high‐affinity laminin receptor, which might account for γ/δ T‐cell recognition. © 1994 Wiley‐Liss, Inc.
Alterations in serum levels of insulin‐like growth factors and insulin‐like growth‐factor‐binding proteins in patients with colorectal cancer
Authors: El Atiq Fatima , Garrouste Françoise , Remacle‐Bonnet Maryse , Sastre Bernard , Pommier Gilbert 
Published: February 2007

AbstractIt has been reported that insulin‐like growth factor (IGF) II is associated with human primary colorectal tumors and colon‐carcinoma cell lines. Here, we examine alterations in circulating levels of IGFs and IGF binding proteins (IGFBPs) in patients with colorectal carcinoma, and compare them to age‐ and nutrition‐adjusted references. We report (i) an increase in serum IGF‐11 concentrations (about 2‐fold), whereas IGF‐1 concentrations are regarded as normal when aging is taken into account; (ii) an apparent increase in serum IGFBP‐3 levels when compared to those of healthy elderly subjects, IGFBP‐3 only being detected in the 150‐kDa IGFBP ternary complex as in normal serum; (iii) abnormally elevated serum IGFBP 2 levels taking into account the apparent concentrations of IGFBP‐3. This simultaneous elevation of IGFBP‐3 and IGFBP‐2 in the serum of patients with colorectal tumors appears to be unique in that it reflects a break in the inverse relationship between the serum IGFBP‐3 and IGFBP‐2 levels that is observed in normal and in several physiopathotogical conditions. Moreover, it enables a distinction to be made between 76.5% (13/17) of patients with colorectal carcinoma and normal adults, age‐related healthy aged and malnourished patients. We propose that the disturbed serum IGFBP profile observed in the patients with colorectal cancer may be a consequence of oversecretion of IGF‐11 by the tumor cells. The usefulness of IGFs and IGFBPs as potential colorectal tumor‐associated metabolic markers should be further investigated. © 1994 Wiley‐Liss, Inc.
Successful immunotherapy of the highly metastatic murine ESb lymphoma with sensitized CD8+ T cells and IFN‐α/β
Authors: Kaido Thomas , Maury Chantal , Schirrmacher Volker , Gresser Ion 
Published: February 2007

AbstractDaily IFN‐α/β therapy was totally ineffective in inhibiting the development of visceral metastases in DBA/2 mice injected i.v. with the ESb lymphoma regardless of the number of tumor cells injected. The finding that IFN‐α/β therapy increased the survival time of ESb‐tmmunized mice rechallenged with ESb cells suggested that cooperation between the immune system and IFN‐α/β was important. Adoptive transfer of ESb‐immune spleen cells (but not normal cells) together with IFN‐α/β treatment did inhibit the development of ESb metastases in immunocompetent DBA/2 mice. Either treatment alone was ineffective. The anti‐metastatic effect was specific for the ESb lymphoma as spleen cells from ESb‐immunized mice together with IFN‐α/β treatment did not inhibit the development of metastases in mice challenged with IFN‐α/β‐resistant 3C18 FLC. Depletion of CD8+ T cells (but not CD4+ T cells or B lymphocytes) prior to transfer eliminated the protective effect of ESb‐immune splenocytes in IFN‐α/β‐treated mice. As few as 1 × 106 ESb‐immune spleen cells highly enriched for CD8+ cells increased the survival time of IFN‐α/β‐treated ESb‐challenged DBA/2 mice. The combined therapy of ESb‐specific immune cells and IFN‐α/β resulted in long‐term immunity to this tumor. © 1994 Wiley‐Liss, Inc.
The lectin Griffonia simpucifolia I‐A4 (GS I‐A4) specifically recognizes terminal α‐linked N‐acetylgalactosaminyl groups and is cytotoxic to the human colon cancer cell lines LS174t and SW1116
Authors: Chen Yu‐Fang , Boland C. Richard , Kraus Eugene R. , Goldstein Irwin J. 
Published: February 2007

AbstractThe lectin GS I‐A4 binds to terminal α‐N‐acetylgalactosaminyl (GaINAc) groups (which include the Tn antigen), but not to the closely related tumor‐associated epitope, sialylated Tn antigen. The lectin also precipitates asialo OSM, but not its native sialylated form. Lectin histochemistry with human colonic tissues showed that GS I‐A4 specifically stained specimens of colon cancer and colonic tissues from individuals with FAP; however, normal colonic tissues from patients without colonic disease were rarely stained with this lectin. Glycoconjugates bound by GS I‐A4 were observed on the surface membranes of 2 human colon cancer cell lines, LS174t and SW1116, when fluorescein isothiocyanate (FITC)‐conjugated GS I‐A4 was used. GS I‐A4 was toxic to these 2 human colon cancer cell lines in monolayer culture, A dose‐response study conducted using 10‐160 μg/ml of GS I‐A4 demonstrated significant dose‐related toxicity against LS174t and SW1116 cells. At concentrations > 80 μg/ml, > 99% of LS174t and > 90% of SW1116 cells were killed. Four mM GaINAc specifically inhibited the cytotoxic effect of GS I‐A4 (p < 0.001), whereas 4mM N‐acetylglucosamine (GlcNAc) had no effect. Two other lectins that recognize terminal α‐GalNAc residues, DBA and LBL, were significantly less cytotoxic to the colon cancer cells than GS I‐A4. In the light of these findings, we speculate that GS I‐A4 may have potential use as a diagnostic agent against colorectal cancer. © 1994 Wiley‐Liss, Inc.
Anti‐tumor activity of mycophenolate mofetil against human and mouse tumors in vivo
Authors: Tressler Robert J. , Garvin Laura J. , Slate Doris L 
Published: February 2007

AbstractCultured tumor cell lines, tumor xenografts grown in athymic nude mice, and a murine experimental metastasis model were used to assess the in vitro and in vivo anti‐tumor activity of the potent IMP dehydrogenase (IMPDH) inhibitor, mycophenolic acid (MPA), and its morpholinoethyl ester pro‐drug, mycophenolate mofetil (MM). The growth of all the cell lines tested was inhibited by MPA in vitro, with EC50 values ranging from less than 0.1 μM to 3.9 μM. Mice were monitored for s.c. tumor outgrowth in the case of human tumor xenograft models or survival time for the murine experimental metastasis model. Treatment with MM p.o. was started 24 hr after tumor challenge or after tumors became palpable. Treatment of athymic nude mice bearing A3.01 (T‐lymphoblast), Molt‐4 (T‐cell leukemia), CaPan‐2 (pancreatic adenocarcinoma), CaLu‐3 (non‐small‐cell lung adenocarcinoma), LS174T and T84 (colon adenocarcinoma), and Daudi (B‐cell lymphoma) human tumor xenografts with MM significantly inhibited s.c. tumor growth. Treatment of BALB/c mice with MM after i.v. injection of murine RAW 117‐H10 lymphoma cells in an experimental metastasis assay resulted in increased survival time for treated animals. No significant inhibitory effect on s.c. tumor outgrowth was seen with MM treatment of SK‐Hep‐1, a human hepatic endothe‐lioma, or Hep‐3B, a liver adenocarcinoma, at any of the doses tested. © 1994 Wiley‐Liss, Inc.
Harly endothelium activation and polymorphonuclear cell invasion precede specific necrosis of human melanoma and sarcoma treated by intravascular high‐dose tumour necrosis factor alpha (rTNFα)
Authors: Renard N. , Liénard D. , Lespagnard L. , Eggermont A. , Heimann R. , Lejeune F. 
Published: February 2007

AbstractTwenty‐seven patients treated with high‐dose rTNFα, IFNγ and melphalan by isolated limb perfusion were histologically documented. There were 20 cases of melanoma‐in‐transit metastases and 7 cases of high‐grade soft‐tissue sarcoma. Biopsies were taken before IFN7, after IFNγ, before TNFα and between 2 hr and 60 days after the TNFα perfusion. Immunohistochemistry was performed for adhesion molecules ICAM‐I, ELAM‐I (E selectin), VCAM‐I and PECAM. During the first hours after beginning perfusion, the endothelial cells of the tumour capillaries appeared swollen. Significant tumour necrosis was already observed 3 hours after the perfusion in melanoma cases. The overall predominant feature was coagulative necrosis associated or not with haemorrhagic necrosis. TNFα induced increased expression of ELAM‐I and VCAM‐I adhesion molecules on intratumoral endothelial cells. The activated tumour vessels were progressively destroyed. Significant intra‐vascular recruitment of polymorphonuclear cells (PMNs) was observed 3 hr after starting TNFα; it was followed by diapedesis and tumour colonization 3 days later. T lymphocytes and macrophages were detected during the first 7 days and B lymphocytes during the second week. Melanoma in transit metastases treated with alkylating agent alone did not show significant necrosis and did not express high levels of adhesion molecules (ELAM‐1, VCAM‐I) nor infiltration by PMN.
Expression of Ca2+‐binding proteins of the S100 family in malignant human breast‐cancer cell lines and biopsy samples
Authors: Pedrocchi Michele , Schäfer Beat W. , Mueller Heinz , Eppenberger Urs , Heizmann Claus W. 
Published: February 2007

AbstractIn order to examine whether the expression of calcium‐binding proteins of the SI00 family may correlate with the transformation grade of human mammary‐tumor cells, we studied the expression patterns of 4 members of this family (CACY, CAPL, S100L, S100α/β) in human breast‐cancer cell lines. Each S100 protein is shown to be individually regulated in the human breast‐cancer cell lines we studied, but it appears that the expression levels of S100 proteins do not strictly correlate with prognostic factors or the tumorigenicity of the cells. However, 2 aggressive cell lines, MDA‐MB‐231 and HS‐578T, show elevated expression of CAPL, We show that methylation may account for partial regulation of the SI00 genes, whereas neither genomic rearrangements in the S100 gene cluster region nor gene dosis effects seem to influence their expression pattern in MDA‐MB‐231 and MCF‐7 cells. On the basis of our genomic analyses, we can localize the gene for SIOOL within 5 kb upstream of S100E, thus extending the SIOO gene cluster by one gene. A series of primary breast tumors was collected and tested for expression of CAPL, CACY and S100α/β. The results show that all human breast‐cancer tissues tested express CACY, whereas the presence of CAPL is more restricted. There if a significant correlation between enhanced expression of CAPL and presence of the invasivity marker urokinase‐type plasminogen activator (uPA). This observation suggests that CAPL may play an important role in the acquisition of metastatic potential of human mammary epithelial cells.
Anti‐tumor effect of combined treatment with thymosin alpha 1 and interleukin‐2 after 5‐fluorouracil in liver metastases from colorectal cancer in rats
Authors: Rasi Guido , Silecchia Gianfranco , Sinibaldi‐Vallebona Paola , Spaziani Erasmo , Pierimarchi Pasquale , Sivilia Mariliana , Tremiterra Salvatore , Garaci Enrico 
Published: February 2007

AbstractWe studied the effect of combined chemo‐immunotherapy, 5‐FU followed by thymosin α1 (Tα1) and interleukin‐2 (IL‐2) at low doses, on liver metastases from colorectal cancer, induced by splenic injection of DHD/K12 cells (1,2‐dimethylhydraiine‐induced colon adenocarcinoma) in syngeneic BDIX rats. The presence of liver metastases was checked by laparotomy 14 days after tumor‐cell injection. Evaluable rats were assigned randomly to 5 experimental groups designated as control, 5‐FU, IL‐2, 5‐FU/IL‐2 and S‐FU/Tαl/IL‐2. S‐FU was administered i.v. as a continuous infusion for 7 days by an osmotic device implanted surgically. Tα1 and IL‐2 were administered for 4 days and repeated after 11 days. Combined chemo‐immunotherapy was shown both to significantly reduce the growth of liver metastases and to prevent extra‐hepatic spread. 5‐FU/Tαl/IL‐2 also improved survival rate. Combined immunotherapy after 5‐FU restored NK activity of the peripheral‐blood‐mononuclear‐cell (PBMC) in tumor and/or 5‐FU immunode‐pressed rats and enhanced PBMC cytotoxic activity against the OHD/K12autologous cell line. This model was devised to mimic the clinical situation of unresectable liver metastases.
HTLV‐I messenger RNA is expressed in vivo in adult T‐cell leukemia/lymphoma patients: An in situ hybridization study
Authors: Setoyama Mitsuru , Fujiyoshi Toshinobu , Mizoguchi Shimako , Katahira Yoshihiko , Yashiki Shinji , Tara Mitsutoshi , Kanzaki Tamotsu , Sonoda Shunro 
Published: February 2007

AbstractAdult T‐cell leukemia/lymphoma (ATLL) is a malignancy involving peripheral blood, lymph nodes, skin and other organs. Human T‐cell leukemia virus type 1 (HTLV‐1) is etiologically associated with ATLL but cannot be detected by conventional methods in fresh samples of peripheral blood and skin taken from ATLL. The aim of this study was to investigate the feasibility of an in situ hybridization technique for detection of HTLV‐1 mRNA in atypical lymphoid cells of peripheral blood and skin lesions of patients with ATLL. We detected variable amounts of HTLV‐1 tax mRNA in the nuclei and cytoplasm of these cells in fresh peripheral blood samples and skin lesions from ATLL patients, and also in asymptomatic HTLV‐1 infected donors to a lesser extent. Out of 10 patients with ATLL, 7 showed strong positive in situ hybridization whereas the other 3 were only weakly positive. However, in the last 3 cases, the reaction became strongly positive after cells had been cultured for 24 hr. Furthermore, all 3 asymptomatic HTLV‐1‐infected donors exhibited a weakly positive response in their apparently mature lymphoid cells.
Trends in pancreatic cancer mortality in Europe, 1955–1989
Authors: Fernandez Esteve , la Vecchia Carlo , Porta Miquel , Negri Eva , Lucchini Franca , Levi Fabio 
Published: February 2007

AbstractTrends in death certification rates from pancreatic cancer over the period 1955–1989 were analyzed for 25 European countries (excluding the former Soviet Union and a few smaller countries). In 1985–1989, rates for males ranged between 5.3/100,000 (age‐standardized world population) in Spain and 10.3/100,000 in Hungary and Czechoslovakia. Other high‐mortality areas were located in Northern Europe (Finland, Iceland, Ireland, Denmark) and Central Europe (Austria, Poland, Germany), whilst mortality was lower in Southern Europe (Portugal, Greece). Between 1955 and 1989, mortality rates increased in all the countries considered, the change ranging between 6% in Scotland and 279% in Spain; the rises were higher in the Mediterranean and Eastern European countries than in Northern Europe. Among females, Nordic countries such as Iceland, Sweden and Denmark had the highest mortality rates in 1985–1989 (over 6/100,000) and, as for males, Southern Europe (Spain, Portugal, Greece) appeared as a low‐mortality area (around 3/100,000). During the 1955–1989 period, upward trends were observed in all the countries studied, with the highest increase in Greece, Italy, Bulgaria, Poland and Spain. A negative correlation was observed between the percent change in mortality rates between 1955–1959 and 1985–1989 and the rate in 1955–1959 among both males (r = −0.95, p <0.001) and females (r = −0.81, p <0.001). Thus, a systematic levelling of rates was observed in most countries, with the exception of the UK and some Nordic countries, whose rates were already high in the late 1950s. Tobacco smoking and dietary factors could account for some of the generalized upward trends. Improved diagnostic and death certification of the disease might also partially explain the observed figures. © 1994 Wiley‐Liss, Inc.
Detection of immunoglobulin heavy‐chain gene rearrangement at the single‐cell level in malignant lymphomas: No rearrangement is found in hodgkin and reed‐sternberg cells
Authors: Roth Judith , Daus Heiner , Trümper Lorenz , Gause Angela , Salamon‐Looijen Monika , Pfreundschuh Michael 
Published: February 2007

AbstractHodgkin and Reed‐Sternberg (HRS) cells, the neoplastic cells of Hodgkin's disease (HD), represent only a minority of the cellular infiltrate in affected tissue. Therefore, rearrangements of the immunoglobulin heavy‐chain (IgH) gene detected in DNA extracted from an entire Hodgkin's lymph node cannot be attributed to the HRS cells and cannot be used as an argument for the B‐cell origin of HRS cells. We developed a new method for the amplification of rearranged DNA of the IgH gene from single cells. Using 6 “forward primers” which were constructed corresponding to consensus sequences of the 6 known families of the IgH variable (V) region (framework region I) and a mix of 2 “reverse primers” corresponding to consensus sequences of the different joining (J) segments, rearrangements of all 6 V‐families were detected in human peripheral blood lymphocytes. Rearranged IgH DNA could be amplified from single cells of B‐cell lymphoma‐cell lines and from 13 patients with B‐cell non‐Hodgkin's lymphomas. However, analysis of HRS cells isolated from lymph nodes of 13 patients with Hodgkin's disease did not show any rearrangement of the IgH gene locus. These findings, obtained by polymerase chain reaction (PCR) on isolated single HRS cells, contrast with previous studies that used Southern‐blot analysis of entire tissues affected by Hodgkin's disease. We conclude that the neoplastic HRS cells in Hodgkin's disease‐with the possible exception of the nodular paragranuloma subtype‐are probably not derived from B cells. © 1994 Wiley‐Liss, Inc.
Cellular immunodeficiency enhances the progression of human papillomavirus‐associated cervical lesions
Authors: Petry Karl Ulrich , Scheffel Danicla , Bode Ulrike , Gabrysiak Thomas , Köchel Heinrich , Kupsch Eckehardt , Glaubitz Michael , Niesert Stefan , Kühnle Henning , Schedel Ingolf 
Published: February 2007

AbstractMost cases of low‐grade cervical intraepithelial neoplasia (CIN) associated with oncogenic human papillomavirus (HPV) types regress spontaneously within years. Unknown co‐factors seem to be necessary for a progression to malignancy. To determine the possible role of cellular immunodeficiency as such a co‐factor in the genesis of genital neoplasia, 48 HIV‐infected women and 52 allograft recipients were examined periodically during a 3‐year period. Colposcopy, cytology and HPV‐DNA typing (Vira Type) were performed at each visit. Each cervical lesion was matched prospectively with 2 lesions from immunocompetent controls. In all, 29/100 patients suffered from cervical neoplasms, including 2 advanced cervical cancers and 9 CIN3 lesions. Correlation between grade of lesion and HPV DNA 16/18 was significant. Low‐grade lesions among patients progressed more often than among controls and recurrent lesions after destructive treatment were seen more frequently among patients than among controls. All patients with CD4‐lymphocyte counts of <400/μl or immunosuppression for more than 3 years suffered from progressive lesions. We conclude that malfunction of the cellular immune response following either HIV‐induced depletion or iatrogenic inhibition of CD4‐lymphocyte activation, enhances the progression of HPV‐induced cervical lesions to malignancy. © 1994 Wiley‐Liss, Inc.