bluuebunny/crossref_metadata_2025_split huggingface dataset:
Histomorphologic and immunophenotypic spectrum of primary gastro‐intestinal B‐Cell lymphomas
Authors: Mielke Birgit , Möller Peter 
Published: February 2007

AbstractIn order to compare primary gastro‐intestinal (GI) B‐cell lymphomas histomorphologically and immunophenotypically with orthologous steps of B‐cell differentiation within the mucosa‐associated lymphoid tissue (MALT) of the GI tract, a comprehensive panel of well characterized leucocyte differentiation antigens was composed. It comprised immunoglobulin constituents CD5, CD10, CD11c, CD20, CD23, CD24, CD30, CDw32, CD38, CD39, CDw75, CD76, and vimentin. These antigens yield characteristic immunoprofiles for the following B‐cell compartments of the MALT, per se closely linked to cytologically distinct B‐cell phenotypes: mantle zone (MZ), extrafollicular compartment (EF), follicle center (FC), and plasma‐cell compartment (PC). An unselected series of 31 MALT B lymphomas (13 of low and 18 of high grade malignancy) was classified histologically in routine preparations and subsequently characterized immunohistochemically using fresh frozen tissue, monoclonal antibodies (MAbs) against the antigen panel listed above, and an indirect immunoperoxidase method. The final classification considered both morphology and immunoprofile of tumor cells. Ten tumors were “typical” in both respects: 2 closely corresponded to MZ, 5 to EF, 2 to FC and 1 to PC. The remaining 21 cases were characterized as “atypical” because of anaplastic cytology and/or abnormal co‐expression and/or loss of antigens. A hybrid EF/FC phenotype was most frequently observed together with centrocyte‐like or centrocytic anaplastic cytology of tumor cells. We conclude that MALT B‐cell neoplasia comprises a broad spectrum of histo‐ and immunophenotypes ranging from well differentiated forms closely mimicking normal B‐cell development to highly abnormal tumors which cannot be subclassified.
Socio‐economic indicators, infectious diseases and hodgkin's disease
Authors: Serraino Diego , Franceschi Silvia , Talamini Renato , Barra Salvatore , Negri Eva , Carbone Antonino , La Vecchia Carlo 
Published: February 2007

AbstractThe relationship between socio‐economic indicators, family size, history of tonsillectomy, infectious mononucleosis (IM) and other diseases and the risk of Hodgkin's disease (HD) was investigated in a hospital‐based case‐control study, conducted in the province of Pordenone, North‐east Italy, between June, 1985 and March, 1990. One hundred and fifty‐two HD cases (88 men and 64 women) and 613 controls (357 men and 256 women) were interviewed. Patients with 14 or more years of education had a 2‐fold increased HD risk (95% confidence interval, CI: 1.0‐3.9); such risk tended to be higher in patients with nodular sclerosis (NS) HD (odds ratio, OR: 4.4, 95% CI 1.8‐11.0). Sibship size, birth order and tonsillectomy were not associated with HD risk. Cases and controls did not differ in the frequency or age at occurrence of common childhood infections. A history of IM, however, was found to be an important predictor of HD risk, in particular among NS HD (OR = 13.1, 95% CI 1.0‐176.7). Past episodes of herpes zoster and of skin and genital warts were also associated with significantly increased HD risks. These data lend further support to the role of the IM agent (i.e., the Epstein‐Barr virus) and, perhaps, of other viral infections and immunological alterations in the development of HD.
Production of fibronectin by human tumor cells and interaction with exogenous fibronectin: Comparison of cell lines obtained from colon adenocarcinomas and squamous carcinomas of the upper aerodigestive tract
Authors: Varani James , Schuger Lucia , Fugiel Suzanne E. G. , Inman Dennis R. , Chakrabarty Subhas 
Published: February 2007

AbstractCell lines derived from 13 different human colon adenocarcinomas were examined for production of fibronectin by ELISA and for cell‐surface expression of fibronectin by indirect immunofluorescence. Two squamous epithelial cell lines obtained from tumors of the upper aerodigestive tract were used as controls. None of the 13 colon carcinoma lines produced detectable amounts of fibronectin or showed detectable cell‐surface staining with anti‐fibronectin. The 2 squamous epithelial cell lines, in contrast, produced large amounts of fibronectin which could be detected in the culture medium and bound to the substratum. The squamous carcinoma cells also stained brightly when examined in the viable state by immunofluorescence with anti‐fibronectin. In addition to being studied for fibronectin production, each cell line was also examined for the ability to interact with exogenous fibronectin in an adhesion assay. None of the colon carcinoma cells were adherent to fibronectin‐coated culture dishes while the 2 squamous carcinoma cells rapidly attached and spread on this substratum. These data suggest that cell lines derived from adenocarcinomas of the colon are deficient in production of fibronectin and in their ability to interact with exogenous fibronectin. In their degree of deficiency, the colon carcinoma cells are significantly different from several different types of human tumor cell. The failure of the colon carcinoma cells to synthesize detectable amounts of fibronectin endogenously or to interact with exogenous fibronectin may explain, in part, the low degree of adhesive interaction which these cells have for their substratum. This, in turn, may influence the in vitro and in vivo properties of colon carcinoma cells.
Sequence variations in ltr and env regions of HTLV‐I do not discriminate between the virus from patients with HTLV‐I‐associated myelopathy and adult T‐cell leukemia
Authors: Kinoshita Tomohiro , Tsujimoto Atsumi , Shimotohno Kunitada 
Published: February 2007

AbstractFor detailed comparison of human T‐cell leukemia virus type I (HTLV‐I) in adult T‐cell leukemia (ATL) and HTLV‐I‐associated myelopathy (HAM), the nucleotide sequences of parts of the long terminal repeat (LTR) and env regions of the HTLV‐I proviruses from 12 patients with HAM, 8 patients with ATL and one with both diseases were analyzed. About 340 bp of the LTR U3 region, about 4S0 bp of the 5′ region and about 280 bp of the 3′ region of env were sequenced directly in DNAs amplified by the polymerase chain reaction (PCR) with 2 or 3 sets of primers for each region. Nucleotide insertions, deletions or point mutations were observed at 50 positions in these regions of about 1,000 nucleotides length. None of these changes was specific to either HAM or ATL, and some changes were observed in proviruses from both cases of HAM and ATL. Moreover, the sequences of proviruses isolated from pairs of cell lines established from cerebrospinal fluid (CSF) and peripheral blood mononuclear cells (PBMCs) of the 4 patients with HAM also had different sequences. These results indicate that the proviruses from HAM and ATL are indistinguishable in these sequenced regions, suggesting that these 2 diseases are caused by infection with genetically indistinguishable HTLV‐I. Therefore, the reason why these two distinct diseases, HAM and ATL, develop in HTLV‐I carriers may be based on a host factor(s) or some other factor(s) rather than variation in the virus itself.
Altered dosage of the sex chromosomes in human testicular cancer: A molecular genetic study
Authors: Peltomäki PÄIvi , Lothe Ragnhild , Børresen Anne‐Lise , Fosså Sophie D. , Brøgger Anton , De La Chapelle Albert 
Published: February 2007

AbstractThirty‐one males with testicular germ‐cell tumors were studied by Southern hybridization using X‐ and Y‐chromosome‐specific probes as well as a pseudoautosomal probe. Densitometric analysis showed changes in the relative dosage of Y‐chromosomal fragments in tumor DNA from 12 out of 31 patients (39%) as compared to normal DNA from the same patients. In 11 tumors the relative intensity ratios of Y‐chromosome‐specific fragments had decreased from the normal value of I to values between 0 and 0.77. An increase in the Y‐chromosomal dosage was observed in I case. The entire Y chromosome was apparently involved in most patients but 2 tumors revealed regional variation. Tumor DNA of 2 patients with Y‐chromosomal deficiency showed a concomitant increase in the X chromosomal dosage. The pseudoautosomal region that is shared by both sex chromosomes was involved in a total of 8 tumors (26%), 2 of which did not show any obvious dosage changes with probes detecting strictly X‐ or Y‐chromosome‐specific fragments. Autosomal alterations in the present tumor series have been described. A dosage change involving the sex chromosomes accompanied loss of heterozygosity at loci in 3p or lip in 10 tumors out of 15 (67%). Seminomas tended to be affected more often than non‐seminomas by either type of alteration. Our results indicate that changes in the sex chromosomes occur in a substantial proportion of male germ‐cell tumors and, together with other defects, may constitute an important step in tumor development and/or progression.
Increased susceptibility of ifn‐γ‐treated neuroblastoma cells to lysis by lymphokine‐activated killer cells: Participation of ICAM‐1 induction on target cells
Authors: Naganuma Hirofumi , Kiessling Rolf , Patarroyo Manuel , Hansson Mona , Handgretinger Rupert , Grönberg Alvar 
Published: February 2007

AbstractWe have investigated the effect of interferon‐gamma (IFN‐γ) treatment of neuroblastoma cells on the susceptibility to lysis by lymphokine‐activated killer (LAK) cells and examined the participation of cell‐adhesion molecules on the target cells in LAK cell lysis. Untreated neuroblastoma cells expressed lymphocyte‐function‐associated antigen 3 (LFA‐3) and neural‐cell‐adhesion molecule (NCAM), but did not express MHC‐class‐I, MHC‐class‐II, or intercellular‐adhesion molecule 1 (ICAM‐1). IFN‐γ treatment of neuroblastoma cells induced the expression of MHC‐class‐I and ICAM‐1 antigens, but did not affect the expression of MHC‐class‐II, LFA‐3, and NCAM. This was accompanied by an increased susceptibility to lysis by LAK cells. Anti‐ICAM‐1 antibody inhibited partially the increased sensitivity of IFN‐γ‐treated neuroblastoma cells to LAK cell lysis, and blocked completely the increase in binding of LAK cells observed after IFN‐γ treatment of the target cells. These results suggest that the increased LAK sensitivity of IFN‐γ‐treated neuroblastoma cells is partially attributable to the induction of ICAM‐1 on neuroblastoma cells and indicate that post‐binding events also play a role in the increased sensitivity to LAK cell lysis observed after IFN‐γ treatment.
The role of the peyer's patch in the carcinogenesis of lymphoid cells
Authors: Garrett Lenora R. , Byers Paul , Cuchens Marvin A. 
Published: February 2007

AbstractThe dose response to 3‐methylcholanthrene (3‐MC), the promoter effects of 2,6,10,14‐tetramethylpentadecane (pristane) and the target‐organ specificity in the preferential induction of B‐lymphoid malignancies versus thymic tumors were examined. Lymphoid malignancies were induced in approximately 30% of the Copenhagen rats treated with injections in Peyer's patches (PP) of low, intermediate or high doses of 3‐MC. A low dose of 3‐MC induced B‐lymphocytic leukemias or B lymphomas, whereas thymic tumors were detected in rats treated with high doses. Co‐treatment of rats with pristane and 3‐MC resulted in increased incidences and decreased latency of the lymphoid malignancies observed, suggesting that pristane acts as a tumor promoter. To address the possible role of PP in the induction events, PP were surgically removed after 3‐MC treatment and the remaining small intestine anastomosed. Thymic tumors, but no B‐lymphoid malignancies, were observed, indicating that the PP environment was important in the induction of the B‐lymphoid malignancies. Radiotracer studies also revealed that appreciable amounts of 3‐MC were disseminated to the thymus within 24 hr after treatment of PP with a high dose of 3‐MC. Furthermore, direct intrathymic injection of the thymus with 3‐MC resulted in the development of thymic tumors only. These results support the hypothesis that the PP has an important role in early events in the carcinogenesis of B lymphocytes and in the dissemination of 3‐MC to the thymus.
The effect of radiosensitizers on radio‐immunotherapy, using 131I‐Labelled anti‐cea antibodies in a human colonic xenograft model
Authors: Barbara Pedley R. , Begent Richard H. J. , Boden Joan A. , Boden Robert , Adam Theresa , Bagshawe Kenneth D. 
Published: February 2007

AbstractAnti‐CEA antibodies were used for radio‐immunotherapy in an established LSI74T colonic xenograft in nude mice. A single IV dose of either l3lI‐PK4S (polyclonal) or ‐A5B7 (monoclonal) antibody produced tumour regression, and significantly delayed subsequent tumour growth. Administration of a clearing second antibody, 24 hr post 1311‐PK4S and at 5 times the dose, significantly reduced the therapeutic effect of radio‐antibody alone. Tumours of mice given non‐specific antibody or unlabelled anti‐CEA antibody grew like those of untreated controls. In an attempt to enhance therapy without increasing dose, radiosensitizers normally employed with external beam radiation were used in combination therapy. When the hypoxic cell radiosensitizer misonidazole was combined with 1311‐A5B7, it significantly prolonged tumour‐growth inhibition over radio‐antibody alone. Conversely, the therapeutic effect of either radio‐antibody was significantly reduced when used in combination with the halogenated pyrimidine radiosensitizer 5‐iododeoxyuridine. Neither sensitizer alone affected tumour growth.
Activation of ras oncogenes and expression of tumor‐specific transplantation antigens in methylcholanthrene‐induced murine fibrosarcomas
Authors: Carbone Giusi , Borrello Maria Grazia , Molla Alessandra , Rizzetti Maria Grazia , Pierotti Marco A. , Porta Giuseppe Della , Parmiani Giorgio 
Published: February 2007

AbstractThe DNA of 22 fibrosarcomas, newly induced in BALB/c mice by subcutaneous doses of 3‐methylcholanthrene (3‐MCA), was tested in NIH 3T3 transformation assay. Activation of K‐ras and N‐ras was found in 7 and 3 cases respectively. No H‐ras activation was detected. Polymerase chain reaction and oligonucleotide hybridization performed on the DNA of the 22 sarcomas revealed 5 cases of K‐ras mutation at codon 12, 3 at codon 13 and I at both codons. One case of K13 mutation was not detectable by transfection. Three cases of mutation at codon 61 of N‐ras were also found, one of which was simultaneous with a K12 mutation. Tumor‐specific transplantation antigens (TSTA) were assessed in the 22 original tumors. Altogether 16 sarcomas were immunogenic, with the highest frequency of TSTA tumors (10/11 and 5/6) in the groups given 1.0 and 0.1 mg of 3‐MCA respectively, the lowest (1/5) in that with 0.01 mg of carcinogen; ras mutations occurred in the DNAs of 11 out of the 16 TSTA+ sarcomas, but none of the DNAs of the 6 TSTA‐ tumors showed ras mutation. The results suggest that 3‐MCA‐induced transformation of subcutaneous fibroblasts can involve mutations in codons 12, 13 or 61 of K‐ and N‐ but not H‐ras gene and that such mutation is accompanied by the expression of TSTA.
Involvement of ornithine decarboxylase in the control of proliferation of the HT29 human colon cancer cell line. effect of vasoactive intestinal peptide on enzyme activity
Authors: Gamet Laurence , Cazenave Yolande , Trocheris Véronique , Denis‐Pouxviel Colette , Murat Jean‐Claude 
Published: February 2007

AbstractInvolvement of ornithine decarboxylase (ODC) in proliferation of the HT29 cell line and its control by either fetal calf serum (FCS) or vasoactive intestinal peptide (VIP) as an external signal increasing cAMP level were investigated. Activation of the polyamine‐producing system appears to be a necessary step in the proliferative response of HT29 cells since cell growth is arrested by addition of difluoromethylornithine (DFMO, an inhibitor of ODC), then restored by further addition of putrescine into the culture medium. FCS deprivation results in decreased activity of ODC and arrest of cell growth. Addition of FCS induces reactivation of ODC peaking at 9 hr and re‐initiates proliferation but does not affect cAMP level. VIP strongly and rapidly stimulated cAMP accumulation, which resulted in significant activation of ODC. When VIP‐induced cAMP formation was hindered by the alpha2‐adrenergic agonist UK 14304, activation of ODC was no longer observed. The dose‐response curve for ODC activation by VIP indicates an EC50 value of 0.078 nm which falls within the range of physiological concentrations for this peptide. However, VIP fails to stimulate proliferation when cells are cultured either in an FCS‐free medium or in the presence of a growth‐limiting concentration of FCS. We conclude that the mechanisms of ODC activation by either FCS or VIP are different, the latter involving cAMP formation. Activation of ODC to produce polyamines is necessary to support the proliferative process in our model but the VIP‐induced activation of the enzyme alone is not sufficient to promote cell growth.
Presence of circulating anti‐c‐myb oncogene product antibodies in human sera
Authors: Sorokine Irène , Ben‐Mahrez Kamel , Bracone Annie , Thierry Dominique , Ishii Shunsuke , Imamoto Fumio , Kohiyama Masamichi 
Published: February 2007

AbstractBacterially expressed mouse c‐myb protein was purified from E. coli extracts and used as antigen to screen human sera for circulating anti‐c‐myb oncogene product antibodies. Using Western blotting, we have found that human sera contain IgG antibodies to the c‐myb gene product. The percentage of positive sera in cancer patients appears to be dependent upon cancer type and is significantly higher in breast‐cancer patients than in normal donors: 43% of sera from breast‐cancer patients are positive, whereas in neuroblastoma cancer patients the production of IgG anti‐c‐myb appears to be rare. No significant correlation was observed between the presence of circulating anti‐c‐myb antibodies and the expression of the c‐myb gene in breast tumors.
Increasing incidence of cancers associated with the human immunodeficiency virus epidemic
Authors: Rabkin Charles S. , Biggar Robert J. , Horm John W. 
Published: February 2007

AbstractWe examined data from San Francisco and other areas participating in the Surveillance, Epidemiology, and End Results (SEER) Program to determine the effect of the human immunodeficiency virus (HIV) epidemic on cancer incidence between 1973 and 1987. In this period, non‐Hodgkin's lymphoma incidence has increased over 10‐fold and Kaposi's sarcoma incidence has increased over 5000‐fold in single San Francisco men 20 to 49 years of age. Increases in non‐Hodgkin's lymphoma have been restricted to high‐grade and diffuse large‐cell (intermediate‐grade) histological types. With the exceptions of non‐Hodgkin's lymphoma and Kaposi's sarcoma, no other tumor has significantly increased in incidence. During 1987, we estimate that HIV‐seropositive men in San Francisco had a 0.47% risk of developing non‐Hodgkin's lymphoma and a 1.6% risk of developing Kaposi's sarcoma. The relative risks for non‐Hodgkin's lymphoma and Kaposi's sarcoma associated with HIV infection were 104 and 40,000, respectively. For 1987, HIV was associated with 14% of all reported cancers (except non‐melanoma skin cancer) in men aged 20 to 49. We expect that 1,890 to 2,730 excess cases of non‐Hodgkin's lymphoma and 6,490 to 8,320 excess cases of Kaposi's sarcoma will occur in the United States in 1990.
The high lysability by lak cells of colon‐carcinoma cells resistant to doxorubicin is associated with a high expression of ICAM‐1, LFA‐3, NCA and a less‐differentiated phenotype
Authors: Rivoltini Licia , Cattoretti Giorgio , Arienti Flavio , Mastroianni Antonio , Melani Cecilia , Colombo Mario P. , Parmiani Giorgio 
Published: February 2007

AbstractA human colon‐carcinoma ceil subline resistant to doxorubicin (LoVo/Dx), previously shown to be more lysed than the chemosensitive subline LoVo/H by different immune effectors, is reported here to be similarly susceptible to direct, anti‐proliferative effect of soluble cytokines (TNF‐α and/or IFN‐γ). More adhesion molecules ICAM‐1, LFA‐3 and NCA were expressed on LoVo/Dx than on LoVo/H, while no significant amounts of CEA were detectable on the cell surface or in culture supernatant of either tumor subline. Anti‐ICAM‐1, anti‐LFA‐3 and anti‐NCA monoclonal antibodies (MAbs) caused a marked reduction of lysis by interleukin‐2 (IL‐2) activated lymphocytes (LAK) of LoVo/Dx, whereas a lower effect was evident on LoVo/H. A pool of these antibodies was able to further increase the inhibition of the LAK lysis of both sublines. LoVo/Dx displayed a less differentiated phenotype as assessed by morphology, in vitro growth and altered or increased expression of markers such as desmoplakin and vimentin respectively, and disappearance of mucin. Treatment of LoVo sublines with differentiating agents (dimethylformamide and retinoic acid) led to a decreased expression of all adhesion molecules studied, accompanied by increased resistance to LAK‐mediated lysis. These data indicate that sensitivity of chemoresistant tumor cells to cytotoxic effectors depends on the level of expression of adhesion molecules, including NCA, and is related to differentiation stage.
Type‐II insulin‐like growth‐factor receptor in conditioned medium from HT‐29 human colon carcinoma cell line
Authors: Garrouste Françoise , Remacle‐Bonnet Maryse , Culouscou Jean M. , Marvaldi Jacques , Pommier Gilbert 
Published: February 2007

AbstractThe HT‐29 human colon cancer cell line has previously been shown to secrete high amounts of insulin‐like growth factor II (IGF‐II). The recent demonstration that soluble IGF‐II/ mannose 6‐phosphate receptor was present in fetal serum prompted us to search for a release of type‐II IGF receptor by these human colonic carcinoma cells. Serum‐free conditioned medium from the HT‐29 cell line was gel filtered on Sephadex G‐200. There was significant binding of [125I]IGF‐II to the void volume fractions in addition to binding to the 40‐kDa IGF‐binding protein (IGF‐BP) fractions. Competitive binding studies using [l25I]IGF‐II and the void volume pool showed a pattern typical of the type‐II receptor. It exhibited a high affinity for IGF‐II (KD = 0.4 nM), but had a low affinity for IGF‐I (KD = 6.8 nM), and no detectable affinity for insulin. Additional evidence was provided by affinity cross‐linking of [l25I]IGF‐II to the same high‐molecular‐weight material which demonstrated a major specific band at 250kDa after reduction of disulfide bonds. In contrast, the type‐I IGF receptor was undetectable. The extracellular type‐II IGF receptor was not a significant carrier for IGF‐II since virtually all IGF‐II secreted by HT‐29 cells was associated with IGF‐BP. The presence of a soluble IGF‐II/mannose 6‐phosphate receptor in the culture medium from colonic cancer cells suggests that it may play an important role in tumor pathogenesis.