bluuebunny/crossref_metadata_2025_split huggingface dataset:
Involvement of leukocyte (β2) integrins (CD18/CD11) in human monocyte tumoricidal activity
Authors: Bernasconi Sergio , Peri Giuseppe , Sironi Marina , Mantovani Alberto 
Published: February 2007

AbstractAppropriately activated mononuclear phagocytes mediate contact‐dependent tumoricidal activity. Adhesion structures involved in contact‐dependent tumor cytotoxicity have not been defined. The present study was aimed at identifying the adhesion structures involved in the tumoricidal activity of activated (IFN‐γ + LPS) human monocytes. Tumor cells of different histological origin were used as targets in a 48‐hr cytolysis assay. Anti‐CD18 (integrin β2 chain) monoclonal antibodies (MAbs) substantially (50–40%) inhibited human monocyte cytotoxicity. When the role of different a‐chains was studied, anti‐αL (CD11a, LFA1), anti‐αM (CD11b, Mac‐1) and anti‐αX (CD11c, p150.95) caused marginal inhibition, but the effect of the 3 combined was comparable to that of anti‐CD18. Anti‐CD 18 MAb did not affect the release of various cytotoxic molecules (e.g. TNF) by activated human monocytes. Activated monocytes showed augmented binding to target cells and anti‐CD18 MAb inhibited the binding of resting and activated monocytes to tumor target cells. While IFN‐γ alone augmented expression of leukocyte integrins and LPS had no effect, the 2 activation signals, combined for optimal stimulation of tumoricidal activity, resulted in no appreciable increase in these leukocyte adhesion molecules, as assessed by flow cytometry. Our results suggest that the augmented CD 18‐dependent binding of activated monocytes on tumor cells depends mainly upon changes in the adhesive properties of these molecules rather than upon increased numbers on the cell surface. Anti‐1CAM‐1 MAb significantly reduced monocyte cytotoxicity on tumor cells, which is consistent with a role of the CD11/CD18 adhesion pathway. These results implicate “activated”︁ leukocyte (β2) integrins (CD11 /CD18) as important adhesion molecules in the contact‐dependent tumoricidal activity of human monocytes.
Comparison of neutralization of BPV‐1 infection of C127 cells and bovine fetal skin xenografts
Authors: Ghim Shinje , Christensen Neil D. , Kreider John W. , Bennett Jenson A. 
Published: February 2007

AbstractBPV‐I induces focus formation in murine C127 cells and fibropapillomas in bovine fetal skin xenografts. In this study, we compared the specificity of neutralization of BPV‐I in both assay systems, using sera and monoclonal antibodies (MAbs) selected to define neutralizing epitopes. Sera from rabbits and cattle, inoculated with intact BPV‐1 or BPV‐2 virions, neutralize BPV‐1 infectivity in both C127 cells and xenografts. Selected human sera and murine MAbs that react with intact BPV‐1 particles, serum of a rabbit immunized with denatured BPV‐1 particles, and sera from calves vaccinated with a recombinant L1 fusion protein did not neutralize BPV‐1 infection in either system. It was concluded that neutralization of BPV‐1 infection of C127 cells and bovine fetal skin xenografts by hyperimmune sera is specific and concordant for both assay systems, and involves conformational BPV‐1 capsid epitopes.
The receptor encoded by the human C‐MET oncogene is expressed in hepatocytes, epithelial cells and solid tumors
Authors: Prat Maria , Narsimhan Radha P. , Crepaldi Tiziana , Rita Nicotra M. , Natali Pier G. , Comoglio Paolo M. 
Published: February 2007

AbstractThe human c‐MET oncogene encodes a transmembrane tyrosine kinase (p 190c‐met) with structural and functional features of a growth‐factor receptor. Monoclonal antibodies (MAbs) have been used to investigate the distribution of the c‐Met protein in human normal and neoplastic tissues. By immunofluorescence microscopy homogeneous expression was detected in normal hepatocytes as well as in epithelial cells lining the stomach, the small and the large intestine. Positive staining was also found in epithelial cells of the endometrium and ovary, and in basal keratinocytes of esophagus and skin. By Northern blot analysis, high levels of c‐met messenger RNA were detected in specimens of liver, gastro‐intestinal tract and kidney. c‐met‐specific mRNA was also found in thyroid, pancreas and placenta, in which organs c‐Met protein was barely detectable by immunofluorescence. The antibodies revealed expression of c‐MET protein in hepatomas (11/14), carcinomas of colon and rectum (19/21), stomach (11/22), kidney (16/19), ovary (9/17) and skin (7/17). Carcinomas of the lung (13/20), thyroid (11/13) and pancreas (5/7) were also positive. In these last cases (lung, thyroid and pancreas) tumor cells were homogeneously stained by the antibodies, whereas in their normal counterparts staining was barely detectable. These data suggest that the receptor encoded by c‐MET plays a physiological role in epithelial cell growth and that its expression is altered in human carcinomas.
Herpes simplex virus type 2: A possible interaction with human papillomavirus types 16/18 in the development of invasive cervical cancer
Authors: Hildesheim Allan , Mann Valerie , Brinton Louise A. , Szklo Moyses , Reeves William C. , Rawls William E. 
Published: February 2007

AbstractA case‐control study of 766 histologically confirmed incident cases of invasive cervical cancer and 1,532 hospital and community controls was conducted in Latin America to evaluate the etiologic role of herpes simplex virus type 2 (HSV‐2) and to examine whether HSV‐2 interacts with other risk factors. In addition to a personal interview, all subjects were asked to donate blood samples and cervical swabs for assessment of exposure to HSV‐2 and human papillomaviruses (HPVs) respectively. Ninety‐eight percent of cases and 91% of controls agreed to the interview and blood collection. Women testing positive for HSV‐2 antibodies were found to have a 60% increased risk of cervical cancer compared with seronegative women (95% CI = 1.3, 1.9). Control for education, sexual and reproductive behavior, prior Pap‐smear screening, smoking, oral contraceptive use, HPV‐6/11 DNA, or HPV‐16/18 DNA detection did not materially affect this estimate. No effect modification of HSV‐2 by age, HPV‐6/11 DNA, pregnancies, oral contraceptive use or cigarette smoking was observed. However, a significant interaction was detected between HSV‐2 and HPV‐16/18. Compared with women testing negative to both virus types, those positive for HSV‐2 alone had a RR of 1.2 (95% CI = 0.9, 1.6), those positive for HPV‐16/18 DNA alone had a RR of 4.3 (95% CI = 3.0,6.0), and those positive for both viruses had a RR of 8.8 (95% CI = 5.9, 13.0). These findings corroborate recent laboratory evidence of a possible biological interaction between HSV‐2 and HPV‐16/18 in the development of cervical cancer. Further confirmatory studies are needed, given concerns with potential misclassification of exposure by the laboratory assays utilized.
Cysteine endopeptidase activity levels in normal human tissues, colorectal adenomas and carcinomas
Authors: Shuja Sania , Sheahan Kieran , Murnane Mary Jo 
Published: February 2007

AbstractWe have assayed cysteine endopeptidase activities in 17 types of normal human tissue and in matched sets of colorectal mucosa, adenoma and carcinoma samples. Our data indicate that cathepsin B enzyme levels vary 70‐fold and cathepsin L enzyme levels vary 20‐fold from one normal tissue to another. Cathepsin B specific activity in normal tissues fell into 3 categories. High activity, with a mean of 156.7 ± 41.5 nmoles min−1 mg−1 protein, was measured in liver, thyroid, kidney and spleen; intermediate activity, with a mean of 60.2 ± 8.3 nmoles min−1 mg−1 protein, was measured in heart, colon, adrenal and lung; and low activity, with a mean of 18.4 ± 9.7 nmoles min−1 mg−1 protein, was measured in prostate, testis, nerve, stomach, pancreas, brain, skeletal muscle, skin and breast. Cathespin L specific activity fell into 2 categories. High activity, with a mean of 51.1 ± 4.9 nmoles min−1 mg−1 protein, was measured in thyroid, liver and kidney; and low activity, with a mean of 11.4 ± 5.5 nmoles min−1 mg−1 protein, was measured in spleen, colon, heart, adrenal, lung, testis, brain, nerve, skin, stomach, pancreas, skeletal muscle, prostate and breast. Our characterization of these enzyme levels provides a reference standard for normal cathepsin B and L activities in human tissues that should enhance the detection of their deregulation in disease states. For example, in studies of colorectal carcinoma and normal mucosa, we observed a significant tumor‐specific increase in cathepsin B and L activities with particularly high activity levels in earlier (Dukes′ A and B) compared to later (Dukes′ C and D) stages of colorectal cancer. In contrast, adenomas from colorectal cancer patients expressed normal levels of cathepsin B activity, providing evidence that the increase in expression of cathepsin B may be a sensitive marker for progression from the pre‐malignant to the malignant state in the development of colorectal cancer.
Expression of integrin receptors on 45 clinical neuroblastoma specimens
Authors: Favrot Marie C. , Combaret Valérie , Goillot Evelyne , Lutz Patrick , Frappaz Didier , Thiesse Philippe , Thyss Antoine , Dolbeau Dominique , Bouffet Eric , Tabone Eric , Philip Thierry 
Published: February 2007

AbstractImmunohistological expression of integrins has been analyzed on 45 neuroblastoma specimens representative of the different clinical and histological forms of the tumor. None of the specimens expressed the α5 chain of the integrins. The β1 chain was expressed on all specimens, the α1 chain on 44 specimens and the α3 chain on 42; the 4 specimens which lacked α1 or α3 were stage‐4 neuroblastomas. The α2 chain was expressed on 18 specimens, and the α6 chain on 17;15 reacted with both. Their reactivity was related to the maturation of the tumor rather than the stage of the disease: they were expressed on lowgrade, well‐differentiated specimens; stage 3‐4 neuroblastoma specimens analyzed at diagnosis were negative, but usually expressed both chains when analyzed after in vivo differentiation by chemotherapy. αv reacted with 18 specimens and β3 with 12, without strict relation with the stage of the disease and/or its degree of differentiation; 9 well‐differentiated specimens expressed the β4 chain; only 4 well‐differentiated specimens expressed the α4 chain. The 4 specimens which lacked α1‐β1 or α3‐β1 expression had n‐myc amplification, whereas those which expressed either α4, β4, β3, or αv had no amplification. Furthermore, the expression of the 3 heterodimers α4‐β1, αv‐β3 and α6‐β4 was essentially observed on primary tumors which developed in the mediastinum. The expression of α2‐β1 and α6‐β1 was observed on both n‐myc‐positive and ‐negative specimens. β1 and α3, were diffusely expressed on all counterparts of these tumors, from undifferentiated neuroblasts to ganglion and Schwann cells. The α1 chain reacted with undifferentiated and intermediate neuroblasts as well as with Schwann cells, but ganglion cells were negative. α2 and α6 chains were negative on undifferentiated neuroblasts, variably expressed on intermediate neuroblasts, and restricted to Schwann cells in ganglioneuroma. The expression of α4 and β4 was restricted to Schwann cells. αv and β3 occasionally reacted with undifferentiated and intermediate neuroblasts; αv was strongly positive on Schwann cells but negative on ganglion cells, whereas β3 was positive on both neuronal and non‐neuronal populations.
Epidemiologic assessment of interactions of hepatitis‐C virus with seromarkers of hepatitis‐B and ‐D viruses, cirrhosis and tobacco smoking in hepatocellular carcinoma
Authors: Tzonou Anastasia , Trichopoulos Dimitrios , Kaklamani Evangelia , Zavitsanos Xenophon , Koumantaki Yvonni , Hsieh Chung‐Cheng 
Published: February 2007

AbstractA recently introduced enzyme immunoassay procedure for antibodies against the hepatitis‐C virus (HCV) was used to test samples from 185 cases with hepatocellular carcinoma (HCC) and 432 hospital controls. The anti‐HCV results were examined in conjunction with previously reported data from this study concerning hepatitis‐B virus (HBV) serology, hepatitis‐D virus (HDV) antibodies, presence of cirrhosis and tobacco smoking. There was evidence for interaction between HBV and HCV in the causation of HCC: as previously reported, the rate ratio (RR) linking the presence of anti‐HCV to HCC among subjects positive for hepatitis‐B surface antigen (HBsAg) was substantially higher than the corresponding RR among those negative for this marker; furthermore, among HCC patients positive for HBsAg, a high proportion (33/61) of those who were positive for hepatitis‐Be antigen (HBeAg) or its antibody were positive for anti‐HCV, whereas among HBsAg‐positive controls who were also positive for HBeAg or its antibody, none was positive for anti‐HCV (0/18; p < 10−4. The anti‐HCV‐related RR for HCC was also higher among HCC patients with cirrhosis than among those without evidence of co‐existing cirrhosis (RR 11.4 vs. 4.4; p = 0.06). In addition, there was some evidence of interaction between tobacco smoking and HCV in the origin of HCC; after controlling for age, sex and HBsAg status, the RR for subjects positive for anti‐HCV was 6.8 among smokers but only 3.2 among non‐smokers (p = 0.26). By contrast, there was no suggestion of an interaction between anti‐HCV and anti‐HDV, in agreement with the presumed minimal role, if any, of HDV in HCC etiology. These results support the notion that HCV is involved in the etiology of HCC by advancing, through a chronic liver disease process, carcinogenesis initiated by other factors.
Epstein‐barr virus antibody patterns preceding the diagnosis of non‐hodgkin's lymphoma
Authors: Mueller Nancy , Mohar Alejandro , Evans Alfred , Harris Nancy L. , Comstock George W. , Jellum Egil , Magnus Knut , Orentreich Norman , Frank Polk B. , Vogelman Joseph 
Published: February 2007

AbstractImmunosuppressed patients who develop non‐Hodgkin's lymphoma (NHL) have abnormal antibody responses against the Epstein‐Barr virus (EBV) prior to the diagnosis of malignancy. To see if this is also true of „spontaneous”︁ cases in the general population, we undertook a collaborative serologic case‐control study. From 4 serum banks containing specimens from over 240,000 persons, 104 subjects were identified for whom a blood specimen had been stored an average of 63 months before diagnosis of NHL, and 259 controls matched for age, sex, ethnic group and date of serum collection. The relative risks (RR) for subsequent development of NHL associated with elevated levels of IgG and IgM antibodies against viral capsid antigen were 2.5 (95% confidence interval = 1.1‐5.7) and 3.2 (1.3‐7.5), respectively; these associations increased with age at diagnosis. For the nuclear antigen, the distribution of titers for cases was more restricted than that of controls, with fewer cases having either elevated or low titers, RR = 0.5 (0.2‐1.4) and 0.5 (0.2‐1.2), respectively. Cases had significantly lower antibody titers against the cytomegalovirus, RR = 0.4 (0.2‐0.9). These findings suggest that, at least for some patients, NHL is preceded by an enhanced level of endogenous immunosuppression with resultant EBV activation. This observation supports the role of EBV either directly in the development of NHL or as a primary marker of immune dysfunction.
Expression of lymphocyte homing receptor gene is lost in multi‐drug‐resistant variants of human T‐lymphoblastoid CCRF‐CEM cells
Authors: Cianfriglia M. , Yassen A. , Tombesi M. , Samoggia P. , Barca S. , Caserta M. 
Published: February 2007

AbstractThe 2.2‐kb human cDNA clone PBL32, encoding for the lymphocyte homing receptor (LHR) was used to study the expression of this determinant in multi‐drug‐resistant (MDR) variants of human T‐lymphoblastoid CCRF‐CEM (CEM) cells. LHR is significantly associated with the drug‐sensitive phenotype, its expression being progressively and quantitatively reduced in MDR variants of CEM cells according to the extent of drug resistance.
Anti‐tumoral activity of L and D isomers of aspartic acid β‐hydroxamate on L5178Y leukemia
Authors: Thomasset Nicole , Hamedi‐Sangsari Farid , Tournaire Roselyne , Navarro Claudine , Malley Serge , Goetsch Liliane , Grange Jacques , Vila Jorge 
Published: February 2007

AbstractD and L isomers of aspartic acid β‐hydroxamate (respectively DAH and LAH) were compared for their in vitro and in vivo activity against the murine leukemia L5178Y and their tolerance in vivo in DBA/2 mice. DAH and LAH displayed comparable cytotoxic activity against L5178Y leukemia in vitro. Death of leukemia cells was observed at concentrations above 1.2 mM for both DAH and LAH. High concentrations of L‐asparagine partially reversed the growth‐inhibitory effects of DAH and LAH on L5178Y cells for concentrations of DAH and LAH lower than 0.6 mM. Intraperitoneal administration of DAH and LAH to mice showed that the LD10, LD50 and LD90 of DAH was 3‐ to 4‐fold greater for DAH than for LAH. DAH was able to eradicate L5178Y tumors in mice without inducing toxic deaths, whereas LAH at comparable doses killed all the animals treated.
Establishment of a new human cancer cell line secreting protease nexin‐II/amyloid β protein precursor derived from squamous‐cell carcinoma of lung
Authors: Itoh Hiroshi , Kataoka Hiroaki , Koita Hiroyuki , Nabeshima Kazuki , Inoue Teruhiko , Kangawa Kenji , Koono Masashi 
Published: February 2007

AbstractA new cell line (LC‐1/sq) of human lung squatnous‐cell carcinoma was established from a surgically resected specimen of primary lung cancer. Upon continuous propagation in serum‐free culture medium, it secreted trypsin inhibitors into the conditioned medium. The major fraction of the trypsin inhibitor (TI‐1) was purified to apparent homogeneity by anion‐exchange and gel‐filtration high‐performance liquid chromatography (HPLC) and sodium dodecyl sulfate polyacrylamide gel electro‐phoresis (SDS‐PAGE) followed by transblotting to Immobilon. TI‐1 effectively inhibited trypsin. Chymotrypsin, plasmin and kallikrein were inhibited to a lesser extent, but urokinase‐type plasminogen activator, elastase, thrombin and papain were not inhibited. The activity of TI‐1 was acid‐stable and heat‐resistant, and its molecular weight was 115 kDa by SDS‐PAGE. It exhibited single NH2‐terminal sequence, and its first 20 NH2‐terminal amino‐acid residues were identical with those of protease nexin‐II (PN‐II)/amyloid β‐protein precursor (APP). These characteristics of TI‐1 suggest that the major trypsin inhibitor secreted by LC‐1/sq is indistinguishable from PN‐II/APP. LC‐1/sq is the first lung squamous carcinoma cell line that secretes functionally active trypsin inhibitor, PN‐II/APP, in vitro and is useful for studying its biological significance in malignant tumor.
Recombinant human granulocyte colony‐stimulating factor inhibits the metastasis of hematogenous and non‐hematogenous tumors in mice
Authors: Matsumoto Y. , Saiki I. , Murata J. , Okuyama H. , Tamura M. , Azuma I. 
Published: February 2007

AbstractWe studied the effects of in vivo administrations of recombinant human granulocyte colony‐stimulating factor (rhG‐CSF) on the metastasis of murine hematogenous and non‐hematogenous tumors in spontaneous and experimental metastasis models. Spontaneous lung metastasis caused by intra‐footpad injections of B16‐BL6 melanoma and Lewis‐lung‐carcinoma (3LL) cells were inhibited by intravenous (i.v.) and subcutaneous (s.c.) injections of rhG‐CSF after excision of the primary tumors. Recombinant hG‐CSF significantly inhibited liver metastasis when administered i.v. after i.v. injection of L5178Y‐ML25 T‐lymphoma cells. Multiple i.v. administration of rhG‐CSF after the tumor inoculation prolonged the survival times of mice inoculated i.v. with L5178Y‐ML25 lymphoma cells. Recombinant hG‐CSF did not directly affect the growth of B16‐BL6 and L5178Y‐ML25 cells in vitro. During the administration periods, both i.v. and s.c. injections of rhG‐CSF increased the number of total white blood cells (WBC) in peripheral blood to approximately 3 times the normal level in normal and tumor‐bearing mice. We also found that the administration of rhG‐CSF stimulates neutrophils to become cytostatic against these tumor cells. Our results indicate that the injection of rhG‐CSF is effective in inhibiting lung and liver metastases by activating neutrophils and increasing cell number.
Inhibition by retinoic acid of hepatocarcinogenesis induced by N‐nitrosomorpholine and of expression of myc oncogene protein in sprague‐dawley rats
Authors: Baba Miyako , Iishi Hiroyasu , Yamamoto Reiko , Tatsuta Masaharu 
Published: February 2007

AbstractThe effects of all‐trans‐retinoic acid (RA) on hepato‐carcinogenesis induced by N‐nitrosomorpholine (NNM) and on the expression of myc p 110 proteins were investigated in male Sprague‐Dawlay rats. Rats received i.m. injections of RA twice week and, from the beginning of the experiment, were given drinking water containing NNM for 8 weeks. Pre‐neoplastic and neoplastic lesions staining positively for gamma‐glutamyl transpeptidase (GGT), glutathione‐S‐transferase placental type (GST‐P) or myc p 110 protein were examined histochemically. At week 18, quantitative histological analysis showed that prolonged administration of RA resulted in a significant reduction in the number, size and volume of GGT‐positive and GST‐P‐positive hepatic lesions. Administration of RA also caused significant increase in the proportion of myc p 110‐negative lesions to the total pre‐neoplastic lesions observed. Myc p 110‐negative lesions had a significantly lower mitotic index than myc p 110‐positive lesions. These findings indicate that RA inhibits hepatocarcinogenesis and suggest that this effect may be related to its influence in reducing the expression of myc gene proteins and its subsequent inhibition of cell proliferation pre‐neoplastic lesions.
Risk factors for cancer of the oesophagus in Kerala, India
Authors: Sankaranarayanan R. , Duffy Stephen W. , Padmakumary G. , Nair S. Muralidharan , Day Nicholas E. , Padmanabhan T. K. 
Published: February 2007

AbstractA case‐control study of oesophageal cancer was carried out in Trivandrum, Kerala, involving 267 cases and 895 controls. Risk factors studied in males were pan (betel)‐tobacco chewing, bidi and cigarette smoking, drinking alcohol and taking snuff. Only pan‐tobacco chewing was investigated in females as very few indulged in the other habits. Among males significant associations with higher risk were observed for bidi smoking (p < 0.001), bidi plus cigarette smoking (p > 0.05) and drinking alcohol (p < 0.001). While a significant effect of duration of pan‐tobacco chewing (p < 0.005) was observed in males, there was no significant trend, the risk first falling then rising as duration of use increased. This was partly due to confounding with smoking. No effect of pan‐tobacco use was observed in females. A step‐wise model was fitted, retaining only those risk factors which were significant when adjusted for other factors; the risk factors included were duration of pan‐tobacco chewing, duration of bidi smoking, daily frequency of bidi and cigarette smoking and alcohol use (yes or no). An adjusted relative risk of 2.03 was observed for a pan‐tobacco habit of more than 40 years' duration, of 4.70 for more than 20 years of bidi smoking, of 4.80 for more than 20 bidis/cigarettes per day, and of 2.33 for regular alcohol use (in each category relative to a baseline of those never indulging in the relevant habit).