bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prevalence of epstein‐barr virus DNA in different T‐cell lymphoma entities in a European population
Authors: Ott German , Ott M. Michaela , Feller Alfred C. , Seidl Stephan , Müller‐Hermelink Hans Konrad 
Published: February 2007

AbstractThe Epstein‐Barr virus (EBV) has been classically associated with nasopharyngeal carcinoma and Burkitt's lymphoma, a monoclonal B‐cell non‐Hodgkin's lymphoma. Since the EBV genome has also been found in post‐transplant lymphomas and lymphomas arising in individuals infected with the human immunodeficiency virus, evidence has now accumulated that EBV might be the initiator of a multi‐step process leading from polyclonal B‐cell hyperplasias to monoclonal lymphoma. In a retrospective study of 60 T‐cell lymphomas of various types, we found EBV DNA in 21 (35%) using Southern‐ and/or dot‐blot techniques. Eight of 14 nodal samples of angio‐immunoblastic lymphadenopathy (57%) were shown to harbour detectable EBV DNA. The tumour with the next highest frequency, 47% (7/15 cases analyzed) was pleomorphic T‐cell lymphoma, medium‐ and large‐cell type; EBV was found both in nodal and in extranodal lymphomas of this type. Lymphoepitheloid (Len‐nert's) lymphoma and large‐cell anaplastic lymphoma were positive in 2/5 and 3/8, respectively, of the cases analyzed. No viral DNA could be demonstrated in 3 T‐immunoblastic and 5 T‐lymphoblastic lymphomas. Clonotypic analysis revealed monoclonal as well as oligoclonal virus populations. Our data suggest that, at least in some of these entities, the presence of the EBV genome might be due to secondary mechanisms such as escape from immune surveillance.
Immunorecognition of different ganglioside epitopes on human normal and melanoma tissues
Authors: Bernhard Helga , Roth Sigrid , Bauerschmitz Jürgen , Büschenfelde Karl‐Hermann Meyer Zum , Dippold Wolfgang 
Published: February 2007

AbstractThere is increasing evidence that cell‐surface gangliosides play a role in tumor growth, progression and metastases. In order to determine the frequency of ganglioside GD3 in patients with metastatic malignant melanoma for further therapeutic trials, GD3 ganglioside expression was determined in 119 tissue samples. Of these melanomas, 93% (111/119) were R‐24‐positive, which indicates the value of this diagnostic marker for melanoma. To study the structural epitopes of gangliosides, 10 ganglioside antibodies with defined specificities and affinities were tested on over 100 fresh‐frozen tissue specimens of human normal and melanoma tissues. All the antibodies tested recognize the ganglioside GD3, but vary in their cross‐reactivity with other gangliosides. According to their epitope specificity, they can be divided into 5 groups. For example, the antibodies Z‐21 and A‐4 react like the previously established MAb R‐24 with gangliosides GD3 and GQIb, and one MAb (Q‐4) detects all gangliosides containing 2 connected sialic acids (GD3, GD2, GDIb, GTIb, GQIb). Specificity on TLC does not always correlate with specificity to melanoma tissues and vice‐versa. For example, MAb A‐4, which recognizes only GD3 and GQI b on TLC, shows no specific reactivity on tissues. Furthermore, antibodies with the same ganglioside specificity do not have the same staining pattern on human tissues. For example, MAb Z‐21, which is directed against the same gangliosides as MAb R‐24 on TLC, does not cross‐react with as many neuroectodermal tissues as MAb R‐24. Because of their distinct properties, some of these antibodies may be even more useful for immunodiagnosis and immunotherapy of malignant melanoma than MAb R‐24.
High HTLV‐I proviral DNA level associated with abnormal lymphocytes in peripheral blood from asymptomatic carriers
Authors: Tachibana Nobuyoshi , Okayama Akihiko , Ishihara Shirou , Shioiri Shigemasa , Murai Koichi , Tsuda Kazunori , Goya Naoko , Matsuo Yasuko , Essex Max , Stuver Sherri , Mueller Nancy 
Published: February 2007

AbstractThe level of proviral DNA in peripheral blood mononuclear cells from a representative group of asymptomatic HTLV‐I carriers in Miyazaki district, an HTLV‐I endemic area in Japan, was determined by a single‐cycle polymerase chain reaction method (PCR). Of 217 subjects, 26% had a high level of proviral DNA, 43% a medium level, 18% a low level, and 13% an undetectable level. In the high‐DNA group, 60% had at least 0.6% abnormal lymphocytes on peripheral blood smears, significantly higher than in those with low DNA levels (19%). This association was present for men of all ages and for women under 55. Men were more than twice as likely to have abnormal lymphocytes as well as high levels of proviral DNA. These differences may reflect different host responses to the virus by sex or by the time or route of infection. This study supports the utility of PCR for molecular screening in epidemiologic studies of the natural history of HTLV‐I, and may lead to the identification of those carriers who are at greatest risk of developing HTLV‐l‐induced malignancy.
Enhancement by stable butyrate derivatives of antitumor and antiviral actions of interferon
Authors: Pouillart Philippe , Cerutti Italina , Ronco Gino , Villa Pierre , Chany Charles 
Published: February 2007

AbstractThe use of n‐butyric acid has been associated with induction of cell differentiation and bypassing of genetic defects in the suppression of malignancy. This biological response modifier satisfies the requirements for specificity and low toxicity, and its use can be considered as an alternative approach to conventional cancer chemotherapy. However, a lack of clinical efficacy has been observed with butyrate and attributed mainly to the rapid metabolism of the compound. Butyric acid pro‐drugs derived from monosaccharides such as 3‐O‐butanoyl‐1,2‐O‐isopropylidene‐α‐D‐glucofuranose (MAG=3but) have consequently been devised. Pharmacokinetic and biological advantages of MAG=3but have been previously described. In the present report, we have studied the effect of MAG=3but on murine interferon‐α,β (IFN) anticellular, antitumor and antiviral activities, In vitro, it appears that MAG=3but predisposes malignant MSV cells to a later, complete establishment of the antiproliferative and the cell‐differentiating effects of IFN, and the antiviral action of the latter in the same line of cells infected with encephalomyocarditis (EMC) virus. In vivo, combined treatment with MAG=3but and IFN protects mice effectively against the fatal development of ascitic sarcoma 180 TG and the lethal effect of EMC virus infection.
The growth rate of two transplantable murine tumors, 3ll lung carcinoma and b16f10 melanoma, is influenced by Hyal‐1, A locus determining hyaluronidase levels and polymorphism
Authors: de Maeyer Edward , De Maeyer‐Guignard Jaqueline 
Published: February 2007

AbstractThe effect of 2 different levels of serum hyaluronidase on tumor development was studied by comparing the development of 2 transplantable tumors, the 3LL lung carcinoma and the B16F10 melanoma, in mice of the C57BL/6 and the congenic HW23 strains. The reasoning behind the study was that, in vitro, removal by hyaluronidase of the hyaluronan present in the extracellular matrix of tumor cells renders the latter more accessible to effector T cells. In the mouse, the levels and molecular forms of circulating hyaluronidase are under the influence of different alleles at the Hyal‐1 locus on chromosome 9. C57BLJ.6 mice which have the Hyal‐1b allele have only a 60,000‐kDa form of hyaluronidase in the circulation, whereas the congenic HW23 strain has, on a C57BL/6 background, the BALB/c‐derived Hyal‐1,2 allele, characterized by the presence of the 60‐, 120‐ and 140‐kDa forms and of 3 times as much enzyme activity as the CS7BL/6 strain. These 2 mouse strains that are genetically almost identical can therefore be used to compare the effect of different levels of circulating hyaluronidase on tumor development. Two different tumors were studied: the 3LL lung carcinoma and the B16F10 melanoma. After intra‐footpad inoculation, both tumors developed more slowly in the congenic Hyal‐1,2 HW23 strain, as measured by a slower rate of increase in local tumor size and by a prolonged survival time. These results are in favor of the hypothesis that the Hyal‐1,2 allele, determining higher hyaluronidase levels, enhances resistance to tumor development.
Inhibitions by 6‐hydroxydopamine and neostigmine singly or together of gastric carcinogenesis induced by N‐methyl‐N′‐nitro‐n‐nitrosoguanidine in wistar rats
Authors: Tatsuta Masaharu , Iishi Hiroyasu , Baba Miyako , Taniguchi Haruo 
Published: February 2007

AbstractThe effects of chemical sympathectomy induced by 6‐hydroxydopamine (6‐OHDA) and administration of the acetylcholinesterase inhibitor neostigmine, singly or together, on gastric carcinogenesis induced by N‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG), and on the tissue catecholamine concentration of the gastric wall and the labeling index of the gastric mucosa, were investigated in inbred Wistar rats. Rats received s.c. injections of neostigmine (0.075 mg/kg), and/or i.p. injections of 6‐OHDA (42 mg/kg twice within 24 hr, and then 105 mg/kg every 2 weeks from I week later) 25 weeks after oral treatment with MNNG. Prolonged administration of 6‐OHDA or neostigmine significantly reduced the incidence of gastric cancers by week 52, and in combination they had a significantly greater inhibitory effect. 6‐OHDA and/or neostigmine had no influence on the histology of gastric cancers. Administration of 6‐OHDA, but not neostigmine, significantly decreased the norepinephrine concentration in the antral portion of the gastric wall. The labeling index of the antral mucosa was decreased significantly by treatment with 6‐OHDA or neostigmine, and decreased even more significantly by 6‐OHDA plus neostigmine. Our findings indicate that 6‐OHDA and neostigmine have protective effects against gastric carcinogenesis and that in combination their effects are additive. These results imply that the activities of the sympathetic and parasympathetic autonomic systems together influence gastric carcinogenesis. © 1992 Wifey‐Liss, Inc.
A combination of two immunotoxins exerts synergistic cytotoxic activity against human breast‐cancer cell lines
Authors: Crews Jennie R. , Maier Lisa A. , Yu Yin Hua , Hester Susan , O'Briant Kathy , Leslie David S. , Desombre Karen , George Stephen L. , Boyer Cinda M. , Argon Yair , Bast Robert C. 
Published: February 2007

AbstractIn previous studies, combinations of immunotoxins reactive with different cell‐surface antigens have exerted additive cytotoxicity against tumor cells in culture. In this report we describe a combination of 2 immunotoxins that produce synergistic cytotoxic activity. Recombinantly derived ricin A chain (RTA) was conjugated with murine monoclonal antibodies (MAbs) 317G5, 260F9, 454A12 and 741F8 that bound to cell‐surface determinants of 42, 55, 180 (transferrin receptor) and 185 kDa (HER‐2/neu) expressed by the SKBr3 human breast‐cancer cell line. When inhibition of clonogenic growth was measured in a limiting dilution assay, the combination of 260F9‐RTA and 454A12‐RTA produced synergistic cytotoxic activity against SKBr3 and 2 other breast‐cancer cell lines. All other combinations produced only additive inhibition of clonogenic growth. Simultaneous binding of 260F9 and 454A12 was not supra‐additive, but sub‐populations of cells which lacked one or the other antigen could be detected. Kinetic studies of internalization, using antibodies conjugated with gold particles, indicated that 454A12 remained within peripheral endosomes for a longer interval in the presence of 260F9. This change in the traffic of the transferrin receptor may contribute to synergy between 260F9‐RTA and 454A12‐RTA. © 1992 Wifey‐Liss, Inc.
The effect of parity, tumor latency and transplantation on the activation of int loci in mmtv‐induced, transplanted C3H mammary pre‐neoplasias and their tumors
Authors: Schwartz Marlene S. , Smith Gilbert H. , Medina Daniel 
Published: February 2007

AbstractMouse mammary tumor virus (MMTV) infection of mammary glands results in proviral insertion into host DNA and activation of cellular genes. Clonal expansion of cells bearing insertional mutations results in hyperplastic alveolar nodules (HAN) and tumors. HAN, transplanted into epithelium‐cleared mammary fat pads, form hyperplastic alveolar outgrowths (HOGs). Previous work indicates the commonly MMTV‐activated genes wnt‐1 and int‐2 are rarely affected in HOGs and HOG‐derived tumors. To determine the basis of the dichotomy between the frequency of wnt/int gene activation in HOG‐derived tumors and tumors from breeders of the identical inbred mouse strain, we compared the activation of wnt‐1, int‐2 and int‐3 in tumors from virgin and breeding C3H mice, in consecutive primary tumors arising in individual C3H breeders and in C3H HOGs at early passages. Activation of wnt‐1 or int‐2 was rare in HOG‐derived tumors (6% and 0%) compared with primary tumors in breeders (52% and 14%). int‐3 was never found to be activated, wnt‐1 was activated in the same percentage of primary tumors from virgins as from breeders, int‐2 was activated only in tumors from breeders, wnt‐1 activation also did not correlate with shorter tumor latency in multiple tumors from individual breeders, wnt‐1 RNA was not detected in HOGs at early transplant generations, however, low levels of wnt‐1 RNA were variably found in the epithelium of virgin mammary glands. We cannot explain why C3H HOGs and their derivative tumors develop without wnt‐1 expression when the majority of C3H primary mammary tumors possess an MMTV‐activated wnt‐1 gene. © 1992 Wifey‐Liss, Inc.
Accumulation of allelic loss on arms of chromosomes 13q, 16q and 17p in the advanced stages of human hepatocellular carcinoma
Authors: Nishida Naoshi , Fukuda Yoshihoro , Kokuryu Hiroyuki , Sadamoto Tetuo , Isowa Gohei , Honda Kazuo , Yamaoka Yoshio , Ikenaga Mituo , Imura Hiroo , Ishizaki Kanji 
Published: February 2007

AbstractWe examined loss of heterozygosity at 13 loci on 5 chromosomes in hepatocellular carcinomas (HCCs) from 56 patients. In 42 of these cases, regenerative nodules of liver cirrhosis were also analyzed. High frequencies of allelic losses were detected on chromosomes 13q (47%), 16q (40%) and 17p (64%), whereas losses on chromosome 4p and 11 p were observed in less than 22% of cases in HCCs. In contrast, LOH was not detected on any loci in cirrhotic nodules. On chromosome 13q, the common region of allelic loss was mapped to the region including the retinoblastoma (RB) locus, by using 8 polymorphic probes. Furthermore, one case with 13q loss had an interstitial deletion of the RB gene, indicating the involvement of inactivation of the RB gene in hepatotumorigenesis. Losses were associated with portal‐vein thrombosis or intrahepatic metastasis, increased tumor size, a poorly differentiated phenotype and clinical stage. Losses occurring together on 13q, 16q and 17p were significantly higher in patients in clinical stage IV or histologically poorly differentiated tumors, suggesting that the accumulation of allelic loss occurs in advanced tumors and that patients with multiple allelic losses may have a worse prognosis than those with a single loss.
Immunocytodiagnosis of atypical hyperplasia and endometrial carcinoma in post‐menopausal women
Authors: Mottolese Marcella , Vocatjro Amina , Bartolazzi Armando , Vocaturo Giuseppe , Benevolo Maria , Sedati Alfonso , Atlante Giuseppe , Prat Maria , Bigotti Aldo , Natali Pier Giorgio 
Published: February 2007

AbstractIn the present study we have evaluated whether monoclonal antibodies (MAbs) B72.3 and AR‐3 which display, on histological preparations, a differential reactivity with normal and transformed endometrium, could be a useful adjunct to endometrial cytology in the identification of pre‐neoplastic and neoplastic conditions. Immunocytochemical (ICC) tests, using the 2 reagents, were performed on normal cycling endometrium and on hyperplastic and malignant lesions collected by the endocyte technique both from 86 surgically resected specimens and from 62 postmenopausal symptomatic and asymptomatic outpatients. The results obtained showed that the combination of the 2 MAbs can complement conventional morphology in the identification of pre‐malignant atypical lesions and endometrial carcinoma of unclear cytological features, thus allowing a selection of those patients who are candidates for fractional curettage.
Expression of c‐sis and c‐fos genes in human meningiomas and neurinomas
Authors: Riva P. , Larizza L. 
Published: February 2007

AbstractThe HindIII c‐sis RFLP was analyzed in constitutional and tumor DNAs of 19 meningioma patients. Loss of a c‐sis allele (allele 1 in all cases) was observed in 6 out of 10 tumors from heterozygous patients. No alteration in the structure or dosage of the c‐sis gene was detected in any tumor sample. Northern analysis of c‐sis evidenced sis transcripts in 7 out of 8 meningiomas which were amenable to analysis. All tumors expressing c‐sis also expressed c‐fos, suggesting that the autocrine loop elicited by sisactivation may have c‐fos as its nuclear target. Co‐expression of c‐sis and c‐fos was also observed in 5 neuromas out of 7 analyzed. Very high levels of fos‐mRNA were observed in 2 neuromas, but were not found to be caused by apparent alteration or amplification of the c‐fos gene.
HOX gene expression in normal and neoplastic human kidney
Authors: Cillo C. , Barba P. , Freschi G. , Bucciarelli G. , Magli M. C. , Boncinelli E. 
Published: February 2007

AbstractAs a consequence of transformation, cancer cells generally lose some of their differentiative properties. Thus, alterations interfering with the genetic mechanisms required to maintain embryonic determination could lead to tumorigenesis. Ho‐meobox genes are a network of genes encoding nuclear proteins containing DNA‐binding homeodomains that are highly conserved throughout evolution. They are expressed in a stage‐related fashion in the developing embryo and, in adult life, in normal tissues. In mice and humans, homeobox genes of the HOX family are organized in 4 clusters on different chromosomes which have presumably evolved by duplication of a primordial gene cluster. Strikingly, the order of genes within each cluster is also highly conserved throughout evolution, suggesting that the physical organization of HOX genes might be essential for their expression. Recent reports indicate that homeobox mutant mice display morphological abnormalities or show neoplastic alterations, and that growth factors can turn on homeobox genes. We have studied the expression of the Antennapedia‐like HOX genes in normal human kidney and in renal carcinomas. The great majority of the HOX genes analyzed are expressed in a peculiar manner in normal kidney: blocks of genes, even entire HOX loci, are coordinately regulated. Alterations in HOX gene expression in renal carcinoma can be observed in 2 genes of the HOX‐2 locus, HOX‐2A and HOX‐2E, which are actively expressed in normal kidney and silent in cancer biopsies. The HOX‐3H gene is not expressed in normal kidney whereas the HOX‐3H transcripts are present in renal carcinomas. Homeobox genes within the 4 HOX loci can be aligned on the basis of the maximal sequence homology of their homeodomains: this alignment defines 13 paralogous gene groups. In renal carcinomas, genes of group 10 (HOX‐1D, 2F, 3E, 4B) display a marked difference in their transcript classes when compared to those of normal kidney. Our findings suggest an association between altered HOX gene expression and kidney cancer.
Alcoholism and liver cirrhosis in the etiology of primary liver cancer
Authors: Adami Hans‐Oiov , Hsing Ann W. , McLaughlin Joseph K. , Trichopoulos Dimitrios , Hacker David , Ekbom Anders , Persson Ingemar 
Published: February 2007

AbstractThe aim of this study was to determine the risk of developing primary liver cancer in patients with a diagnosis of alcoholism, liver cirrhosis, or both. Three population‐based, mutually exclusive cohorts were defined on the basis of hospital discharge diagnoses between 1965 and 1983. Complete follow‐up through 1984—excluding the first year of follow‐up—showed that among 8,517 patients with a diagnosis of alcoholism, 13 cancers occurred, vs. 4.2 expected (standardized incidence ratio (SIR) = 3.1; 95% confidence interval (CI) = 1.6 to 5.3); among 3389 patients with liver cirrhosis, 59 cancers occurred, vs. 1.7 expected (SIR = 35.1; 95% CI = 26.7 to 45.3), and among 836 patients with both diagnoses, 11 cancers occurred, vs. 0.3 expected (SIR = 34.3; 95% CI = 17.1 to 61.3). Thus, alcoholism alone entailed a moderately increased risk and alcoholism with liver cirrhosis did not increase the high relative risk for liver cancer more than cirrhosis alone. We conclude that alcohol intake may be a liver carcinogen only by being causally involved in the development of cirrhosis; and further, that the risk of developing liver cancer following cirrhosis in this population is similar to or higher than that after chronic hepatitis‐B‐virus infection in other Western countries.
The effect of schedule, protein binding and growth factors on the activity of suramin
Authors: Lopez Rafael Lopez , Peters Godefridus J. , van Loenen Arie C. , Pizao Paulo E. , van Rijswijk Ruud E. N. , Wagstaff John , Pinedo Herbert M. 
Published: February 2007

AbstractSuramin has been shown to have antiproliferative activity, either by blocking the binding of growth factors to their receptors or by inhibiting critical cellular enzymes. In 6 different cell lines from 5 tumour types (MCF‐7, MCF‐7/ADRR, PC3, HT‐29, UM‐SCC‐IIB and SW‐1573/1R500), we studied the effect of scheduling of suramin, of FCS and of human serum albumin (HSA), of epidermal growth factor (EGF) and of the addition of growth factors in serum‐free medium on the activity of suramin. The concentration of suramin which gave 50% growth inhibition (IC50) varied from 45 μM in SW‐I573/IR500 to 153 μM in PC3 cells grown in medium supplemented with 5% FCS, after 6 days of continuous exposure. Exposure for more than 4 days did not enhance the sensitivity to suramin, except in PC3. At exposure to suramin for 1 day followed by 5 days recovery, high IC50 values (>0.5 mM) were observed in MCF‐7 cells. In medium with 1% and 0.5% FCS these values were 3 to 8 and 14 to 26 times lower respectively. Addition of HSA increased the IC50 in PC3 and MCF‐7 cells. Suramin binding to protein was dependent on the concentration of protein and of suramin. Excess of EGF in medium with different FCS concentrations did not change the IC50 values of suramin in PC3 and MCF‐7 cells. Addition of EGF, fibroblast growth factor or platelet‐derived growth factor in PC3 cells cultured in serum‐free medium did not increase the IC50 values. Suramin was active against these 6 cell lines at clinically achievable concentrations. This activity varied depending on the cell line, exposure time and suramin concentration. The most significant factor interfering with sensitivity to suramin was the amount of protein present in the culture medium.