bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interaction of topoisomerase I inhibitors with radiation in cis‐diamminedichloroplatinum(II)‐sensitive and ‐resistantcells In Vitro and in the fsaiic fibrosarcoma In Vivo
Authors: Bosciai Roseanne E. , Korbut Timothy , Holden Sylvia A. , Ara Gulshan , Teicher Beverly A. 
Published: February 2007

AbstractThe cytotoxicity of the topoisomerase‐I inhibitors, camptothecin and topotecan, toward the SCC‐25 human head‐and‐neck squamous‐carcinoma cells and the SCC‐25/CDDP sub‐line made resistant to cis‐diamminedichloroplatinum(II) was assessed alone and in combination with radiation. Topotecan was less cytotoxic than camptothecin in cell culture and the SCC‐25/CDDP cell line was more sensitive to either topoisomerase‐I inhibitor than was the parental SCC‐25 cell line. Both camptothecin and topotecan were effective radiation sensitizers of hypoxic SCC‐25 and SCC‐25/CDDP cells under normal pH or acidic pH conditions. Sensitizer‐enhancement ratios ranged between I.5 and I.6 for hypoxic SCC‐25 cells and between I.3 and I.5 for hypoxic SCC‐25/CDDP cells. When the ability of campothecin or topotecan to sensitize the FSallC fibrosarcoma to single‐dose radiation was assessed using the tumor‐cell‐survival assay, a sensitizer‐enhancement ratio of I.2 was found with each drug. However, using tumor growth delay of the FSallC fibrosarcoma to determine the effect of camptothecin or topotecan to enhance the efficacy of a daily fractionated radiation regimen, topotecan produced a sensitizer‐enhancement ratio of I.4, while that for camptothecin was I.2. These results indicate that topoisomerase‐I inhibitors may retain activity in CDDP‐resistant cells and may be effective adjuncts to radiation therapy.
Macrophage‐induced cytotoxicity and anti‐metastatic activity of a 43‐kDa human urinary protein against the lewis tumor
Authors: Fontan Elisabeth , Saklani Hélène , Fauve Robert M. 
Published: February 2007

AbstractResident, inflammatory or bone‐marrow macrophages from C57BI/6 mice incubated in vitro with a pure human urinary protein (HGP.43) decreased the growth rate of Lewis tumor cells (3LL). This inhibition of 3LL growth was the result of a cytotoxic activity of these macrophages which was independent of oxygen metabolites and nitrous oxide. Murine monoclonal antibodies (MAbs) against HGP.43 inhibited macrophage‐mediated cytotoxicity. This cytotoxic activity was not due to the release of cytotoxic factors in the culture supernatant, showing that a contact between macrophages and tumor cells was required to express cytotoxicity. The presence of HGP.43 was absolutely necessary during the incubation of macrophages with target cells. In vivo, in HGP.43‐treated mice, the growth of the primary tumor was not delayed but the size and number of lung metastases were significantly reduced 21 days after tumor inoculation.
Effect of drug‐light interval on photodynamic therapy with meta‐tetrahydroxyphenylchlorin in malignant mesothelioma
Authors: Ris Hans‐Beat , Altermatt Hans Jörg , Nachbur Bernhard , Stewart J. Charles M. , Wang Qiang , Lim Chang Kee , Bonnett Raymond , Althaus Ulrich 
Published: February 2007

AbstractThe influence of the time interval (TI) between drug administration and laser activation on selectivity of meta‐tetrahydroxy‐ phenylchlorin(mTHPC)‐mediated photodynamic therapy (PDT) for tumour tissue was assessed in BALB/c nude mice bearing human malignant mesothelioma xenografts. Following i.p. administration of 0.3 mg/kg mTHPC, a light dose of 10 J/cm2 and 0.1 W/cm2 was delivered at 650 nm on the tumour and an equal‐sized area of the hind leg after 4. I2, 24 and 36 hr and 2,3, 4,5 and 6 days to groups of 6 animals (surface irradiance). Then, 72 hr after light delivery, the depth of necrosis was measured in the tumour and in the skin and underlying muscle of the hind leg. Photosensitized necrosis occurred in normal tissue at TI from 4 hr to 3 days and in the tumour at TI from I2 hr to 4 days. The therapeutic ratio of mTHPC‐PDT varied significantly with the time interval between drug administration and laser activation and was greatest at an interval of 3 days. mTHPC concentration was measured in 3 control unirradiated animals at all time points in normal tissues and in tumour tissue, and found to be the same in both tissues. Thus the tissue concentration of mTHPC was of limited use as regards the prediction of photosen‐sitizing effects in the tumour model.
Epstein‐barr virus (EBV) nuclear‐antigen‐2‐induced up‐regulation of cd21 and cd23 molecules is dependent on a permissive cellular context
Authors: Cordier‐Bussat Martin , Billaud Marc , Calender Alain , Lenoir Gilbert M. 
Published: February 2007

AbstractThe Epltein‐Barr virus (EBV) induces unlimited growth of B lymphocytes in vitro, a phenomenon known as immortalization. The elucidation of the mechanisms by which EBV de‐regulates 8‐cell protiiferation in vitro will permit an undemtanding of how the vim contributes in vivo to the genesis of Burkitt's lym‐ phoma (BL) and of lymphopmliierations in immunosuppressed patients. At present, no singie EBV immortalizing gene has been identified, and the hypothesis has been made that many viral genes cooperate in establishing an autocrine loop of secretion leading to irnmortdization. Constitutive expression of B‐cell surface molecules such as CD2l and CD23, specifically impli‐ cated in the control of B‐cell proliferation, is indeed induced at the surface of immortalized B lymphocytes. The expression of the v i d nuclear antigen 2 (EBNA2) has been shown to be in part responsible for CD2l and CD23 upregulation, and EBNA2 is suspected to be a transactivahr of cellular genes, although this point remains to be demonstrated. The role of EBNA2 gene, independently of other vim1 genes, has beeriinvestigated by transfeetion into B‐lymphoma lines, but conflicting results have been reported. To further investigate its role in the regulation ofCD2l and CD23 molecules, we have compared the effects of EBNA2 expression in 2 sets of B‐lymphoma lines infected with P3HRI EBV strain, and/or tmnsfected with EBNA2 gene. We report here that: (i) EBNAZ expression is not a sufficient conditiw to induce CD21 and CD23 upregulation, EBNA2′s effects are highly dependent on the cellular context, and momover can be modffied by infection with P3HRl virus; (ii) EBNA2 inducer acthation of CD23 expression in a very pvticutar way, namely, an increased quantity of CD23 steady‐ state RNA coding for the form A of the protein, which is not detectable at the cell surface but directly secreted. ® 1993 Wiley‐Liss, Inc.
Identification of T‐ and B‐cell epitopes associated with a restricted component of the epstein‐barr virus‐induced early antigen complex
Authors: Pothen Susan , Cao Tin , Smith Richard , Levine Paul H. , Levine Alexandra , Pearson Gary R. 
Published: February 2007

AbstractExperiments were designed in an attempt to identify T‐and B‐cell epitopes expressed on the 17‐kDa early‐antigen‐restricted (EA‐R) polypeptide of the EBV‐induced early antigen complex. Using Berzofsky's algorithm, 3 hypothetical T‐cell epitopes on p 17 were synthesized and employed in EBV‐specific lymphoproliferative assays. Lymphocytes from all EBV‐infected donors responded against one of these epitopes (p 17.1) irrespective of their serological status relative to antibodies to EA‐R. Both CD4+ and CD8+ T‐cell subpopulations from seropositive donors proliferated in the presence of p17.1 in short‐term cultures. These experiments therefore identified one T‐cell epitope on the 17‐kDa polypeptide. In contrast, sera from anti‐EA antibody‐positive individuals reacted with all 3 synthetic peptides to varying degrees, with p 17.1 being the most frequently reactive epitope. When the sera were grouped according to diagnosis, it was noted that 82% of the sera from patients with aggressive lymphomas, whether Africans with Burkitt's lymphoma or North Americans with intermediate‐grade large‐cell or high‐grade B‐cell lymphoma, contained antibody reactive with p17.1, while 64% were reactive with p 17.2 and 29% with p 17.3. In contrast, high anti‐EA antibody‐positive sera from nasopharyngeal carcinoma patients were relatively less reactive with these synthetic peptides (23% positive with p17.1; 19% with p17.2; and 13% with p17.3). These results therefore identified 3 8‐cell EA‐R epitopes which might be potentially useful for clinical or epidemiological studies of EBV‐associated lymphoproliferative diseases.
The value of the 1981 who histological classification in inter‐observer reproducibility and changing pattern of lung cancer
Authors: Campobasso Onofrio , Andrion Alberto , Ribotta Marisa , Ronco Guglielmo 
Published: February 2007

AbstractA series of 722 lung carcinomas, surgically resected and typed some years ago according to the 1967 WHO classification, was independently reviewed by 2 observers in order to test the reproducibility of histopathological typing when using the criteria of the 1981 WHO classification. Typing was fully agreed upon in 87% of cases. Agreement was very high for squamous‐cell, small‐cell and adeno‐carcinomas (K = 0.87,0.89 and 0.85, respectively) while adenosquamous (K = 0.56) and large‐cell (K = 0.71) carcinomas were more controversial categories. A consensus diagnosis was formulated for lesions with discrepant diagnoses. When comparing the final typing to the previous typing based on the 1967 WHO classification, squamous‐and large‐cell carcinomas were reduced respectively by 22% and 33% and adenocarcinomas increased by 94% of the original number. The 1981 “adenosquamous carcinoma” category included 2.8% of the tumours, while the corresponding 1967 category “combined epidermoid and adenocarcinoma” was empty. These changes must be taken into account when considering epidemiological studies, especially those aiming at evaluation of the secular trends of lung cancer by cell type.
Site distribution of cutaneous melanoma in queensland
Authors: Green Adèle , Maclennan Robert , And Phillipa Youl , Martin Nicholas 
Published: February 2007

AbstractThe age‐adjusted incidence rates of cutaneous melanoma in Queensland in 1987 have been analysed for 16 anatomic sites, taking into account their surface areas. In men, the incidence of invasive melanoma on the ears, a chronically sun‐exposed site, was extraordinarily high with annual rates of over 200 per 105 units of surface area in the Queensland population. Next highest rates of over 100 melanomas per 105 units were found on the face, neck, shoulders and back in men and the face and shoulders in women. Comparison with site‐specific incidence rates in the same population 7½ years previously showed that incidence of invasive disease had significantly increased for all these sites, though the largest relative increase in this period occurred on the forearm in both men and women. Melanoma was very rare on the buttocks of both sexes and on the scalp in women, sites which receive the least sun exposure. These findings are consistent with the theory that excessive total sun exposure plays a major role in the aetiology of cutaneous melanoma.
Sequence variation in the E7 gene of human papillomavirus type 18 in tumor and non‐tumor patients and antibody response to a conserved seroreactive epitope
Authors: Ter Meulen J. , Schweigler A. C. , Eberhardt H. C. , Luande J. , Mgaya H. N. , Müller M. , Bleul C. , Ulken V. , Ikenberg H. , Pawlita M. , Gissmann L. 
Published: February 2007

AbstractWe have determined nucleotide sequences of the E7 open reading frame (ORF) of human papillomavirus type 18 (HPV‐18) isolates obtained from 18 cervical carcinomas from Tanzanian and German patients and 8 cervical scrapings from Tanzanian non‐tumor patients. The HPV‐18 prototype sequence was detected in only 3 out of 26 isolates. Silent mutations were found at nt positions 640 and 751, whereas the mutations observed at nt positions 770, 806, 864 and 865 all change the respectively encoded amino acid. The HPV‐18 isolates of 3 German carcinomas showed the same mutations (at position 751) as those of 2 established cervical carcinoma cell lines (HeLa and C4‐1), whereas different mutations were found in 16/23 African isolates (at positions 640 and 864), to which the isolate of cell line SW756 was similar (changes at positions 640 and 865). Seven out of 15 HPV‐18‐positive Tanzanian tumor patients (46.7%) reacted in a peptide ELISA against a recently described seroreactive epitope of the HPV‐18 E7 ORF (nt positions 704‐769). Mutational changes of the E7 ORF were excluded as a possible explanation for the lack of antibody response, because there was no correlation with the serological results. The seroreactive region appears to be well conserved despite geographically varying mutations within the E7 ORF of HPV‐18.
Myoepithelial and basement membrane antigens in benign and malignant human breast tumors
Authors: Guelstein V. I. , Tchypysheva T. A. , Ermilova V. D. , Ljubimov A. V. 
Published: February 2007

AbstractSerial cryostat sections of 160 human breast lesions and of 9 lymph‐node metastases were studied by indirect immunofluores‐cence. We used monoclonal antibodies (MAbs) to lining‐epithelium‐specific keratin 8 and to myoepithelium‐specific keratin 17 in combination with polyclonal and monoclonal antibodies to major basement membrane components, laminin, collagen type IV, entactinhidogen, and large heparan sulfate proteoglycan (perlecan) core protein. Continuous basement membranes adjacent to a basal layer of keratin‐17‐positive myoepithelial cells were typical for normal, benign and in situ carcinomatous structures. In invasive and metastatic structures, always formed by keratin‐8‐positive tumor cells, basement membranes were found only rarely and with conspicuous fragmentations. This lack of basement membranes correlated with loss of myoepithelium identified by staining for keratin 17. In comedo structures of invasive ductal carcinomas and in papillary carcinomas, fibrovascular complexes with numerous blood vessels and deposition of basement membrane material were often seen in the stroma. lmmunomorphological analysis of 41 cases of doubtful diagnosis at intra‐operative biopsy was also performed. A combination of MAbs to keratins 8 and 17, and to basement membrane components, made it possible to distinguish between morphologically similar benign and malig‐nant proliferations and to detect single‐cell invasion of the stroma. This combination of antibodies may be recommended as an auxiliary immunomorphological tool for differential diagno‐sis of intra‐operative breast biopsies in dubious cases.
Expression of functionally intact pdgf‐α receptors in highly metastatic 3ll lewis lung carcinoma cells
Authors: Fitzer‐Attas Cheryl , Feldman Michael , Eisenbach Lea 
Published: February 2007

AbstractThe ability of disseminating tumor cells to grow in a target organ is the final limiting step of the metastatic cascade. The growth of a highly lung‐metastatic clone, D122, of the murine 3LL Lewis lung carcinoma was induced in vitro with lungconditioned media (CM) to a greater extent than that of a weakly metastatic clone, A9. With the use of platelet‐derived growth factor (PDGF)‐α‐receptor‐specific antibodies, the possible paracrine mode of metastatic cell growth was further suggested by demonstrating the presence of these receptors on highly metastatic cells only. Receptors for PDGF have been found almost exclusively on cells of mesenchymal and glial origin. Therefore, the functionality of this receptor in the D122 epithelial cell line was verified by immune complex kinase and ligand‐stimulation assays. Moreover, PDGF was shown to specifically induce in vitro growth of D122 highly metastatic cells only and to be abundantly expressed in lung CM but not in kidney or liver CM. Thus, the interaction of PDGF‐like factors in the lung with PDGF receptors on the metastatic tumor cell may be important in the development of metastatic lesions in the target organ.
Hypersensitivity of human testis‐tumour cell lines to chemotherapeutic drugs
Authors: Masters John R. W. , Osborne Edward J. , Claire Walker M. , Parris Christopher N. 
Published: February 2007

AbstractMetastatic testis tumours, in contrast to most other types of cancer, can be cured by drugs. To investigate which classes of chemotherapeutic drug are differentially toxic to testis‐tumour cells, we compared the in vitro dose‐response curves of 5 human testis and 5 bladder‐cancer cell lines to 12 compounds. The testis cells were hypersensitive to drugs that interact directly with DNA (m‐amsa, bleomycin, cisplatin, doxorubicin, methylni‐ trosourea, mitozolomide, etoposide, mitomycin‐C), but little or no difference between the 2 cell types was seen following exposure to drugs whose mechanisms of action do not involve direct interaction with DNA (methotrexate, 5‐fluorouracil, colchicine, vinblastine). We conclude that testis tumour cells are either less tolerant of, or have a reduced capacity to repair, DNA damage.
International variations in the incidence of childhood bone tumours
Authors: Parkin D. M. , Stiller C. A. , Nectoux J. 
Published: February 2007

AbstractBone cancers comprise about 5% of childhood neoplasms. Osteosarcoma, the most common sub‐type, shows a somewhat irregular geographic pattern of incidence, with low rates in some Asian (Indian, Japanese, Chinese) and Latin American populations. Incidence is similar in the sexes and rises steeply with age, accompanied by an increasing proportion of tumours localized in the long bones of the legs. Rates in the USA are higher in blacks than in whites, as a result of a higher incidence at ages 10 to 14 and of tumours of the leg bones. The descriptive epidemiology is consistent with early observations linking risk to the amount of bone growth. Ewing's sarcoma is rare in black populations (USA and Africa) and in eastern Asia. Compared with osteosarcoma, a lower percentage of tumours is localized to the long bones, and incidence rises less steeply with age and is accompanied by an increasing proportion of pelvic tumours. Chondrosarcoma is a rare cancer in children (less than 5% of bone cancers), with an age distribution similar to that of osteosarcoma and a sub‐site distribution resembling that of Ewing's sarcoma. Little is known of the aetiology of these tumours; there is clearly a strong genetic predisposition in Ewing's sarcoma but, although the proportion of osteosarcorma cases of genetic origin seems to be small, environmental determinants so far suspected can account for only a small fraction of the total cases.
Analysis of the relationship between stage of differentiation and nk/lak susceptibility of colon carcinoma cells
Authors: Blottière H. M. , Zennadi R. , Grégoire M. , Aillet G. , Denis M. G. , Meflah K. , Le Pendu J. 
Published: February 2007

AbstractNK and LAK cells which are able to lyse tumor target cells in an MHC‐unrestricted manner are not equally effective against targets of the same nature. In the case of colorectal tumors, some cells are highly sensitive, whereas others are resistant to NK and can even be quite resistant to LAK‐mediated lysis. In the present paper, we tried to correlate the stage of differentiation of 17 human colorectal tumor cell lines with their NK‐ or LAK‐cell susceptibility. It was observed that NK cells killed colorectal target cells independently from their stage of differentiation defined according to histopathological criteria from xenografting in nude mice. NK susceptibility was not correlated either with in vitro‐defined criteria of differentiation, such as cell polarity and morphology, brush‐border enzyme expression and CEA production. A LAK‐resistant HT‐29 sub‐line (HT‐29 LAK) was selected which could not be distinguished from HT‐29 in terms of features of differentiation. It was further observed that HT‐29 Glc−/+ cell line, a highly differentiated enterocytic‐like variant of HT‐29, obtained after glucose starvation, was killed by LAK cells as efficiently as the moderately differentiated parental HT‐29, and that Caco‐2 cells, which differentiate spontaneously after confluence in standard culture conditions, were equally sensitive to NK‐mediated lysis whatever their stage of differentiation. In contrast, HT29 MTX10−5, a highly differentiated mucus‐secreting variant of HT29 obtained by methotrexate selection, was much more resistant to LAK cells than parental HT29 cells.
Monocyte‐conditioned media possess a novel factor which increases motility of cancer cells
Authors: Jiang W. G. , Puntis M. C. A. , Hallett M. B. 
Published: February 2007

AbstractA number of cytokines have been reported to increase the cell motility (scatter) of cohesive cell colonies. We report here a novel scattering factor produced by human monocytes. Media from both stimulated and non‐stimulated human monocytes or the monocytic cell line, U937, increased the cell motility of 2 human colon‐cancer cell lines, HT115 and HT29, but not the canine epithelial cell line MDCK. Motility was assayed by cell dissociation from carrier beads and colony scattering. HT115 cells were strongly scattered by the conditioned media but not by interleukins IL‐1,2,4,6,8,10, TNFα, TGFβ, EGF, GM‐CSF, IGF‐1, PDGF, interferon‐γ. This factor is distinct from hepatocyte growth factor/scatter factor (HGF/SF), since the activity was not blocked by anti‐HGF/SF antibody. The activity was reduced by treatment with acid, heat, trypsin and dithiothreitol; this, together with gel filtration, suggests that the factor is a protein (MW 40 to 60 kDa). This new factor, which is secreted from monocytes and the monocytic cell line, U937, has the ability to increase the motility of cancer cells and may be important in controlling the behaviour of tumours in vivo.
Expression and distribution of peripherin protein in human neuroblastoma cell lines
Authors: Pedersen Ward A. , Becker Laurence E. , Yeger Herman 
Published: February 2007

AbstractA series of human neuroblastoma (NB) cell lines was analyzed for expression of peripherin, a class‐III intermediate filament protein expressed at high levels in ganglia of the peripheral nervous system. By Western blotting, peripherin protein was detected in all human NB cell lines examined. The highest level of peripherin was found in the NUB‐7 cell line, previously characterized as homogeneously neuroblastic. By immunofluorescence labeling, peripherin was shown to be organized in a perinuclear filamentous pattern and, exemplified by IMR32 cells, was also shown to be localized to spontaneously formed neurites. Peripherin was expressed in neuroblastic but not substrate‐adherent cells, and was found at low levels in I‐type cells. There was a pronounced redistribution of peripherin to neurites formed in response to dibutyryl cyclic adenosine monophosphate (dbcAMP) and all‐trans‐retinoic acid (RA). In NUB‐7 cells, which do not extend neurites in response to nerve growth factor, there was no change in the level of peripherin protein following treatment with this agent. Both dbcAMP and RA induced a redistribution of peripherin to neurite extensions, but only treatment with RA increased the level of the protein as demonstrated with NUB‐6A4 and NUB‐6C4 subclones. Peripherin was also variably expressed in peripheral neuroepithelioma (NE) cell lines tested, but was organized into a more basket‐like filamentous pattern in these cells. The heterogeneous expression and distribution of peripherin in NB and NE cell lines indicate that this protein is associated with maturation of the neuronal phenotype and hence serves as a differentiation marker for tumors derived from the neural crest.