bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chromosomal assignment of woodchuck hepatitis virus (WHV) dna integration sites in a woodchuck hepatocellular carcinoma‐derived cell line (WH257GE10)
Authors: Mizuno Yasutsugu , Murakami Seishi , Matsushita Fumiaki , Unoura Masashi , Kobayashi Ken‐Ichi , Migita Shunsuke , Hattori Nobu , Ohno Sinsuke 
Published: February 2007

AbstractThe chromosomal sites of woodchuck hepatitis virus (WHV) DNA integration were identified in a woodchuck hepatocellular carcinoma‐derived cell line (WH257GE10) by the in situ hybridization technique using 3H‐labelled WHV whole genome (WHV 2) as a probe. The G‐banded chromosome spreads from WH257GE10 were identified and diagrammed schematicaiiy according to their band patterns. WHV DNA was integrated into 2 sites: 33 region of the long arm of chromosome 6 (6q33) and 31 region of the long arm of chromosome 8 (8q31). Chromosomal sites of WHV DNA integration were stable during successive passage periods analyzed in vitro.
Preparation and in vitro cytotoxicity of a methotrexate‐anti‐MM46 monoclonal antibody conjugate via an oligopeptide spacer
Authors: Umemoto Naoji , Kato Yoshinori , Endo Noriaki , Takeda Yumiko , Hara Takeshi 
Published: February 2007

AbstractA method was developed by which conjugates of methotrexate (MTX) with antibody were prepared via an oligopeptide spacer which, after internalization of the conjugates into the target cells, would be cleaved by lysosomal enzymes to liberate MTX or its derivative(s) for entry of the drug into the cytoplasm through the lysosomal membrane. The conjugate of MTX with a monoclonal antibody (MAb) (aMM46) to mouse mammary carcinoma MM46 cells prepared by this method via Leu‐Ala‐Leu‐Ala showed potent, antibody‐directed cytotoxicity through lysosomal degradation of the conjugate, most likely at the tetrapeptide spacer. This was supported by the following observations: (a) the cytotoxicity of the aMM46 conjugate was more potent than that of the corresponding normal γ‐globulin conjugate, the antibody alone not being cytotoxic; (b) the conjugate retained its potent cytotoxicity to MM46 cells even after removal, by hydroxylamine treatment, of a less stably bound MTX derivative which might have been released extracellularly and have caused non‐specific cytotoxicity by entering the cells via the membrane active transport system for MTX; (c) the cytotoxicity was not inhibited by thiamine pyrophosphate, an inhibitor of the MTX transport system; (d) the cytotoxicity was inhibited significantly with ammonium chloride, which inactivates lysosomal enzymes by raising the pH; and (e) the cleavability of the Leu‐Ala‐Leu‐Ala spacer by the lysosomal enzymes was verified by using bio‐undegradable poly(D‐lysine) and biodegradable poly(L‐lysine) as the lysosomotropic macromolecular carriers: unlike the poly(L‐lysine) counterpart, the direct MTX‐poly(D‐lysine) conjugate showed very weak cytotoxicity while the tetrapeptide‐mediated conjugate of MTX with poly(D‐lysine) exhibited potent cytotoxicity.
Evaluation of the carcinogenicity of different preparations of areca nut in mice
Authors: Rao A. Ramesha , Das Padma 
Published: February 2007

AbstractAreca nut has been used as a masticatory since antiquity and it is estimated that more than 10% of the world population chews it in a variety of forms. We have evaluated the carcinogenicity of different preparations of areca nut: ripe‐uprocessedsundried nut (R‐UP‐SD), ripe‐processedsundried nut (R‐P‐SD), unripe‐processed‐sundried nut (UR‐P‐SD), ripe‐unprocessed‐sundried‐water‐soaked nut (R‐UP‐SD‐WS) and ripe‐unprocessed‐undried‐water‐soaked nut (R‐UP‐UD‐WS) in mice following diet‐feeding or oral feeding for 12 months. Only unprocessed areca nuts (R‐UP‐SD, R‐UP‐SD‐WS and R‐UP‐UD‐WS), at high doses, displayed a very weak carcinogenicity.
Laminin receptor expression on murine tumor cells: Correlation with sensitivity to natural cell‐mediated cytotoxicity
Authors: Laybourn Katherine A. , Hiserodt John C. , Varani James 
Published: February 2007

AbstractPrevious studies have identified a relationship between the presence of cell surface laminin receptors on murine tumor cells and sensitivity to killing by natural killer (NK) cells. On the basis of these observations, we suggested that laminin and laminin receptors may function to facilitate the interaction of NK‐sensitive murine target cells with NK cells. Our original studies were conducted with a number of genetically unrelated tumor cell lines. In order to extend these earlier observations, studies have now been conducted in which sensitivity to NK‐mediated lysis and responsiveness to laminin were compared in a number of variant populations derived from the NK‐sensitive cell lines Yac‐l and RL‐l and from the NK/ NC‐resistant line P815. All of the lines which interacted with murine NK cells as indicated by sensitivity to killing and/or by ability to “cold‐target” compete with the killing of sensitive Yac‐l cells were able to bind 125l‐laminin and to respond to laminin in an aggregation assay. Of 4 NK‐resistant populations identified in these studies, 3 failed to respond to laminin. These studies indicate that even among genetically related tumor cell lines there is a relationship between laminin receptor expression and interaction with NK cells.
Centchroman—a non‐steroidal anti‐cancer agent for advanced breast cancer: Phase‐II study
Authors: Misra N. C. , Nigam P. K. , Gupta Ruby , Agarwal A. K. , Kamboj V. P. 
Published: February 2007

AbstractTreatment with Centchroman (3,4‐trans‐2,2‐dimethyl‐3‐phenyl‐4‐p‐(βpyrrolidinoethoxy) phenyl‐7‐methoxy chroman) has been evaluated in 4 male and 75 female patients with advanced breast cancer. The overall response rate, including both male and female cases, was 40.5%. Among the female patients, the overall response rate was 38.7%. The median duration of response was 6 months. One of the 4 male patients showed a complete response and 2 showed partial responses. The responses were more marked for bone, pulmonary, soft tissue, skin and lymph‐node metastases than for liver metastases.
A case‐control study of cancer of endometrium in athens
Authors: Koumantaki Yvonni , Tzonou Anastasia , Koumantakis Eugene , Kaklamani Evangelia , Aravantinos Dionisios , Trichopoulos Dimitrios 
Published: February 2007

AbstractEighty‐three women with invasive adenocarcinoma of the endometrium and 164 control women hospitalized for various orthopedic conditions were interviewed regarding demographic, reproductive, socio‐economic and biomedical characteristics, including their use of tobacco, drugs and exogenous estrogens. The data were analyzed by modelling rate ratio (r) through multiple logistic regression. The main results were as follows: women with invasive adenocarcinoma of the endometrium had earlier menarche (r = 0.82 for every additional year; one‐tailed p approx. 0.04), later menopause (r = 1.50 for a 5‐year difference; one‐tailed p approx. 0.004), and fewer live‐born children (r = 0.86 for every additional child; one‐tailed p approx. 0.08); they were also taller (r = 1.33 for a 5‐cm difference; one‐tailed p approx 0.03), whereas weight, adjusted for height, was not a statistically significant risk indicator (one‐tailed p approx. 0.38). Regular use of combination oral contraceptives was associated with a reduced risk of endometrial cancer (r = 0.56), whereas intake of menopausal estrogens for more than 6 months was associated with an increased risk (r = 2.04); however, because of the low frequency of use of exogenous estrogen preparations in Greece, neither of these 2 results was statistically significant. Tobacco smoking was associated with a significantly reduced risk of endometrial cancer; smoking 15–20 cigarettes per day for 20 years was associated with a rate ratio of 0.49 (one‐tailed p approx. 0.03). The protective effect of tobacco smoking was evident only among post‐menopausal women. These results indicate that the risk profile of endometrial cancer is similar in high‐risk and low‐risk countries, and underline the importance of unopposed estrogenic stimulation in the pathogenesis of this cancer.
The use of a monoclonal antibody against a proliferating cell nuclear matrix antigen in the study of solid human tumors
Authors: Yankulov K. Y. , Hadjiolova K. V. , Kounev K. V. , Getov Chr. , Hadjiolov A. A. 
Published: February 2007

AbstractA monoclonal antibody (MAb) identifies the nuclear antigen p125/6.5 associated with the nuclear matrix and present in proliferating human cells. By direct and indirect immunofluorescence, the presence and distribution of the antigen p125/6.5 in cryostat sections from primary and metastatic solid human tumors has been investigated. The antigen is present in nuclei of malignant and benign tumor cells, but is not detected in adjacent normal tissues. The antigen displays a speckled nucleoplasmic distribution, while nucleoli are negative. The intensity of the immunofluorescence reaction is markedly higher in the nuclei of some individual or grouped tumor cells.
Systemic immunity against a murine colon tumor (CT‐26) produced by immunization with syngeneic cells expressing a transfected viral gene product
Authors: Schackert Hans K. , Itaya Toshiyuki , Schackert Gabriele , Fearon Eric , Vogelstein Bert , Frost Philip 
Published: February 2007

AbstractWe have previously shown that CT‐26 tumor cells expressing the transfected hemagglutination antigen of influenza virus elicit an immune response in syngeneic hosts that is cross‐protective against an s.c. challenge with non‐transfected parental cells. Since CT‐26 is a murine colorectal carcinoma we sought to determine whether the same immuno‐protective effect could be achieved after a challenge with parent tumor cells injected into the usual sites of colon tumor growth and metastasis. We now show that the protection afforded by this immunization protocol is systemic and that animals can be protected against tumor growth in the cecum, lymphatics of the mesentery, liver and lung.
Different class I antigen oligosaccharides on a murine tumor and a lectin‐resistant variant are not responsible for the differential recognition of the tumors by CTL
Authors: Degen Eric , Laferte Suzanne , Elliott Bruce E. , Williams David B. 
Published: February 2007

AbstractPrevious studies have shown that whereas a highly malignant mouse cell line termed MDAY‐D2 (d haplotype) does not elicit a detectable response by cytotoxic T lymphocytes (CTL) in DBA/2 mice, strong anti‐tumor CTL are generated against a wheat‐germ‐agglutinin‐resistant variant, designated MDW3. Additional evidence suggests these anti‐MDW3 CTL may not be a consequence of a unique antigenic determinant on the variant cells. Because MDW3 cells are expected to differ from MDAY‐D2 cells in their surface carbohydrate structures (due to their lectin resistance) and Class 1 major histocompatibility molecules play a crucial role in CTL‐mediated responses, we speculated that the Asn‐linked oligosaccharides present on Class 1 molecules of MDAY‐D2 and MDW3 might be different and could potentially influence recognition by the anti‐MDW3 CTL. High‐resolution gel filtration analyses and Con A‐Sepharose affinity chromatography clearly demonstrated that the oligosaccharides isolated from the H‐2Dd molecule of MDAY‐D2 cells are larger and more highly branched than those of the MDW3 variant. Taken together with the finding that anti‐MDW3 CTL are restricted by H‐2Dd, these results suggested that the larger H‐2DD oligosaccharides on MDAY‐D2 cells could potentially mask or perturb determinants required for recognition by these CTL. To test this postulate, the surface Class I oligosaccharides of both MDAY‐D2 and MDW3 cells were converted to simpler hybrid structures by treatment with the oligosaccharide processing inhibitor, swainsonine. However, no effect was observed on the lysis or binding of either MDAY‐D2 or MDW3 cells by anti‐MDW3 CTL. Thus, the results do not support the possibility that the larger H‐2Dd oligosaccharides on MDAY‐D2 cells are, in themselves, responsible for the poor recognition of the parent tumor by anti‐MDW3 CTL. Our data to indicate, however, that CTL target binding and effector functions are not dependent on the fine structure of complex Asnlinked carbohydrates present on Class 1 molecules and possibly on other, accessory molecules at the target cell surface, since MDW3 cells maintained their sensitivity to lysis by CTL following swainsonine treatment.
Human lung cancer—a comparative study of the levels of circulating immune complexes in pulmonary blood draining the tumor area and peripheral venous blood
Authors: Bukh A. , Kimose H.‐H. , Aguado M. T. , Linnet L. , Mösller N. P. H. 
Published: February 2007

AbstractOur objective was to investigate whether low levels of circulating immune complexes (cICs) in peripheral venous blood of cancer patients could be due to removal of cIC released at the tumor site during passage to the peripheral veins. In 54 patients with primary lung cancer, we therefore compared the cIC levels as detected by 3 different assays in paired samples from the pulmonary vein draining the tumor area and from a peripheral vein. Only 6 of the 54 patients had significantly increased pulmonary vein cIC levels as compared to the corresponding peripheral vein levels. The peripheral vein levels of these 6 patients were all within the normal range, and in none of these patients was the difference between the 2 sites of analysis—although significant—of such a magnitude that the pulmonary vein cIC level appeared higher than the normal range, i.e., “positive” for cIC. Positive cIC levels were only found in 11% of lung cancer patients (irrespective of the site of measurement). Thus, our present data, together with our previous findings indicating no significant difference between peripheral venous blood cIC levels in cancer patients and normal controls, contradict the theory of tumor cells expressing new antigens resulting in the formation of tumor‐associated cICs.
Generation and partial characterization of melanoma sublines resistant to lymphokine activated killer (LAK) cells. Relevance to doxorubicin resistance
Authors: Rivoltini Licia , Gambacorti‐Passerini Carlo , Supino Rosanna , Parmiani Giorgio 
Published: February 2007

AbstractTo see whether a tumor cell population may contain cells resistant to lymphokine‐activated killer (LAK) lymphocytes, cells from a LAK‐sensitive melanoma line (Me 665/2) were co‐cultured with LAKs. Three sublines were obtained after 1, 2 or 3 immunoselection cycles. Immunoselected (IS) sublines show reduced proliferation, decreased reactivity to the monoclonal antibody (MAb) R24 and appeared morphologically more differentiated in comparison with the parental Me 665/2 line. A progressively reduced sensitivity to LAKs was observed in IS sublines with a more than 8‐fold reduction in LAK susceptibility. A reduced complement (C)‐mediated lysis was also observed in IS sublines. Since we have previously shown that LAK sensitivity of melanoma cells may be associated with Doxorubicin (Dx) resistance, the sensitivity to Dx was tested in these lines. An augmented sensitivity to Dx was noted in IS sublines as compared with Me 665/2. The differences in LAK susceptibility between the IS sublines and the parental Me 665/2 line remained stable for 2 weeks but declined and disappeared thereafter. These results indicate that (1) a LAK‐sensitive tumor line may contain a subpopulation of cells which are significantly less lysed by LAKs; (2) a correlation between LAK sensitivity and susceptibility to C‐mediated lysis is also present; and (3) increased sensitivity to Dx is evident in the IS sublines.
Acidic cellular environments: Activation of latent tgf‐β and sensitization of cellular responses to tgf‐β and egf
Authors: Jullien P. , Berg T. M. , Lawrence D. A. 
Published: February 2007

AbstractTransient (about 2 hr) acidification to approx. pH 5.0 of agar‐gelled overlayers containing untransformed NRK‐49F or KiMSV‐transformed NRK‐49F cells in the presence of fetal calf serum or crude 49F‐cell conditioned medium, as sources of latent TGF‐β, elicited EGF‐dependent colony formation of 49F cells and inhibited spontaneous growth of transformed cells. Pure, active TGF‐β (porcine, type 1) had the same effects on these respective cell types, suggesting that the above results were due to activation of latent TGF‐β in the transiently acidic cellular environment. Similar acidifications in the absence of a source of latent TGF‐β enhanced the positive growth response of 49F and AKR‐2B cells to EGF and active TGF‐β and also the negative growth response of KiMSV‐transformed 49F cells to active TGF‐β. These results are compatible with the idea that acidic cellular environments, particularly in tumor tissues, are conducive to activation of latent TGF‐β, perhaps in conjunction with other activating mechanisms, and to an enhanced response to some growth factors. However, the heterogeneity of cell populations within tumoral masses presents an obstacle to a clear understanding of the consequences of such activation.
Stimulatory role of transforming growth factors in multistage skin carcinogenesis: Possible explanation for the tumor‐inducing effect of wounding in initiated nmri mouse skin
Authors: Förstenberger Gerhard , Rogers Michael , Schnapke Ruben , Bauer Georg , Höufler Petra , Marks Friedrich 
Published: February 2007

AbstractMechanical wounding provides a convertogenic (“stage 1 tumor‐promoting”) stimulus in initiated NMRI mouse skin, indicating that this stage of carcinogenesis can be entirely controlled by endogenous factors. A search for such factors led to the finding that both platelet‐derived Epstein‐Barrvirus‐inducing factor (EIF), alias human TGFβ1 and porcine TGFβ, exhibited—upon intracutaneous injection—convertogenic efficacy in initiated NMRI‐mouse skin in vivo provided that their injection was combined with a single topical application of the non‐convertogenic tumor promoter 12‐O‐retinolyphorbol‐13‐acetate (RPA). Since TGFβ inhibits epidermal cell proliferation, the RPA treatment is thought to provide a mitogenic stimulus required for conversion. The RPA treatment can be replaced by intracutaneous injection of transforming growth factor α (TGFα). These results indicate that the stage of conversion consists of two components, one of which is related to mitogenesis (RPA or TGFα), the other to a still unknown activity exhibited by TGFβ‐like factors. Thus, endogeneous factors with the quality of “wound hormones” may be involved in multistage skin carcinogenesis. This finding could explain the convertogenic effect of skin wounding.
A carcinoembryonic antigen‐directed immunotoxin built by linking a monoclonal antibody to a hemolytic toxin
Authors: Avila A. D. , Mateo Acosta C. De , Lage A. 
Published: February 2007

AbstractHybrid molecules prepared by linking toxins to monoclonal antibodies (MAbs) are cytotoxic to cells bearing the target antigen. The toxin most widely used has been the plant toxin ricin as the toxic component, which inhibits protein synthesis at the ribosome level. Immunotoxins based on membraneactive, hemolytic toxins can be a useful alternative when directed towards antigens which do not mediate internalization, as is the case for most carcinoma antigens. We present an alternative for toxic components using a hemolytic toxin acting at the membrane level, due to its phospholipase activity. The hemolytic toxin (HT), isolated from the sea anemone Stoichactis helianthus, has been conjugated to a MAb directed against carcinoembryonic antigen (CEA), by means of an artificial disulphide bridge. The hybrid α CEA‐HT exhibits no hemolytic activity unless it is reduced. It is toxic for cells (MDA‐MB‐134) expressing CEA and not toxic for cells (MDA‐MB‐231) not bearing CEA. An excess of free antibody reverses toxicity.
Cytogenetics of undifferentiated nasopharyngeal carcinoma xenografts from southern chinese
Authors: Huang D. P. , Ho J. H. C. , Chan W. K. , Lau W. H. , Lui M. 
Published: February 2007

AbstractThree undifferentiated nasopharyngeal carcinoma (NPC) tumour lines were successfully established from fresh biopsy material injected s.c. into athymic mice and passaged for many generations. These xenografts were found to be free of infiltrating lymphoid cells and remained undifferentiated up to passage 30. They were designated NPC/HK2117 (Xeno‐1), NPC/HK1915 (Xeno‐2) and NPC/HK1530 (Xeno‐3), respectively. Passage 16 from Xeno‐1, passage 1 from Xeno‐2 and passage 14 from Xeno‐3 were studied cytogenetically using G‐banding with the trypsin‐Giemsa method. Two xenografts were hyperdiploid with chromosome modal numbers ranging from 49 to 76, and one was hypodiploid with modal numbers ranging from 28 to 38. Five marker chromosomes have been identified with involvement of chromosomes 1, 3, 11, 12 and 17. Marker chromosomes derived from chromosomes 12q, 1q and 3q were consistent in one of the 2 xenografts successfully G‐banded, and chromosomes 12, 11 and 17 were consistent in another. Three out of the 6 markers involve 12q13 qter. An abnormal chromosome 3 with most of the p arm deleted was also observed.
A functional and phenotypic comparison of murine natural killer (NK) cells and lymphokine‐activated killer (LAK) cells
Authors: Hoskin D. W. , Stankova J. , Anderson S. K. , Roder J. C. 
Published: February 2007

AbstractLymphokine‐activated killer (LAK) cells have been defined as interleukin 2 (lL‐2)‐activated cytolytic effector cells exhibiting non‐MHC restricted killing against a wide range of NK‐sensitive and NK‐resistant tumor cells. There has been considerable debate as to whether LAK cells are derived from NK cells or from a unique precursor population. In the present study, we compare LAK cells derived from T‐cell‐depleted nylon‐wool‐non‐adherent spleen cells with endogenous NK cells and NK cells activated with the interferon inducer polyl.C., in terms of their phenotype and functional characteristics. The predominant splenic LAK precursor in the mouse was found to be a nylon‐wool‐non‐adherent, thyl‐, MICG,‐,Jlld.2, asialo GM1+ cell. This phenotype is shared by endogenous NK cells. A significant number of activated NK cells express macromolecular insoluble cold globulin (MICG) in addition to asialo GM1. Neither endogenous nor activated NK cells express a heat‐stable antigen found on bone‐marrow cells, immature T cells, and most B cells and defined by monoclonal antibody (MAb)Jlld.2. However, Jlld.2 is expressed on some LAK precursor and effector cells. The asialo GM1 marker is common to all LAK effector cells, while many are also thyl+, and or MICG+. LAK effector cells are therefore a heterogeneous population sharing some phenotypic characteristics in common with NK cells. In addition, there is a positive correlation between LAK and NK activity in “high NK” and “low NK” mouse strains, suggesting that NK cells and LAK cells share a common lineage. Monoclonal antibodies to the alpha and beta chains of LFA‐1 inhibit LAK and activated NK function, while endogenous NK and CTL killing is affected only by anti‐alpha chain antibodies. LAK cells, like MHC‐restricted and non‐restricted CTL clones, express mRNA transcripts of the C11 serine protease gene. We conclude that LAK cells share several features in common with cells of the NK lineage and may therefore represent NK cells in a unique state of activation. LAK cells appear to employ cytolytic machinery common to other lytic cell types.