bluuebunny/crossref_metadata_2025_split huggingface dataset:
Isolation of simian immunodeficiency virus from african green monkeys and seroepidemiologic survey of the virus in various non‐human primates
Authors: Ohta Yoshihiro , Masuda Takao , Tsujimoto Hajime , Ishikawa Koh‐Ichi , Kodama Toshiaki , Morikawa Shigeru , Nakai Masuyo , Honjo Shigeo , Hayami Masanori 
Published: February 2007

AbstractSixteen isolates of simian retrovirus closely related to human immunodeficiency virus (HIV) were obtained from healthy African green monkeys (AGM) (Cercopithecus aethiops). The first isolate was obtained from a monkey seropositive for HIV, and the others were isolated from monkeys harboring antibodies to the first isolate. These simian retro‐viruses were referred to as simian immunodeficiency virus from AGM, SIV[AGM], due to their cross‐reactivities with HIV structural proteins. These SIV[AGM] isolates were found by Western blotting analysis to have virus‐specific proteins of 120, 66, 55, 32–40, 24 and 17 kDa, which were all similar in size to the analogous proteins of HIV. Putative gas proteins of p55, p24 and pl7 were recognized by sera of human AIDS patients, but the corresponding env proteins of 32–40 and 120 kDa showed only weak cross‐reactivity with those of HIV. The transmembrane glycoproteins of these 3 SIV[AGM] isolates showed size heterogeneity, being 32, 35 and 40 kDa. This virus had particles that were morphologically similar to those of HIV, and had Mg2+ ‐dependent reverse transcriptase. Furthermore, the SIV[AGM] showed tropism and cytopathic effects on CD4‐positive human cell tines. In a sero‐epidemiological survey of SIV[AGM] in various non‐human primates, 2 other African monkey species, the mandrill and de Brazza's monkey, were also found to have antibodies to SIV[AGM]. These HIV‐related simian retroviruses will be important in determining the origin and transmission of HIV group viruses, and may provide useful animal models for studies on the infection and pathogenesis of HIV and AIDS.
Interferon treatment markedly inhibits the development of tumor metastases in the liver and spleen and increases survival time of mice after intravenous inoculation of friend erythroleukemia cells
Authors: Gresser Ion , Maury Chantal , Woodrow David , Moss Jill , Grütter Marcus G. , Vicnaux Françoise , Belardelli Filippo , Maunoury Marie‐Thérèse 
Published: February 2007

AbstractTo investigate the effect of interferon treatment on the development of tumor metastases, DBA/2 mice were injected i.v. with 2 × 106 Friend erythroleukemia cells (FLC) (equivalent to about 5 × 105 LD50). FLC multiplied rapidly in the liver and spleen and all untreated or control treated mice died between 7 and 12 days. Daily treatment of mice with potent preparations of mouse interferon α/β was initiated 3 to 72 he after i.v. inoculation of tumor cells, at times when FLC were already present in the liver and spleen. Interferon treatment resulted in a 100 to 1,000‐fold inhibition of the multiplication of FLC in the liver and spleen and a marked increase in mean survival time. Small numbers of tumor cells persisted in the liver and spleen in some interferon‐treated mice and could be recovered by bioassay several weeks after tumor inoculation‐Most interferon‐treated mice died with tumor in the ensuing months. Three of 34 Interferon‐treated mice were considered cured as they were alive at 386, 325 and 284 days after tumor inoculation. Daily treatment of tumor‐inoculated mice with human recotnbinant interferons αD and αBDDD, which had antiviral activity on mouse cells in culture, also increased the survival time of mice injected i.v. with FLC. The use of the interferon‐resistant 3C 18 line of FLC suggests that the marked inhibition of development of established liver and spleen metastases was not due to a direct effect of Interferon on the tumor cells, but was host‐mediated.
Distribution and survival of passively transferred lymphoblasts in normal and tumor‐bearing mice
Authors: Normann S. J. , Cornelius J. 
Published: February 2007

AbstractAlthough most circulating lymphocytes are long‐lived small lymphocytes, it is the recently‐divided medium and large‐sized lymphoblasts that most clearly migrate to sites of inflammation, and they do so without regard to immunologic commitment. The tumor‐bearing state frequently suppresses macrophage accumulation at inflammatory sites but it is not known whether lymphocyte traffic is similarly affected. We addressed this issue using passively transferred radiolabelled lymphoblasts. Lymphoblasts readily entered s.c. fibrosarcomas transplanted to C57BL/6 mice. Large and small tumors acquired the same number of lymphoblasts per gram of tumor, indicating the absence of an anti‐inflammatory reaction. However, the intra‐tumoral survival of lymphoblasts was shorter in large than in small tumors. Shortened survival was noted also in spleen and whole body of animals bearing tumors. Shortened survival rather than impaired emigration may contribute to the increase in turn or lymphocyte ratio observed with large tumors. The adverse effect of tumor bearing on lymphoblast survival may be limited to tumors which acquire a high percentage of passively transferred lymphocytes since intraperitoneal P‐815 maitocytomas in DBA/2 mice acquired few labelled lymphoblasts and did not alter lymphoblast survival. These results are important for host resistance to tumor growth and therapeutically for the use of lymphocyte cytotoxic cells induced to proliferate in vitro.
Refining the prognostic significance of dna ploidy status in colorectal cancer: A prospective flow cytometric study
Authors: Jones D. J. , Moore M. , Schofield P. F. 
Published: February 2007

AbstractA consecutive series of 123 colorectal cancers, prospectively followed for 3 years, was studied to determine if the prognostic significance of DNA ploidy related to: (a) thresholds used to define DNA aneuploidy, or (b) aneuploid sub‐groups defined by DNA index (DI) and peak size. Aneuploidy was defined using 3 methods depending on the minimum proportion of nuclei considered to constitute an aneuploid peak; type 1, 5%; type 2, 10%; type 3, 10% if Dl is 1.1–1.8, but 15% if Dl is 1.9–2.1. DNA aneuploidy rates were type 1, 75%; type 2, 67%; type 3, 58%. The significance of clinical and pathological correlations varied with the use of different methods. All were associated with a significant DNA diploid survival advantage which was strongest for type 3 (p=0.006). Dl was unrelated to survival irrespective of the presence or absence of an associated S/G2; 33% with a Di of 1.1–1.8 and 35% with a Dl of 1.9–2.1 survived. Prognosis was inversely proportional to aneuploid peak size, 48% with small peaks (<20%), 30% with intermediate peaks (>20%<40%), but none with large peaks (>40%) survived (p=0.03). We conclude that: (a) thresholds used to define DNA aneuploidy affect the prognostic significance of DNA ploidy; (b) survival is independent of the Dl of aneuploid peaks; and (c) measurement of aneuploid peak size refines the prognostic value of DNA ploidy.
Interaction between epidermal growth factor and its receptor in progression of human gastric carcinoma
Authors: Yasui Wataru , Hata Jotaro , Yokozaki Hiroshi , Nakatani Hiroshi , Ochiai Atsushi , Ito Hisao , Tahara Eiichi 
Published: February 2007

AbstractThe expressions of epidermal growth factor (EGF) and its receptor were studied immunohistochemically in a total of 156 gastric carcinomas; 26 early and 130 advanced. No EGF immunoreactivity was found in early carcinomas, while EGF‐positive tumor cells were detected in 38 (29.2%) of the 130 advanced carcinomas. EGF receptor immunoreactivity was detected in one (3.8%) of the 26 early carcinomas and in 44 (33.8%) of the 130 advanced carcinomas, the incidence being significantly different (p<0.01). Out of the 130 advanced carcinomas, 17 (13.1%) had synchronous expression of EGF and its receptor and most of the tumors with strong expression of EGF were positive to EGF receptor. A significant correlation was observed between the depth of tumor invasion and EGF or its receptor immunoreactivity in tumor cells (p<0.05). Furthermore, a good correlation was demonstrated between the synchronous expression of EGF and its receptor and the depth of tumor invasion or the tumor staging. The incidence of cases with EGF in metastatic tumors was significantly higher than that in primary tumors (p<0.05). Patients with synchronous expression of EGF and its receptor had a far poorer prognosis than those without EGF and receptor.
D‐verapamil and L‐verapamil are equally effective in increasing vincristine accumulation in leukemic cells in vitro
Authors: Gruber Astrid , Peterson Curt , Reizenstein Peter 
Published: February 2007

AbstractLeukemic cells isolated from peripheral blood from 6 patients with chronic lymphocytic leukemia, immunocytoma and prolymphocytic leukemia were incubated with vincristine (10nM) with and without racemic verapamil and its L‐ and D‐ isomers (6.6 μM). Verapamil increased vincristine accumulation in all cells, the increase varying between 100 and 700%. Racemic verapamil and the L‐ and D‐isomer increased cellular vincristine accumulation to the same extent. The verapamil effect could not be reversed by increasing the calcium concentration in the incubation medium (final concentration 2.5–5.0mm). The results indicate that the mechanism behind the effect of verapamil on cellular accumulation of vincristine does not depend upon changes in calcium transport.
Macrophages associated with murine tumours express plasminogen activator activity
Authors: Mussoni Luciana , Riganti Monica , Acero Raffaella , Erroi Annalaura , Conforti Grazia , Mantovani Alberto , Donati Maria Benedetta 
Published: February 2007

AbstractThe fibrinolytic activity of cancer cells has been repeatedly implicated in mechanisms of local spread and tumour invasiveness. Mononuclear phagocytes associated with solid tumours might also contribute to fibrin dissolution at the tumour/host interface through the expression of plasminogen activator (PA) activity. We have investigated the PA activity of tumour‐associated macrophages (TAM) from 4 transplanted murine tumours in syngeneic hosts; peritoneal macrophages (native and thioglycolate‐elicited) from both tumour‐bearing and control animals were studied as reference cells. TAM from 3 tumours (MSV, mFS6, MN/MCA1) had basal levels of PA activity (20% plasminogen‐independent) comparable to or higher than those of thioglycolate‐elicited peritoneal macrophages from the same tumour‐bearing animals. TAM isolated from I tumour (MS2) had a PA which was very low (60% plasminogen‐independent), but higher than the activity of unstimulated peritoneal macrophages. Molecular analysis of PA by SDS‐PAGE electrophoresis and fibrin autography revealed in all macrophages a single species having an apparent MW of 48 kDA. It thus appears that, in some experimental neoplasms, tumour cell vicinity may represent an in vivo stimulus for macrophage PA expression.
Species‐dependent antigenicity of the 34‐kDa glycoprotein found on the membrane of various primate lymphocytes transformed by human t‐cell leukemia virus type‐I (HTLV‐I) and simian T‐cell leukemia virus (STLV‐I)
Authors: Tozawa Hideki , Andoh Satoshi , Takayama Yoshinaga , Tanaka Yuetsu , Lee Bunsho , Nakamura Hideo , Hayami Masanori , Hinuma Yorio 
Published: February 2007

AbstractSixteen monoclonal antibodies (MAbs) against TA34 antigen found on the surface of human T‐cell leukemia virus type‐I (HTLV‐I) infected cells were prepared. These MAbs and one previously prepared anti‐TA34 MAb (TAG34) recognized 34‐kDa peptide not only in HTLV‐I‐infected cells, but also in cells infected with simian T‐cell leukemia virus (STLV‐I), which is analogous in antigenicity and gene structure to HTLV‐I. Radioimmuno‐precipitation (RIP) tests with the MAbs showed that TA34 antigen had at least 3 overlapping epitope groups. The antigenicities of the TA34 antigens of HTLV‐I‐infected cells derived from various primates were investigated by immunofluorescence staining using 9 anti‐TA34 MAbs. Cells from humans, apes and Old World monkeys reacted with all these antibodies, whereas cells from New World monkeys were stained by most of the antibodies, but little if at all by the remaining 2 (5A8 and TAG34). Similar results were obtained with various primate cells infected with STLV‐I. All 17 MAbs used recognized a 22‐kDa peptide in HTLV‐I‐infected cells cultured in the presence of tunicamycin. When incubated with 1% 2‐mercaptoethanol at ph 7.2 at 37°C, TA34 antigen lost its reactivity with TAG34, suggesting that the antigen has an intramolecular S‐S bond. Twenty sera of adult T‐cell leukemia (ATL) patients did not react with TA34 antigen in RIP tests.
Inhibition by tetragastrin of experimental carcinogenesis in rat colon: Effect of wheat bran consumption
Authors: Tatsuta Masaharu , Iishi Hiroyasu , Yamamura Hisako , Taniguchi Haruo 
Published: February 2007

AbstractThe effect of dietary wheat bran consumption on the anticarcinogenic action of tetragastrin upon colon carcinogenesis induced by azoxymethane was investigated in 122 inbred Wistar rats. Rats were given a control fiber‐free diet or the same basal diet plus 20% wheat bran. From week 5, they were given 250 μg per kg body weight of tetragastrin in depot form every other day until the end of the experiment at week 45. Prolonged administration of tetragastrin resulted in a significant reduction of the incidence and number of colonic tumors per rat in the group given the fiber‐free diet. The adenocarcinomas that did develop in this group had high mucin‐producing activity, unlike the cancers produced in controls without tetragastrin. However, administration of tetragastrin had little or no influence on the incidence, number or histology of colonic tumors in the group given basal diet plus wheat bran. Dietary supplementation with wheat bran alone had little or no effect on the development or histology of colonic tumors. Before and during the administration of carcinogens, addition of fiber to the diet resulted in a significant fall in the colonic ph and a significant increase in the crypt column length, but administration of tetragastrin did not have an additive effect on the crypt column length in rats fed diet supplemented with fiber.
Mouse monoclonal antibodies detecting disialogangliosides on mouse and human t lymphomas
Authors: Kawashima Ikuo , Tada Nobuhiko , Ikegami Shuji , Nakamura Shuji , Ueda Ryuzo , Tai Tadashi 
Published: February 2007

AbstractSix monoclonal antibodies (MAbs) (4 IgG3 and 2 IgM) were produced by hybridomas obtained from A/J mice immunized with EL4(C57BL/6 derived‐T lymphoma). They were found to react with antigens expressed on both mouse and human T‐lymphomas but not on B lymphomas or normal cells. All of these antibodies reacted with the disialoganglioside GD2, GalNAcβI→4(NeuAcα2→8NeuAcα2→3)GalβI→4Glc‐Cer, by 3 different assay systems including the immune adherence inhibition test, enzyme‐linked immunosorbent assay, and enzyme immunostaining on thin‐layer chromatography. The binding specificities of these MAbs to disialogangliosides differed. Four MAbs (AI‐201, AI‐287, AI‐410. and AI‐425) showed restricted specificities, detecting only GD2, whereas the other 2 (AI‐245 and AI‐267) had a broader specificity, recognizing GD2, GD3, and GDlb. No evidence was obtained for the presence of the antigenic epitope in glycoproteins of mouse and human tumor cells. The ganglioside content of EL4 was low in comparison with that of M14 (a human melanoma cell line).
Stability of cytogenetic alterations in a human melanoma cell line and five clonal derivatives
Authors: de Lucca Edmundo Jose , Pathak Sen , Cheung Mei‐Chi Peng 
Published: February 2007

AbstractA cytogenetic study was done on a human malignant melanoma cell line and its 5 clones. Chromosome banding analysis indicated the presence of 7 “shared” markers (M) and 9 unique markers (m) that were present only in the clones. Chromosomes 1, 5, 9, 12, 17 and 21 were involved in M‐markers and chromosomes 1, 2, 4, 6, 8, 9, 11, 16, 17, 18 and 21 were involved in m‐marker formation. Both parental and clonal lines had near‐triploid chromosome numbers. A number of M‐markers were isochromosomes of the short (p) and long (q) arms of chromosome I. Our cytogenetic data indicate that the parental line contained subpopulations of cells that were in different stages of karyotypic evolution.
Conjugates of elliptinium acetate with mouse monoclonal anti‐α‐fetoprotein antibodies or fab fragments: In vitro cytotoxic effects upon human hepatoma cell lines
Authors: Alberici Gilles F. , Pallardy Marc , Manil Luc , Dessaux Jean‐Jacques , Fournier Jacqueline , Mondesir Jean‐Marc , Bohuon Claude , Gros Pierre 
Published: February 2007

AbstractElliptinium acetate (EA) is a new anti‐cancer compound displaying cytostatic activity against various malignancies including hepatoma. Using 3 hepatoma cell lines, we compared the in vitro activity of doxorubicin (reference drug), of EA and of conjugates made up with this latter drug and monoclonal antibodies (MAbs). The linkage was performed by a direct oxidation method. Specific immunoconjugates were prepared with an anti‐alphafetoprotein (AFP) MAb (AF01) or its Fab fragment (Fab AF01). Non‐specific conjugates were obtained with an anti‐thyroglobulin MAb (TG01) or its Fab (Fab TG01). Direct membrane injury (51Cr‐release), DNA and protein synthesis as well as AFP release were investigated for all compounds. Free EA displayed only weak activity on DNA and protein synthesis, at 10‐fold higher molar concentration than doxorubicin. Conjugation of EA with whole AF01 allowed significant potentiation of protein synthesis inhibition without affecting the 3 other tests. In contrast, Fab AF01 × EA conjugates displayed a marked effect in the 4 tests; in particular, this conjugate was at least 100 times more efficient than any other compound when tested in the 51Cr‐release test. Neither Fab AF01 nor free EA alone or in combination exhibited such an effect. Fab TG01 × EA conjugate was not directly cytotoxic but potentiated inhibition of DNA and protein synthesis between 2‐ and 10‐fold. The mechanism of the direct cytotoxic effect of anti‐AFP Fab × EA conjugate, which has never been described in any other immunodrug model, was investigated.
Eradication of mouse melanoma by combined treatment with recombinant human interleukin 2 and recombinant murine interferon‐gamma
Authors: Silagi Selma , Dutkowski Regina , Schaefer Annette 
Published: February 2007

AbstractSuccessful immunotherapy of early s.c. or i.p. (B16) melanoma in syngeneic C57BL/6 (B6) mice was achieved with s.c. perilesional injections (for s.c. tumors) or i.p. injections (for i.p. tumors) of recombinant human interleukin 2 (rIL‐2) and recombinant murine interferon‐gamma (rIFN‐γ). Over a 28‐day period, rIL‐2 and rIFN‐γ were injected 14 times. Results with this combination were additive with s.c. tumors and synergistic with i.p. tumors. Treatment with 6,250 U‐25,000 U of rIL‐2 and 2 μg of rIFN‐γ began 1‐3 days after s.c. inoculation of melanoma. On day 50, 87% (72/83) of mice thus treated were completely free of tumor. None of the 78 control mice (tumor + buffer) survived. Of mice receiving either rIL‐2 or rIFN‐γ alone, 59% (47/79) and 53% (44/83), respectively, were tumor‐free. I.p. tumors were also eradicated by i.p. injections of rIL‐2 (50,000 U) with rIFN‐γ (5, 10, and 15 μg) as judged by absence of tumor in 81% (21/26) of mice autopsied between days 45 and 65. No control mice survived, and only 17% (2/12) and 20% (6/30) given either rIL‐2 or rIFN‐γ separately (i.p.) were tumor‐free. Doses of rIFN‐γ from 1‐4 μg were more beneficial in eliminating 1‐day s.c. melanomas than were higher doses, and local s.c. treatment was far superior to distant or systemic treatment. Non‐adherent peritoneal or splenic cells from mice bearing 6‐day‐old i.p. melanomas and treated with one or both lymphokines on days 3 and 4 were used in cytotoxicity assays in vitro. Significant cytotoxicity against cultured melanoma cells was displayed by cells harvested from lymphokine‐treated mice, but there was no evidence of the synergism observed with combination treatment of i.p. tumors in vivo. rIFN‐γ inhibited proliferation of melanoma cells in vitro, whereas rIL‐2 stimulated proliferation at 1,000 U/ml. Plating efficiency was increased by at least 30% by culture with 100 U or 1,000 U of rIL‐2/ml and both concentrations neutralized the inhibitory effect of 0.05 ng/ml of IFN‐γ but not of 0.5 or 5.0 ng/ml.
Expression of the gangliosides GM3, GD3 and GD2 in tissue sections of normal skin, naevi, primary and metastatic melanoma
Authors: Hersey P. , Jamal O. , Henderson C. , Zardawi I. , D'Alessandro G. 
Published: February 2007

AbstractExpression of the gangliosides GM3, GD3 and GD2 was studied in tissue sections from 19 naevi, 29 primary and 83 metastatic melanoma using the ABC immunoperoxidase technique. GM3 was not detected in normal skin whereas GD2 was detected on the basal and stratum spinosum of the epidermis and on peripheral nerves in the dermis. GD3 was expressed on melanocytes but not on most other components of normal skin. However, GD3 was strongly expressed on epidermis adjacent to naevi and primary melanoma whereas GD2, in contrast to that in normal skin, was not expressed on the epidermis adjacent to 26/29 primary melanoma. All naevi were positive for GM3 and GD3 except that GM3 was not detected on junctional components of naevi. GD2 was not expressed on naevi except in areas showing neuroid differentiation. Studies on melanoma revealed that approximately 60% of primary and 75% of metastatic melanoma expressed GM3 to a varying extent. With 2 exceptions, all primary and metastatic melanomas expressed GD3 although there was variable expression within most of the individual tumours. GD2 was detected in only approximately 25% of primary and 50% of metastatic melanomas. Both GD2 and GD3 were detected on lymphocytes surrounding melanoma. The higher expression of GD2 on metastases compared to primary melanomas was consistent with the view that GD2 expression was associated with increased metastatic potential. However, the low proportion of metastases expressing GD2 and the absence of any correlation with thickness of the primary tumour suggested that GD2 expression was not a reliable marker of metastatic potential. No differences could be detected in ganglioside expression on metastases in skin or lymph nodes. These results appear to have implications for the use of MAbs against gangliosides in therapy of melanoma and in the study of melanocytic differentiation.