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      1. Author :
        Cirstoiu-Hapca, A; Buchegger, F; Lange, N; Bossy, L; Gurny, R; Delie, F
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Journal of controlled release: official journal of the Controlled Release Society
      6. Products :
      7. Volume :
        144
      8. Issue :
        3
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Antibodies, Monoclonal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents, Phytogenic; Bioware; Cell Line, Tumor; Drug Carriers; Female; Humans; Mice; Nanoparticles; Ovarian Neoplasms; Paclitaxel; Receptor, erbB-2; SKOV3-luc-D3 cells; Tissue Distribution; Xenograft Model Antitumor Assays
      12. Abstract :
        The benefit of polymeric immuno-nanoparticles (NPs-Tx-HER), consisting of paclitaxel (Tx)-loaded nanoparticles coated with anti-HER2 monoclonal antibodies (Herceptin, trastuzumab), in cancer treatment was assessed in a disseminated xenograft ovarian cancer model induced by intraperitoneal inoculation of SKOV-3 cells overexpressing HER2 antigens. The study was focused on the evaluation of therapeutic efficacy and biodistribution of NPs-Tx-HER compared to other Tx formulations. The therapeutic efficacy was determined by two methods: bioluminescence imaging and survival rate. The treatment regimen consisted in an initial dose of 20mg/kg Tx administered as 10mg/kg intravenously (IV) and 10mg/kg intraperitonealy (IP), followed by five alternative IP and IV injections of 10mg/kg Tx every 3 days. The bioluminescence study has clearly shown the superior anti-tumor activity of NPs-Tx-HER compared to free Tx. As a confirmation of these results, a significantly longer survival of mice was observed for NPs-Tx-HER treatment compared to free Tx, Tx-loaded nanoparticles coated with an irrelevant mAb (Mabthera, rituximab) or Herceptin alone, indicating the potential of immuno-nanoparticles in cancer treatment. The biodistribution pattern of Tx was assessed on healthy and tumor bearing mice after IV or IP administration. An equivalent biodistribution profile was observed in healthy mice for Tx encapsulated either in uncoated nanoparticles (NPs-Tx) or in NPs-Tx-HER. No significant difference in Tx biodistribution was observed after IV or IP injection, except for a lower accumulation in the lungs when NPs were administered by IP. Encapsulated Tx accumulated in the organs of the reticulo-endothelial system (RES) such as the liver and spleen, whereas free Tx had a non-specific distribution in all tested organs. Compared to free Tx, the single dose injection (IV or IP) of encapsulated Tx in mice bearing tumors induced a higher tumor accumulation. However, no difference in overall tumor accumulation between NPs-Tx-HER and NPs-Tx was observed. In conclusion, the encapsulation of Tx into NPs-Tx-HER immuno-nanoparticles resulted in an improved efficacy of drug in the treatment of disseminated ovarian cancer overexpressing HER2 receptors.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20219607
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9012
      1. Author :
        Kozloff KM, Volakis LI, Marini JC and Caird MS
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Journal of Bone and Mineral Research
      6. Products :
      7. Volume :
        25
      8. Issue :
        8
      9. Page Numbers :
        N/A
      10. Research Area :
        Physiology
      11. Keywords :
        FMT; bone; OsteoSense; FRFP; in vivo imaging
      12. Abstract :
        Bisphosphonate use has expanded beyond traditional applications to include treatment of a variety of low-bone-mass conditions. Complications associated with long-term bisphosphonate treatment have been noted, generating a critical need for information describing the local bisphosphonate-cell interactions responsible for these observations. This study demonstrates that a fluorescent bisphosphonate analogue, far-red fluorescent pamidronate (FRFP), is an accurate biomarker of bisphosphonate deposition and retention in vivo and can be used to monitor site-specific local drug concentration. In vitro, FRFP is competitively inhibited from the surface of homogenized rat cortical bone by traditional bisphosphonates. In vivo, FRFP delivery to the skeleton is rapid, with fluorescence linearly correlated with bone surface area. Limb fluorescence increases linearly with injected dose of FRFP; injected FRFP does not interfere with binding of standard bisphosphonates at the doses used in this study. Long-term FRFP retention studies demonstrated that FRFP fluorescence decreases in conditions of normal bone turnover, whereas fluorescence was retained in conditions of reduced bone turnover, demonstrating preservation of local FRFP concentration. In the mandible, FRFP localized to the alveolar bone and bone surrounding the periodontal ligament and molar roots, consistent with findings of osteonecrosis of the jaw. These findings support a role for FRFP as an effective in vivo marker for bisphosphonate site-specific deposition, turnover, and long-term retention in the skeleton.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20200982
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4527
      1. Author :
        Neal, Robert E, 2nd; Singh, Ravi; Hatcher, Heather C; Kock, Nancy D; Torti, Suzy V; Davalos, Rafael V
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Breast cancer research and treatment
      6. Products :
      7. Volume :
        123
      8. Issue :
        1
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Bioware; Cell Line, Tumor; Electrochemotherapy; Electrodes; Female; Humans; Mammary Neoplasms, Experimental; MDA-MB-231-D3H1 cells; Mice; Mice, Nude; Needles; Xenograft Model Antitumor Assays
      12. Abstract :
        Irreversible electroporation (IRE) is a therapeutic technology for the ablation of soft tissues using electrodes to deliver intense but short electric pulses across a cell membrane, creating nanopores that lead to cell death. This phenomenon only affects the cell membrane, leaving the extracellular matrix and sensitive structures intact, making it a promising technique for the treatment many types of tumors. In this paper, we present the first in vivo study to achieve tumor regression using a translatable, clinically relevant single needle electrode for treatment administration. Numerical models of the electric field distribution for the protocol used suggest that a 1000 V/cm field threshold is sufficient to treat a tumor, and that the electric field distribution will slightly decrease if the same protocol were used on a tumor deep seated within a human breast. Tumor regression was observed in 5 out of 7 MDA-MB231 human mammary tumors orthotopically implanted in female Nu/Nu mice, with continued growth in controls.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20191380
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8988
      1. Author :
        Kim, Jae-Beom; Urban, Konnie; Cochran, Edward; Lee, Steve; Ang, Angel; Rice, Bradley; Bata, Adam; Campbell, Kenneth; Coffee, Richard; Gorodinsky, Alex; Lu, Zhan; Zhou, He; Kishimoto, Takashi Kei; Lassota, Peter
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        PloS one
      6. Products :
      7. Volume :
        5
      8. Issue :
        2
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        4T1-luc2; Animals; Bicuculline; Bioware; Cell Line, Tumor; Diagnostic Imaging; Female; Genetic Vectors; Lentivirus; Luciferases; Luminescent Measurements; Lung Neoplasms; Mammary Neoplasms, Experimental; Mice; Mice, Inbred BALB C; Mice, Nude; Neoplasm Transplantation; Neoplasms; Sensitivity and Specificity; Time Factors; Transfection; Tumor Burden
      12. Abstract :
        Early detection of tumors can significantly improve the outcome of tumor treatment. One of the most frequently asked questions in cancer imaging is how many cells can be detected non-invasively in a live animal. Although many factors limit such detection, increasing the light emission from cells is one of the most effective ways of overcoming these limitations. Here, we describe development and utilization of a lentiviral vector containing enhanced firefly luciferase (luc2) gene. The resulting single cell clones of the mouse mammary gland tumor (4T1-luc2) showed stable light emission in the range of 10,000 photons/sec/cell. In some cases individual 4T1-luc2 cells inserted under the skin of a nu/nu mouse could be detected non-invasively using a cooled CCD camera in some cases. In addition, we showed that only few cells are needed to develop tumors in these mice and tumor progression can be monitored right after the cells are implanted. Significantly higher luciferase activity in these cells allowed us to detect micrometastases in both, syngeneic Balb/c and nu/nu mice.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20186331
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8938
      1. Author :
        Balibar, Carl J; Shen, Xiaoyu; McGuire, Dorothy; Yu, Donghui; McKenney, David; Tao, Jianshi
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Microbiology (Reading, England)
      6. Products :
      7. Volume :
        156
      8. Issue :
        Pt 5
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Anti-Bacterial Agents; Bacterial Proteins; Bacteriolysis; Bioware; Cell Wall; Gene Expression Profiling; Gene Knockout Techniques; Genes, Reporter; Lysostaphin; Mice; Microbial Sensitivity Tests; Sepsis; Staphylococcus aureus; Virulence; Xen29
      12. Abstract :
        Transcriptional profiling data accumulated in recent years for the clinically relevant pathogen Staphylococcus aureus have established a cell wall stress stimulon, which comprises a coordinately regulated set of genes that are upregulated in response to blockage of cell wall biogenesis. In particular, the expression of cwrA (SA2343, N315 notation), which encodes a putative 63 amino acid polypeptide of unknown biological function, increases over 100-fold in response to cell wall inhibition. Herein, we seek to understand the biological role that this gene plays in S. aureus. cwrA was found to be robustly induced by all cell wall-targeting antibiotics tested – vancomycin, oxacillin, penicillin G, phosphomycin, imipenem, hymeglusin and bacitracin – but not by antibiotics with other mechanisms of action, including ciprofloxacin, erythromycin, chloramphenicol, triclosan, rifampicin, novobiocin and carbonyl cyanide 3-chlorophenylhydrazone. Although a DeltacwrA S. aureus strain had no appreciable shift in MICs for cell wall-targeting antibiotics, the knockout was shown to have reduced cell wall integrity in a variety of other assays. Additionally, the gene was shown to be important for virulence in a mouse sepsis model of infection.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20167623
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9037
      1. Author :
        Zeng, Q.; Yang, Z.; Gao, Y. J.; Yuan, H.; Cui, K.; Shi, Y.; Wang, H.; Huang, X.; Wong, S. T.; Wang, Y.; Kesari, S.; Ji, R. R.; Xu, X.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Eur J Cancer
      6. Products :
      7. Volume :
        46
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MDA-MB-231-D3H2Ln, IVIS, Bioluminescence, Animals; Antineoplastic Combined Chemotherapy Protocols/*therapeutic use; Cell Hypoxia/physiology; Cell Line, Tumor; Cyclophosphamide/*therapeutic use; Female; Immunohistochemistry; Lung Neoplasms/prevention & control/secondary; Mammary Neoplasms, Experimental/*drug therapy/genetics/pathology; Mice; Mice, Nude; Sirolimus/*therapeutic use; Tumor Burden; Xenograft Model Antitumor Assays
      12. Abstract :
        Rapamycin, a mammalian target of rapamycin (mTOR) inhibitor, has been shown to inhibit the growth of oestrogen positive breast cancer. However, triple-negative (TN) breast cancer is resistant to rapamycin treatment in vitro. We set to test a combination treatment of rapamycin with DNA-damage agent, cyclophosphamide, in a TN breast cancer model. By binding to and disrupting cellular DNA, cyclophosphamide kills cells via interfering with their normal functions. We assessed the responses of nude mice bearing tumour xenografts of TN MDA-MB-231 cells to the combination of rapamycin and cyclophosphamide in both orthotopic mammary and lung-metastasis models. We tracked tumour growth and metastasis by bioluminescent imaging and examined the expression of Ki67, CD34 and HIF-1alpha in tumour tissues by immunohistochemistry and apoptosis index with TUNEL assay, and found that MDA-MB-231 cells are sensitive to rapamycin therapy in orthotopic mammary, but not in lung with metastasis. Rapamycin when combined with cyclophosphamide is found to have a more significant effect in reducing tumour volume and metastasis with a much improved survival rate. Our data also show that the sensitivity of TN tumours to rapamycin is associated with the microenvironment of the tumour cells. The data indicate that in a relatively hypoxic environment HIF-1alpha may play a role in mediating the anti-cancer effect of rapamycin and cyclophosphamide may prevent the feedback activation of Akt by rapamycin. Overall our results show that rapamycin plus cyclophosphamide can achieve an improved efficacy in suppressing tumour growth and metastasis, suggesting that the combination therapy can be a promising treatment option for TN cancer.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20156674
      14. Call Number :
        PKI @ kd.modi @ 2
      15. Serial :
        10414
      1. Author :
        Zhang, H; Fagan, D H; Zeng, X; Freeman, K T; Sachdev, D; Yee, D
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Oncogene
      6. Products :
      7. Volume :
        29
      8. Issue :
        17
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Bioware; Cell Line, Tumor; Cell Proliferation; Female; Humans; Insulin; Lung Neoplasms; Lymphangiogenesis; MDA-MB-231-D3H1 cells; Mice; Neoplasm Metastasis; Neoplasms, Experimental; Neovascularization, Pathologic; Phosphorylation; Proto-Oncogene Proteins c-akt; Receptor, Insulin; RNA, Small Interfering; Vascular Endothelial Growth Factor A
      12. Abstract :
        Insulin receptor (IR) and the type I IGF receptor (IGF1R) are structurally and functionally related. The function of IGF1R in cancer has been well documented and anti-IGF1R strategies to treat cancer have shown initial positive results. However, the role of IR in tumor biology, independent of IGF1R, is less clear. To address this issue, short hairpin RNA (shRNA) was used to specifically downregulate IR in two cancer cell lines, LCC6 and T47D. Cells with reduced IR showed reduced insulin-stimulated Akt activation, without affecting IGF1R activation. Cells with reduced IR formed fewer colonies in anchorage-independent conditions. LCC6 IR shRNA xenograft tumors in mice had reduced growth, angiogenesis and lymphangiogensis when compared with LCC6 wild-type cells. Accordingly, LCC6 IR shRNA clones produced less hypoxia-inducible factor-1alpha, vascular endothelial growth factor (VEGF)-A and VEGF-D. Furthermore, LCC6 IR shRNA cells formed fewer pulmonary metastases when compared with LCC6 wild-type cells. Using in vivo luciferase imaging, we have shown that LCC6 IR shRNA cells have less seeding and colonization potential in the lung and liver of mice than LCC6 cells. In conclusion, downregulation of IR inhibited cancer cell proliferation, angiogenesis, lymphangiogenesis and metastasis. Our data argue that IR should also be targeted in cancer therapy.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20154728
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8986
      1. Author :
        Marttila-Ichihara, Fumiko; Castermans, Karolien; Auvinen, Kaisa; Oude Egbrink, Mirjam G A; Jalkanen, Sirpa; Griffioen, Arjan W; Salmi, Marko
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Journal of immunology (Baltimore, Md.: 1950)
      6. Products :
      7. Volume :
        184
      8. Issue :
        6
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Adjuvants, Immunologic; Allylamine; Amine Oxidase (Copper-Containing); Animals; Antibodies, Blocking; Antibodies, Monoclonal; B16-F10-luc-G5 cells; Bioware; Cell Adhesion Molecules; Cell Line, Tumor; Cell Migration Inhibition; Enzyme Inhibitors; Female; Growth Inhibitors; Lymphoma, T-Cell; Melanoma, Experimental; Mice; Mice, Inbred C57BL; Myeloid Cells; Semicarbazides
      12. Abstract :
        Vascular adhesion protein-1 (VAP-1) is an endothelial, cell surface-expressed oxidase involved in leukocyte traffic. The adhesive function of VAP-1 can be blocked by anti-VAP-1 Abs and small-molecule inhibitors. However, the effects of VAP-1 blockade on antitumor immunity and tumor progression are unknown. In this paper, we used anti-VAP-1 mAbs and small-molecule inhibitors of VAP-1 in B16 melanoma and EL-4 lymphoma tumor models in C57BL/6 mice. Leukocyte accumulation into tumors and neoangiogenesis were evaluated by immunohistochemistry, flow cytometry, and intravital videomicroscopy. We found that both anti-VAP-1 Abs and VAP-1 inhibitors reduced the number of leukocytes in the tumors, but they targeted partially different leukocyte subpopulations. Anti-VAP-1 Abs selectively inhibited infiltration of CD8-positive lymphocytes into tumors and had no effect on accumulation of myeloid cells into tumors. In contrast, the VAP-1 inhibitors significantly reduced only the number of proangiogenic Gr-1(+)CD11b(+) myeloid cells in melanomas and lymphomas. Blocking of VAP-1 by either means left tumor homing of regulatory T cells and type 2 immune-suppressing monocytes/macrophages intact. Notably, VAP-1 inhibitors, but not anti-VAP-1 Abs, retarded the growth of melanomas and lymphomas and reduced tumor neoangiogenesis. The VAP-1 inhibitors also reduced the binding of Gr-1(+) myeloid cells to the tumor vasculature. We conclude that tumors use the catalytic activity of VAP-1 to recruit myeloid cells into tumors and to support tumor progression. Small-molecule VAP-1 inhibitors therefore might be a potential new tool for immunotherapy of tumors.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20154208
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8996
      1. Author :
        Holland, Sacha J; Pan, Alison; Franci, Christian; Hu, Yuanming; Chang, Betty; Li, Weiqun; Duan, Matt; Torneros, Allan; Yu, Jiaxin; Heckrodt, Thilo J; Zhang, Jing; Ding, Pingyu; Apatira, Ayodele; Chua, Joanne; Brandt, Ralf; Pine, Polly; Goff, Dane; Singh, Rajinder; Payan, Donald G; Hitoshi, Yasumichi
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Cancer research
      6. Products :
      7. Volume :
        70
      8. Issue :
        4
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Antineoplastic Agents; Benzocycloheptenes; Bioware; Breast Neoplasms; Carcinoma; Female; Hela Cells; Humans; K562 Cells; MDA-MB-231-D3H2LN cells; Mice; Mice, Inbred BALB C; Mice, Nude; Neoplasm Invasiveness; Neoplasm Metastasis; Oncogene Proteins; Protein kinase inhibitors; Proto-Oncogene Proteins; Receptor Protein-Tyrosine Kinases; Survival Analysis; Triazoles; Tumor Cells, Cultured; Xenograft Model Antitumor Assays
      12. Abstract :
        Accumulating evidence suggests important roles for the receptor tyrosine kinase Axl in cancer progression, invasion, metastasis, drug resistance, and patient mortality, highlighting Axl as an attractive target for therapeutic development. We have generated and characterized a potent and selective small-molecule inhibitor, R428, that blocks the catalytic and procancerous activities of Axl. R428 inhibits Axl with low nanomolar activity and blocked Axl-dependent events, including Akt phosphorylation, breast cancer cell invasion, and proinflammatory cytokine production. Pharmacologic investigations revealed favorable exposure after oral administration such that R428-treated tumors displayed a dose-dependent reduction in expression of the cytokine granulocyte macrophage colony-stimulating factor and the epithelial-mesenchymal transition transcriptional regulator Snail. In support of an earlier study, R428 inhibited angiogenesis in corneal micropocket and tumor models. R428 administration reduced metastatic burden and extended survival in MDA-MB-231 intracardiac and 4T1 orthotopic (median survival, >80 days compared with 52 days; P < 0.05) mouse models of breast cancer metastasis. Additionally, R428 synergized with cisplatin to enhance suppression of liver micrometastasis. Our results show that Axl signaling regulates breast cancer metastasis at multiple levels in tumor cells and tumor stromal cells and that selective Axl blockade confers therapeutic value in prolonging survival of animals bearing metastatic tumors.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20145120
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8949
      1. Author :
        Quintela-Fandino, Miguel; Arpaia, Enrico; Brenner, Dirk; Goh, Theo; Yeung, Faith Au; Blaser, Heiko; Alexandrova, Roumiana; Lind, Evan F; Tusche, Mike W; Wakeham, Andrew; Ohashi, Pamela S; Mak, Tak W
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Proceedings of the National Academy of Sciences of the United States of America
      6. Products :
      7. Volume :
        107
      8. Issue :
        6
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Actins; Animals; B16-F10-luc-G5; Bioware; Breast Neoplasms; Cell Line, Tumor; Cell Movement; Cofilin 1; Cytoskeleton; Female; Humans; Immunoblotting; Immunoprecipitation; Male; Mammary Neoplasms, Experimental; MDA-MB-231-D3H2LN cells; Melanoma, Experimental; Mice; Mice, Inbred C57BL; Neoplasm Invasiveness; Neoplasm Metastasis; Phosphorylation; Protein Binding; Protein Kinases; Protein Phosphatase 2; Protein-Serine-Threonine Kinases; RNA Interference; Transplantation, Heterologous
      12. Abstract :
        Metastasis leads to the death of most cancer patients, and basal breast cancer is the most aggressive breast tumor type. Metastasis involves a complex cell migration process dependent on cytoskeletal remodeling such that targeting such remodeling in tumor cells could be clinically beneficial. Here we show that Hormonally Up-regulated Neu-associated Kinase (HUNK) is dramatically down-regulated in tumor samples and cell lines derived from basal breast cancers. Reconstitution of HUNK expression in basal breast cancer cell lines blocked actin polymerization and reduced cell motility, resulting in decreased metastases in two in vivo murine cancer models. Mechanistically, HUNK overexpression sustained the constitutive phosphorylation and inactivation of cofilin-1 (CFL-1), thereby blocking the incorporation of new actin monomers into actin filaments. HUNK reconstitution in basal breast cancer cell lines prevented protein phosphatase 2-A (PP2A), a phosphatase putatively acting on CFL-1, from binding to CFL-1. Our investigation of HUNK suggests that the interaction between PP2A and CFL-1 may be a target for antimetastasis therapy, particularly for basal breast cancers.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20133759
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8951
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