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1,295 results on '"Croce, C. M."'

74. Correction: Fhit modulation of the Akt-survivin pathway in lung cancer cells: Fhit-tyrosine 114 (Y114) is essential

Author

Semba, S., primary, Trapasso, F., additional, Fabbri, M., additional, McCorkell, K. A., additional, Volinia, S., additional, Druck, T., additional, Iliopoulos, D., additional, Pekarsky, Y., additional, Ishii, H., additional, Garrison, P. N., additional, Barnes, L. D., additional, Croce, C. M., additional, and Huebner, K., additional

Published
2019
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78. Chromosome Alterations in Oncogenesis

Author

Nowell, P. C., Emanuel, B. S., Finan, J. B., Erikson, J., Croce, C. M., Heimpel, H., editor, Huhn, D., editor, Mueller-Eckhardt, C., editor, Ruhenstroth-Bauer, G., editor, Neth, Rolf, editor, Gallo, Robert C., editor, Greaves, Melvyn F., editor, and Janka, Gritta, editor

Published
1985
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81. Molecular Genetics of Human B-cell Neoplasia

Author

Tsujimoto, Y., Croce, C. M., Clarke, A., editor, Compans, R. W., editor, Cooper, M., editor, Eisen, H., editor, Goebel, W., editor, Koprowski, H., editor, Melchers, F., editor, Oldstone, M., editor, Vogt, P. K., editor, Wagner, H., editor, Wilson, I., editor, Melchers, Fritz, editor, and Potter, Michael, editor

Published
1986
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82. The Translocated c-myc Oncogene of Burkitt Lymphoma is Differentially Regulated in Lymphoblastoid vs Plasma Cells

Author

Croce, C. M., Erikson, J., Ar-Rushdi, A., Aden, D., Nishikura, K., Cooper, M., editor, Goebel, W., editor, Hofschneider, P. H., editor, Koprowski, H., editor, Melchers, F., editor, Oldstone, M., editor, Rott, R., editor, Schweiger, H. G., editor, Vogt, P. K., editor, Zinkernagel, R., editor, Potter, Michael, editor, Melchers, Fritz, editor, and Weigert, Martin, editor

Published
1984
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83. Human T Cell Hybridomas with Tetanus-Toxoid-Specific Helper Activity

Author

DeFreitas, E. C., Vella, S., Linnenbach, A., Croce, C. M., Koprowski, H., Cooper, M., editor, Henle, W., editor, Hofschneider, P. H., editor, Koprowski, H., editor, Melchers, F., editor, Rott, R., editor, Schweiger, H. G., editor, Vogt, P. K., editor, Zinkernagel, R., editor, Boehmer, H. V., editor, Haas, W., editor, Köhler, G., editor, and Zeuthen, J., editor

Published
1982
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84. Bcl-2α Encodes a Novel Small Molecular Weight GTP Binding Protein

Author

Haldar, S., Beatty, Ch., Croce, C. M., Melchers, Fritz, editor, Albert, E. D., editor, von Boehmer, H., editor, Dierich, M. P., editor, Du Pasquier, L., editor, Eichmann, K., editor, Gemsa, D., editor, Götze, O., editor, Kalden, J. R., editor, Kaufmann, S. H. E., editor, Kirchner, H., editor, Resch, K., editor, Riethmüller, G., editor, Schimpl, A., editor, Sorg, C., editor, Steinmetz, M., editor, Wagner, H., editor, and Zachau, H. G., editor

Published
1989
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88. MicroRNA fingerprints in juvenile myelomonocytic leukemia (JMML) identified miR-150-5p as a tumor suppressor and potential target for treatment

Author

Leoncini, P. P., Bertaina, A., Papaioannou, D., Flotho, C., Masetti, R., Bresolin, S., Menna, G., Santoro, N., Zecca, M., Basso, G., Nigita, G., Veneziano, D., Pagotto, S., D'Ovidio, K., Rota, R., Dorrance, A., Croce, C. M., Niemeyer, C., Locatelli, Franco, Garzon, R., Locatelli F. (ORCID:0000-0002-7976-3654), Leoncini, P. P., Bertaina, A., Papaioannou, D., Flotho, C., Masetti, R., Bresolin, S., Menna, G., Santoro, N., Zecca, M., Basso, G., Nigita, G., Veneziano, D., Pagotto, S., D'Ovidio, K., Rota, R., Dorrance, A., Croce, C. M., Niemeyer, C., Locatelli, Franco, Garzon, R., and Locatelli F. (ORCID:0000-0002-7976-3654)

Abstract

Juvenile myelomonocytic leukemia (JMML) is an aggressive leukemia of early childhood characterized by aberrant proliferation of myelomonocytic cells and hypersensitivity to GM-CSF stimulation. Mutually exclusive mutations in the RAS/ERK pathway genes such as PTPN11, NRAS, KRAS, CBL, or NF1 are found in ~90% of the cases. These mutations give rise to disease at least in part by activating STAT5 through phosphorylation and by promoting cell growth. MicroRNAs (miRs) are small non-coding RNAs that regulate gene expression, which are often deregulated in leukemia. However, little is known about their role in JMML. Here, we report distinctive miR expression signatures associated with the molecular subgroups of JMML. Among the downregulated miRs in JMML, miR-150-5p was found to target STAT5b, a gene which is often over-activated in JMML, and contributes to the characteristic aberrant signaling of this disorder. Moreover, loss of miR-150-5p and upregulation of STAT5b expression were also identified in a murine model of JMML. Ectopic overexpression of miR-150-5p in mononuclear cells from three JMML patients significantly decreased cell proliferation. Altogether, our data indicate that miR expression is deregulated in JMML and may play a role in the pathogenesis of this disorder by modulating key effectors of cytokine receptor pathways.

Published
2016

89. MicroRNA signatures of TRAIL resistance in human non small cell lung cancer. Oncogene

Author

Garofalo M., Quintavalle C., Di Leva G., Zanca C., Romano G., Taccioli C., Liu C. G., Croce C. M., CONDORELLI, GEROLAMA, Garofalo, M., Quintavalle, C., Di Leva, G., Zanca, C., Romano, G., Taccioli, C., Liu, C. G., Croce, C. M., and Condorelli, Gerolama

Subjects
lung cancer, microRNA, apoptosi
Abstract

To define novel pathways that regulate susceptibility to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in non-small cell lung cancer (NSCLC), we have performed genome-wide expression profiling of microRNAs (miRs). We show that in TRAIL-resistant NSCLC cells, levels of different miRs are increased, and in particular, miR-221 and -222. We demonstrate that these miRs impair TRAIL-dependent apoptosis by inhibiting the expression of key functional proteins. Indeed, transfection with anti-miR-221 and -222 rendered CALU-1-resistant cells sensitive to TRAIL. Conversely, H460-sensitive cells treated with -221 and -222 pre-miRs become resistant to TRAIL. miR-221 and -222 target the 3'-UTR of Kit and p27(kip1) mRNAs, but interfere with TRAIL signaling mainly through p27(kip1). In conclusion, we show that high expression levels of miR-221 and -222 are needed to maintain the TRAIL-resistant phenotype, thus making these miRs as promising therapeutic targets or diagnostic tool for TRAIL resistance in NSCLC.

Published
2008

90. MicroRNAs in human cancer: from research to therapy

Author

M. NEGRINI, SABBIONI S, CROCE C. M., FERRACIN, MANUELA, Negrini, M., Ferracin, Manuela, Sabbioni, S, and Croce, C. M.

Subjects
microRNA, oncogene, cancer, tumor suppressor genes, microarray
Abstract

Numerous miRNAs are deregulated in human cancers, and experimental evidence indicates that they can play roles as oncogenes or tumor suppressor genes. Similarly to cancer genes that encode proteins, deregulation of miRNA-encoding genes is associated with genetic or epigenetic alterations, such as deletions, amplifications, point mutations and aberrant DNA methylation. The discovery that miRNAs interact with known oncogenes has established further links with molecular pathways implicated in malignant transformation. Finally, miRNAs can be used as diagnostic markers, and their potential as therapeutic molecules has moved miRNAs from the area of basic research to the field of cancer biotechnology.

Published
2007

91. microRNA signature of hypoxia

Author

KULSHRESHTHA R, WOJCIK S. E, GARZON R, ALDER H, AGOSTO PEREZ F. J, DAVULURI R, LIU C. G, CROCE C. M, M. NEGRINI, CALIN G. A, IVAN M. A., FERRACIN, MANUELA, KULSHRESHTHA R, FERRACIN M, WOJCIK S. E, GARZON R, ALDER H, AGOSTO-PEREZ F. J, DAVULURI R, LIU C. G, CROCE C. M, M. NEGRINI, CALIN G. A, and IVAN M. A

Subjects
Chromatin Immunoprecipitation, Colonic Neoplasm, Oligonucleotide Array Sequence Analysi, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, Apoptosi, MicroRNA, Transfection, Plasmid, Cell Hypoxia, HT29 Cell, Genes, Reporter, Cell Line, Tumor, HCT116 Cell, Female, Luciferase, Breast Neoplasm, Human
Abstract

Recent research has identified critical roles for microRNAs in a large number of cellular processes, including tumorigenic transformation. While significant progress has been made towards understanding the mechanisms of gene regulation by microRNAs, much less is known about factors affecting the expression of these noncoding transcripts. Here, we demonstrate for the first time a functional link between hypoxia, a well-documented tumor microenvironment factor, and microRNA expression. Microarray-based expression profiles revealed that a specific spectrum of microRNAs (including miR-23, -24, -26, -27, -103, -107, -181, -210, and -213) is induced in response to low oxygen, at least some via a hypoxia-inducible-factor-dependent mechanism. Select members of this group (miR-26, -107, and -210) decrease proapoptotic signaling in a hypoxic environment, suggesting an impact of these transcripts on tumor formation. Interestingly, the vast majority of hypoxia-induced microRNAs are also overexpressed in a variety of human tumors.

Published
2007

94. Identification of the genes up- and down-regulated by the high mobility group A1 (HMGA1) proteins: tissue specificity of the HMGA1-dependent gene regulation

Author

Martinez Hoyos J., Kruhoffer M., Arra C., Orntoft T. F., Croce C. M., FEDELE, MONICA, BATTISTA, SABRINA, PENTIMALLI, FRANCESCA, FUSCO, ALFREDO, Martinez Hoyos, J., Fedele, Monica, Battista, Sabrina, Pentimalli, Francesca, Kruhoffer, M., Arra, C., Orntoft, T. F., Croce, C. M., and Fusco, Alfredo

Subjects
HMGA Proteins, Mice, Knockout, HMGA1, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, Stem Cells, Down-Regulation, Gene Expression Regulation, Developmental, Embryo, Mammalian, Neoplasm Proteins, Up-Regulation, Mice, ES cell, Animals, Inhibitor of Differentiation Proteins, Promoter Regions, Genetic, knockout mice, Cell Line, Transformed
Abstract

High mobility group A (HMGA) proteins are chromatinic proteins that do not have transcriptional activity per se, however, by interacting with the transcription machinery, they regulate, negatively or positively, the expression of several genes. We searched for genes regulated by HMGA1 proteins using microarray analysis in embryonic stem (ES) cells bearing one or two disrupted hmga1 alleles. We identified 87 transcripts increased and 163 transcripts decreased of at least 4-fold in hmga1-/- ES cells. For some of them, a HMGA1-dose dependency was observed, because an intermediate level was observed in the heterozygous ES cells. When the expression analysis of these genes was extended to embryonic fibroblasts and adult tissues such as heart, spleen, and liver from hmga1-knockout mice, contrasting results were obtained. In fact, aside some genes showing the same HMGA1 regulation observed in ES cells, there were some genes that did not modify their expression, and others showing a HMGA1-mediated regulation but in an opposite direction. These results clearly indicate that HMGA1-mediated gene regulation depends on the cellular context. Finally for a couple of analyzed HMGA1-regulated genes, electrophoretic mobility shift assay and chromatin immunoprecipitation revealed a direct binding of HMGA1 proteins to their promoters, suggesting a HMGA1-direct regulation of their expression.

Published
2004

97. Monoclonal antibodies and immobilized antibodies

Author

Linhardt, Robert J., Abell C. W., Denney R. M., Altrock B. W., Auerbach R., Bernal S. D., Canfield R. E., Ehrlich P. H., Moyle W. R., Chan T. S., Chang T. W., Chang N. T., Cidlowski J. A., Viceps M. D., Cote R. J., Morrissey D. M., Houghton A. N., Beattie E. J., Oettgen H. F., Old L. J., Croce C. M., Cubicciotti R. S., Karu A. E., Krauss R. M., Cullor J. S., Deutsch A., Brandwein H., Platt H., Hunter D. M., Dubitsky A., Durham S. M., Dolbeare F. A., Gray J. W., Dreesman G. R., Kendall C. E., Egrie J. C., Frackelton A. R., Eisen H. N., Ross A. H., Gay S., Geirnaert G., Geltosky J. E., Goldberg E. H., Goldwasser E., Kavinsky C., Weiss T. L., Gratzner H. G., Hampar B., Zweig M., Showalter S. D., Handley H. H., Glassy M. C., Hagiwara Y., Hagiwara H., Huang C. M., Cohen S. N., Hughes J. V., Scolnick E. M., Tomassini J. E., Jefferis R., Steensgaard J., Kaplan H. S., Teng N. N. H., Earn K. S., Calvo R. F., Kass L., Kettman J. R., Norgard M. V., Khazaeli M. B., Beierwaltes W. H., England B. G., Kung P. C., Goldstein G., Lanier L., Phillips J., Lanier L., Warner N. L., Larrick J. W., Raubitschek A. R., Truitt K. E., Lazarus H., Schwaber J. F., Lewicki J., Lewis C., Olander J. V., Tolbert W. R., Milford E. L., Carpenter C. B., Paradysz J. M., Mosher D. F., Mulshine J. L., Minna J. D., Murray K. A., Neville D. M., Youle R. J., Neville D. M., Youle R. J., Nicolson M., Pastan I., Willingham M. C., Fitzgerald D. J., Pucci A., Smithyman A. M., Slade M. B., French P. W., Wijffels G., Pukel C. S., Lloyd K. O., Travassos L. R., Dippold W. G., Oettgen H. F., Old L. J., Reckel R. P., Harris J. L., Wellerson R., Shaw S. M., Kaplan P. M., Reinherz E. L., Schlossman S. F., Mener S. C., Sakamoto J., Cordon C. C., Friedman E., Finstad C. L., Enker W. E., Melamed M. R., Lloyd K. O., Oettgen J. F., Old L. J., Scannon P. J., Spitler L. E., Lee H. M., Kawahata R. T., Mischak R. P., Schlom J., Colcher D., Nuti M., Hand P. H., Austin F., Shockman G. D., Jackson D. E., Wong W., Steplewski Z., Koprowski H., Herlyn M., Strand M., Trowbridge I. S., Urdal D. L., March C. J., Dower S. K., Wands J. R., Zurawski V. R., White C. A., Dulbecco R., Allen W. R., Arnold E. C., Flasher M., Freedman H. H., Heath T. D., Shek P., Papahadjopoulos D., Ikeda M., Sakamoto S., Suzuki K., Kuboyama M., Harada Y., Kawashiri A., Takahashi E., Lee H. S., Margel S., Neville D. M., Youle R. J., Nowinski R. C., Hoffman A. S., Peterson J. W., Platt K. B., Reed D. E., Real F. X., Mattes M. J., Houghton A. N., Livingston P. O., Lloyd K. O., Oettgen H. F., Old L. J., Rembaum A., Yen R. C. K., Rosenstein R., and Schneider B.

Published
1987
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