521 results on '"Calabretta B."'
Search Results
2. Persistence of Drug-Resistant Leukemic Stem Cells and Impaired NK Cell Immunity in CML Patients Depend on MIR300 Antiproliferative and PP2A-Activating Functions
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Silvestri, G, Trotta, R, Stramucci, L, Ellis, J, Harb, J, Neviani, P, Wang, S, Eisfeld, A, Walker, C, Zhang, B, Srutova, K, Gambacorti-Passerini, C, Pineda, G, Jamieson, C, Stagno, F, Vigneri, P, Nteliopoulos, G, May, P, Reid, A, Garzon, R, Roy, D, Moutuou, M, Guimond, M, Hokland, P, Deininger, M, Fitzgerald, G, Harman, C, Dazzi, F, Milojkovic, D, Apperley, J, Marcucci, G, Qi, J, Polakova, K, Zou, Y, Fan, X, Baer, M, Calabretta, B, Perrotti, D, Silvestri G., Trotta R., Stramucci L., Ellis J. J., Harb J. G., Neviani P., Wang S., Eisfeld A. -K., Walker C. J., Zhang B., Srutova K., Gambacorti-Passerini C., Pineda G., Jamieson C. H. M., Stagno F., Vigneri P., Nteliopoulos G., May P. C., Reid A. G., Garzon R., Roy D. -C., Moutuou M. M., Guimond M., Hokland P., Deininger M. W., Fitzgerald G., Harman C., Dazzi F., Milojkovic D., Apperley J. F., Marcucci G., Qi J., Polakova K. M., Zou Y., Fan X., Baer M. R., Calabretta B., Perrotti D., Silvestri, G, Trotta, R, Stramucci, L, Ellis, J, Harb, J, Neviani, P, Wang, S, Eisfeld, A, Walker, C, Zhang, B, Srutova, K, Gambacorti-Passerini, C, Pineda, G, Jamieson, C, Stagno, F, Vigneri, P, Nteliopoulos, G, May, P, Reid, A, Garzon, R, Roy, D, Moutuou, M, Guimond, M, Hokland, P, Deininger, M, Fitzgerald, G, Harman, C, Dazzi, F, Milojkovic, D, Apperley, J, Marcucci, G, Qi, J, Polakova, K, Zou, Y, Fan, X, Baer, M, Calabretta, B, Perrotti, D, Silvestri G., Trotta R., Stramucci L., Ellis J. J., Harb J. G., Neviani P., Wang S., Eisfeld A. -K., Walker C. J., Zhang B., Srutova K., Gambacorti-Passerini C., Pineda G., Jamieson C. H. M., Stagno F., Vigneri P., Nteliopoulos G., May P. C., Reid A. G., Garzon R., Roy D. -C., Moutuou M. M., Guimond M., Hokland P., Deininger M. W., Fitzgerald G., Harman C., Dazzi F., Milojkovic D., Apperley J. F., Marcucci G., Qi J., Polakova K. M., Zou Y., Fan X., Baer M. R., Calabretta B., and Perrotti D.
- Abstract
Persistence of drug-resistant quiescent leukemic stem cells (LSC) and impaired natural killer (NK) cell immune response account for relapse of chronic myelogenous leukemia (CML). Inactivation of protein phosphatase 2A (PP2A) is essential for CML-quiescent LSC survival and NK cell antitumor activity. Here we show that MIR300 has antiproliferative and PP2A-activating functions that are dose dependently differentially induced by CCND2/CDK6 and SET inhibition, respectively. MIR300 is upregulated in CML LSCs and NK cells by bone marrow microenvironment (BMM) signals to induce quiescence and impair immune response, respectively. Conversely, BCR-ABL1 downregulates MIR300 in CML progenitors to prevent growth arrest and PP2A-mediated apoptosis. Quiescent LSCs escape apoptosis by upregulating TUG1 long noncoding RNA that uncouples and limits MIR300 function to cytostasis. Genetic and pharmacologic MIR300 modulation and/or PP2A-activating drug treatment restore NK cell activity, inhibit BMM-induced growth arrest, and selectively trigger LSC apoptosis in vitro and in patient-derived xenografts; hence, the importance of MIR300 and PP2A activity for CML development and therapy. SIGNIFICANCE: Tumor-naïve microenvironment–induced MIR300 is the only tumor suppressor miRNA that induces CML LSC quiescence while inhibiting NK cell antitumor immune response, and CML LSC/ progenitor cell apoptosis through its anti-proliferative and PP2A-activating functions, respectively. Thus, the importance of MIR300 and PP2A-activating drugs for formation/survival and eradication of drug-resistant CML LSCs, respectively.
- Published
- 2020
3. Antisense strategy for cancer therapy
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Skorski, T., Szczylik, C., Calabretta, B., Azzi, Angelo, editor, Packer, Lester, editor, Mackiewicz, A., editor, and Sehgal, P. B., editor
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- 1998
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4. Expression of Cell-Cycle-Dependent Genes in Phytohemagglutinin-Stimulated Human Lymphocytes
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Kaczmarek, L., Calabretta, B., and Baserga, R.
- Published
- 1985
5. miRNA let-7c promotes granulocytic differentiation in acute myeloid leukemia
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Pelosi, A, Careccia, S, Lulli, V, Romania, P, Marziali, G, Testa, U, Lavorgna, S, Lo-Coco, F, Petti, M C, Calabretta, B, Levrero, M, Piaggio, G, and Rizzo, M G
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- 2013
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6. Gfi-1 inhibits proliferation and colony formation of p210BCR/ABL-expressing cells via transcriptional repression of STAT 5 and Mcl-1
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Soliera, A R, Mariani, S A, Audia, A, Lidonnici, M R, Addya, S, Ferrari-Amorotti, G, Cattelani, S, Manzotti, G, Fragliasso, V, Peterson, L, Perini, G, Holyoake, T L, and Calabretta, B
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- 2012
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7. c-Myb and its target Bmi1 are required for p190BCR/ABL leukemogenesis in mouse and human cells
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Waldron, T, De Dominici, M, Soliera, A R, Audia, A, Iacobucci, I, Lonetti, A, Martinelli, G, Zhang, Y, Martinez, R, Hyslop, T, Bender, T P, and Calabretta, B
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- 2012
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8. Isolation and functional assessment of common, polymorphic variants of the B-MYB proto-oncogene associated with a reduced cancer risk
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Schwab, R, Bussolari, R, Corvetta, D, Chayka, O, Santilli, G, Kwok, J M-M, Amorotti, G F, Tonini, G P, Iacoviello, L, Bertorelle, R, Menin, C, Hubank, M, Calabretta, B, and Sala, A
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- 2008
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9. Expression of CCL9/MIP-1γ is repressed by BCR/ABL and its restoration suppresses in vivo leukemogenesis of 32D-BCR/ABL cells
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Iotti, G, Ferrari-Amorotti, G, Rosafio, C, Corradini, F, Lidonnici, M R, Ronchetti, M, Bardini, M, Zhang, Y, Martinez, R, Blasi, F, and Calabretta, B
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- 2007
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10. Coding sequence and intron–exon junctions of the c-myb gene are intact in the chronic phase and blast crisis stages of chronic myeloid leukemia patients
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Bussolari, R., Candini, O., Colomer, D., Corradini, F., Guerzoni, C., Mariani, S.A., Cattelani, S., Silvestri, C., Pecorari, L., Iacobucci, I., Soverini, S., Fasano, T., Martinelli, G., Cervantes, F., and Calabretta, B.
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- 2007
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11. hIan5: the human ortholog to the rat Ian4/Iddm1/lyp is a new member of the Ian family that is overexpressed in B-cell lymphoid malignancies
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Zenz, T, Roessner, A, Thomas, A, Fröhling, S, Döhner, H, Calabretta, B, and Dahéron, L
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- 2004
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12. Ponatinib and inhibition of the PI3K/Akt/mTOR pathway induces cell death and protective autophagy in TKI-resistant CML stem/progenitor cells: 2
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Helgason, G V, Allan, E, Galavotti, S, Audia, A, Hamilton, A, Mukhopadhyay, A, Karvela, M, Salomoni, P, Calabretta, B, and Holyoake, T L
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- 2012
13. Effect of bcr-abl oligodeoxynucleotides on the clonogenic growth of chronic myelogenous leukaemia cells
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de Fabritiis, P, Skorski, T, De Propris, MS, Paggi, MG, Nieborowska-Skorska, M, Lisci, A, Buffolino, S, Campbell, K, Geiser, T, and Calabretta, B
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- 1997
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14. Cell Cycle Genes as Potential Oncogenes
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Baserga, R., Kaczmarek, L., Calabretta, B., Battini, R., Ferrari, S., Tanner, Widmar, editor, and Gallwitz, Dieter, editor
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- 1986
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15. Erratum: Isolation and functional assessment of common, polymorphic variants of the B-MYB proto-oncogene associated with a reduced cancer risk
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Schwab, R, Bussolari, R, Corvetta, D, Chayka, O, Santilli, G, Kwok, J M-M, Ferrari-Amorotti, G, Tonini, G P, Iacoviello, L, Bertorelle, R, Menin, C, Hubank, M, Calabretta, B, and Sala, A
- Published
- 2008
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16. Different Frequency Classes of Sequences in Heterogeneous Nuclear RNA of Normal Promyelocytes and Lymphoblasts and of Leukemic Blast Cells of Circulating Blood and of the HL60 Line
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Torelli, U., Torelli, G., Narni, F., Donelli, A., Ferrari, S., Franchini, G., Calabretta, B., Heimpel, H., editor, Huhn, D., editor, Mueller-Eckhardt, C., editor, Ruhenstroth-Bauer, G., editor, Neth, Rolf, editor, Gallo, Robert C., editor, Graf, Thomas, editor, Mannweiler, Klaus, editor, and Winkler, Kurt, editor
- Published
- 1981
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17. Expression of CCL9/MIP-1bold italic gamma is repressed by BCR/ABL and its restoration suppresses in vivo leukemogenesis of 32D-BCR/ABL cells
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Iotti, G, Ferrari Amorotti, G, Rosafio, C, Corradini, F, Lidonnici, M, Ronchetti, M, Bardini, M, Zhang, Y, Martinez, R, Blasi, F, Calabretta, B, Lidonnici, MR, Calabretta, B., BARDINI, MICHELA, Iotti, G, Ferrari Amorotti, G, Rosafio, C, Corradini, F, Lidonnici, M, Ronchetti, M, Bardini, M, Zhang, Y, Martinez, R, Blasi, F, Calabretta, B, Lidonnici, MR, Calabretta, B., and BARDINI, MICHELA
- Abstract
Transformation of hematopoietic cells by the BCR/ABL oncogene is caused by perturbation of signal transduction pathways leading to altered patterns of gene expression and activity. By oligonucleotide microarray hybridization of polysomal RNA of untreated and STI571-treated 32DBCR/ABL cells, we identified the beta-chemokine CCL9 as a gene regulated by BCR/ABL in a tyrosine kinasedependent manner. BCR/ABL repressed CCL9 expression at the transcriptional level by mechanisms involving suppression of p38 MAP kinase, and modulation of the activity of CDP/cut and C/EBP alpha, two transcription regulators of myeloid differentiation. However, repression of C/EBP-dependent transcription did not prevent the induction of CCL9 expression by STI571, suggesting that C/EBP alpha is involved in maintaining rather than in inducing CCL9 expression. Restoration of CCL9 expression in 32D-BCR/ABL cells had no effect on the in vitro proliferation of these cells, but reduced their leukemogenic potential in vivo, possibly by recruitment of CD3-positive immune cells. Together, these findings suggest that downregulation of chemokine expression may be involved in BCR/ABL-dependent leukemogenesis by altering the relationship between transformed cells and the microenvironment
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- 2007
18. Inducible activation of C/EBPb, a gene negatively regulated by BCR/ABL, inhibits proliferation and promotes differentiation of BCR/ABL-expressing cells
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Guerzoni, C, Bardini, M, Mariani, S, Ferrari Amorotti, G, Neviani, P, Panno, M, Zhang, Y, Martinez, R, Perrotti, D, Calabretta, B, Mariani, SA, Panno, ML, Calabretta, B., BARDINI, MICHELA, Guerzoni, C, Bardini, M, Mariani, S, Ferrari Amorotti, G, Neviani, P, Panno, M, Zhang, Y, Martinez, R, Perrotti, D, Calabretta, B, Mariani, SA, Panno, ML, Calabretta, B., and BARDINI, MICHELA
- Abstract
Translational regulation by oncogenic proteins may be a rapid and efficient mechanism to modulate gene expression. We report here the identification of the CEBPB gene as a target of translational regulation in myeloid precursor cells transformed by the BCR/ABL oncogene. Expression of CEBPB was repressed in 32D-BCR/ABL cells and reinduced by imatinib (STI571) via a mechanism that appears to depend on expression of the CUG-repeat RNA-binding protein CUGBP1 and the integrity of the CUG-rich intercistronic region of c/ebp beta mRNA. Constitutive expression or conditional activation of wildtype CEBPB induced differentiation and inhibited proliferation of 32D-BCR/ABL cells in vitro and in mice, but a DNA binding-deficient CEBPB mutant had no effect. The proliferation-inhibitory effect of CEBPB was, in part, mediated by the CEBPB-induced GADD45A gene. Because expression of CEBPB (and CEBPA) is low in the blast crisis (BC) stage of chronic myelogenous leukemia (CML) and is inversely correlated with BCR/ABL tyrosine kinase levels, these findings point to the therapeutic potential of restoring C/EBP activity in CML-BC and, perhaps, other types of acute leukemia.
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- 2006
19. Effects of C/EBPalpha and C/EBPbeta in BCR/ABL-Expressing Cells: Differences and Similarities
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Guerzoni, C, Ferrari Amorotti, G, Bardini, M, Mariani, S, Calabretta, B, Mariani, SA, Calabretta, B., Guerzoni, C, Ferrari Amorotti, G, Bardini, M, Mariani, S, Calabretta, B, Mariani, SA, and Calabretta, B.
- Abstract
C/EBP alpha and C/EBP beta, two transcription factors of the C/EBP family play important roles in the proliferation and differentiation of various cell types including myeloid progenitors. Expression of C/EBP alpha and C/EBP beta is repressed in myeloid blast crisis of Chronic Myelogenous Leukemia by mechanisms that involve translation repression which depends on the interaction of RNA-binding proteins with conserved binding sites in the 5'UTR of c/ebp alpha and c/ebp beta mRNA. Ectopic expression of C/EBP alpha and C/EBP beta in myeloid progenitors expressing the BCR/ABL oncogene inhibits proliferation, induces differentiation and suppresses leukemogenesis in mice, but C/EBP a is markedly more effective than C/EBP beta. The more potent effects of C/EBP a probably depends on protein-protein interaction with cell-cycle regulatory proteins, but the pattern of genes modulated by C/EBP alpha and C/EBP beta is not completely overlapping. This suggests that transcription-dependent and -independent effects are both involved and support the therapeutic potential of reactivating C/EBP alpha and C/EBP beta expression in leukemic cells
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- 2006
20. Expression of μ-protocadherin is negatively regulated by the activation of the β-catenin signaling pathway in normal and cancer colorectal enterocytes
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Montorsi, L, primary, Parenti, S, additional, Losi, L, additional, Ferrarini, F, additional, Gemelli, C, additional, Rossi, A, additional, Manco, G, additional, Ferrari, S, additional, Calabretta, B, additional, Tagliafico, E, additional, Zanocco-Marani, T, additional, and Grande, A, additional
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- 2016
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21. Kinetics of hybridization to human DNA of heterogeneous nuclear RNA isolated from normal human lymphoblasts and acute leukemia blast cells
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Torelli, G., Narni, F., Franchini, G., Donelli, A., Ferrari, S., Calabretta, B., Torelli, U., and Bosi, P.
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- 1979
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22. Cell cycle dependent genes inducible by different mitogens in cells from different species
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Gibson, C. W., Rittling, S. R., Hirschhorn, R. R., Kaczmarek, L., Calabretta, B., Stiles, C. D., and Baserga, R.
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- 1986
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23. Erratum: Targeting autophagy potentiates tyrosine kinase inhibitor-induced cell death in Philadelphia chromosome-positive cells, including primary CML stem cells (Journal of Clinical Investigation (2009) 119:5 (1109-1123) DOI: 10.1172/JCI35660)
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Bellodi, C., Lidonnici, M. R., Hamilton, A., Helgason, G. V., Soliera, A. R., Ronchetti, M., Galavotti, S., Young, K. W., Selmi, T., Yacobi, R., Van Etten, R. A., Donato, N., Hunter, A., Dinsdale, D., Tirro, E., Vigneri, P., Nicotera, P., Dyer, M. J., Holyoake, T., Salomoni, P., and Calabretta, B.
- Published
- 2013
24. miRNA let-7c promotes granulocytic differentiation in acute myeloid leukemia. Oncogene
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Pelosi, A, Careccia, S, Lulli, V, Romania, P, Marziali, G, Testa, U, Lavorgna, S, LO COCO, F, Petti, M, Calabretta, B, Levrero, M, Piaggio, G, and Rizzo, M
- Subjects
Settore MED/15 - Malattie del Sangue - Published
- 2012
25. Guidelines for the use and interpretation of assays for monitoring autophagy
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Klionsky, D.J. Abdalla, F.C. Abeliovich, H. Abraham, R.T. Acevedo-Arozena, A. Adeli, K. Agholme, L. Agnello, M. Agostinis, P. Aguirre-Ghiso, J.A. Ahn, H.J. Ait-Mohamed, O. Ait-Si-Ali, S. Akematsu, T. Akira, S. Al-Younes, H.M. Al-Zeer, M.A. Albert, M.L. Albin, R.L. Alegre-Abarrategui, J. Aleo, M.F. Alirezaei, M. Almasan, A. Almonte-Becerril, M. Amano, A. Amaravadi, R. Amarnath, S. Amer, A.O. Andrieu-Abadie, N. Anantharam, V. Ann, D.K. Anoopkumar-Dukie, S. Aoki, H. Apostolova, N. Arancia, G. Aris, J.P. Asanuma, K. Asare, N.Y.O. Ashida, H. Askanas, V. Askew, D.S. Auberger, P. Baba, M. Backues, S.K. Baehrecke, E.H. Bahr, B.A. Bai, X.-Y. Bailly, Y. Baiocchi, R. Baldini, G. Balduini, W. Ballabio, A. Bamber, B.A. Bampton, E.T.W. Bánhegyi, G. Bartholomew, C.R. Bassham, D.C. Bast Jr., R.C. Batoko, H. Bay, B.-H. Beau, I. Béchet, D.M. Begley, T.J. Behl, C. Behrends, C. Bekri, S. Bellaire, B. Bendall, L.J. Benetti, L. Berliocchi, L. Bernardi, H. Bernassola, F. Besteiro, S. Bhatia-Kissova, I. Bi, X. Biard-Piechaczyk, M. Blum, J.S. Boise, L.H. Bonaldo, P. Boone, D.L. Bornhauser, B.C. Bortoluci, K.R. Bossis, I. Bost, F. Bourquin, J.-P. Boya, P. Boyer-Guittaut, M. Bozhkov, P.V. Brady, N.R. Brancolini, C. Brech, A. Brenman, J.E. Brennand, A. Bresnick, E.H. Brest, P. Bridges, D. Bristol, M.L. Brookes, P.S. Brown, E.J. Brumell, J.H. Brunetti-Pierri, N. Brunk, U.T. Bulman, D.E. Bultman, S.J. Bultynck, G. Burbulla, L.F. Bursch, W. Butchar, J.P. Buzgariu, W. Bydlowski, S.P. Cadwell, K. Cahová, M. Cai, D. Cai, J. Cai, Q. Calabretta, B. Calvo-Garrido, J. Camougrand, N. Campanella, M. Campos-Salinas, J. Candi, E. Cao, L. Caplan, A.B. Carding, S.R. Cardoso, S.M. Carew, J.S. Carlin, C.R. Carmignac, V. Carneiro, L.A.M. Carra, S. Caruso, R.A. Casari, G. Casas, C. Castino, R. Cebollero, E. Cecconi, F. Celli, J. Chaachouay, H. Chae, H.-J. Chai, C.-Y. Chan, D.C. Chan, E.Y. Chang, R.C.-C. Che, C.-M. Chen, C.-C. Chen, G.-C. Chen, G.-Q. Chen, M. Chen, Q. Chen, S.S.-L. Chen, W. Chen, X. Chen, X. Chen, X. Chen, Y.-G. Chen, Y. Chen, Y. Chen, Y.-J. Chen, Z. Cheng, A. Cheng, C.H.K. Cheng, Y. Cheong, H. Cheong, J.-H. Cherry, S. Chess-Williams, R. Cheung, Z.H. Chevet, E. Chiang, H.-L. Chiarelli, R. Chiba, T. Chin, L.-S. Chiou, S.-H. Chisari, F.V. Cho, C.H. Cho, D.-H. Choi, A.M.K. Choi, D. Choi, K.S. Choi, M.E. Chouaib, S. Choubey, D. Choubey, V. Chu, C.T. Chuang, T.-H. Chueh, S.-H. Chun, T. Chwae, Y.-J. Chye, M.-L. Ciarcia, R. Ciriolo, M.R. Clague, M.J. Clark, R.S.B. Clarke, P.G.H. Clarke, R. Codogno, P. Coller, H.A. Colombo, M.I. Comincini, S. Condello, M. Condorelli, F. Cookson, M.R. Coombs, G.H. Coppens, I. Corbalan, R. Cossart, P. Costelli, P. Costes, S. Coto-Montes, A. Couve, E. Coxon, F.P. Cregg, J.M. Crespo, J.L. Cronjé, M.J. Cuervo, A.M. Cullen, J.J. Czaja, M.J. D'Amelio, M. Darfeuille-Michaud, A. Davids, L.M. Davies, F.E. De Felici, M. De Groot, J.F. De Haan, C.A.M. De Martino, L. De Milito, A. De Tata, V. Debnath, J. Degterev, A. Dehay, B. Delbridge, L.M.D. Demarchi, F. Deng, Y.Z. Dengjel, J. Dent, P. Denton, D. Deretic, V. Desai, S.D. Devenish, R.J. Di Gioacchino, M. Di Paolo, G. Di Pietro, C. Díaz-Araya, G. Díaz-Laviada, I. Diaz-Meco, M.T. Diaz-Nido, J. Dikic, I. Dinesh-Kumar, S.P. Ding, W.-X. Distelhorst, C.W. Diwan, A. Djavaheri-Mergny, M. Dokudovskaya, S. Dong, Z. Dorsey, F.C. Dosenko, V. Dowling, J.J. Doxsey, S. Dreux, M. Drew, M.E. Duan, Q. Duchosal, M.A. Duff, K. Dugail, I. Durbeej, M. Duszenko, M. Edelstein, C.L. Edinger, A.L. Egea, G. Eichinger, L. Eissa, N.T. Ekmekcioglu, S. El-Deiry, W.S. Elazar, Z. Elgendy, M. Ellerby, L.M. Er Eng, K. Engelbrecht, A.-M. Engelender, S. Erenpreisa, J. Escalante, R. Esclatine, A. Eskelinen, E.-L. Espert, L. Espina, V. Fan, H. Fan, J. Fan, Q.-W. Fan, Z. Fang, S. Fang, Y. Fanto, M. Fanzani, A. Farkas, T. Farré, J.-C. Faure, M. Fechheimer, M. Feng, C.G. Feng, J. Feng, Q. Feng, Y. Fésüs, L. Feuer, R. Figueiredo-Pereira, M.E. Fimia, G.M. Fingar, D.C. Finkbeiner, S. Finkel, T. Finley, K.D. Fiorito, F. Fisher, E.A. Fisher, P.B. Flajolet, M. Florez-McClure, M.L. Florio, S. Fon, E.A. Fornai, F. Fortunato, F. Fotedar, R. Fowler, D.H. Fox, H.S. Franco, R. Frankel, L.B. Fransen, M. Fuentes, J.M. Fueyo, J. Fujii, J. Fujisaki, K. Fujita, E. Fukuda, M. Furukawa, R.H. Gaestel, M. Gailly, P. Gajewska, M. Galliot, B. Galy, V. Ganesh, S. Ganetzky, B. Ganley, I.G. Gao, F.-B. Gao, G.F. Gao, J. Garcia, L. Garcia-Manero, G. Garcia-Marcos, M. Garmyn, M. Gartel, A.L. Gatti, E. Gautel, M. Gawriluk, T.R. Gegg, M.E. Geng, J. Germain, M. Gestwicki, J.E. Gewirtz, D.A. Ghavami, S. Ghosh, P. Giammarioli, A.M. Giatromanolaki, A.N. Gibson, S.B. Gilkerson, R.W. Ginger, M.L. Ginsberg, H.N. Golab, J. Goligorsky, M.S. Golstein, P. Gomez-Manzano, C. Goncu, E. Gongora, C. Gonzalez, C.D. Gonzalez, R. González-Estévez, C. González-Polo, R.A. Gonzalez-Rey, E. Gorbunov, N.V. Gorski, S. Goruppi, S. Gottlieb, R.A. Gozuacik, D. Granato, G.E. Grant, G.D. Green, K.N. Gregorc, A. Gros, F. Grose, C. Grunt, T.W. Gual, P. Guan, J.-L. Guan, K.-L. Guichard, S.M. Gukovskaya, A.S. Gukovsky, I. Gunst, J. Gustafsson, A.B. Halayko, A.J. Hale, A.N. Halonen, S.K. Hamasaki, M. Han, F. Han, T. Hancock, M.K. Hansen, M. Harada, H. Harada, M. Hardt, S.E. Harper, J.W. Harris, A.L. Harris, J. Harris, S.D. Hashimoto, M. Haspel, J.A. Hayashi, S.-I. Hazelhurst, L.A. He, C. He, Y.-W. Hébert, M.-J. Heidenreich, K.A. Helfrich, M.H. Helgason, G.V. Henske, E.P. Herman, B. Herman, P.K. Hetz, C. Hilfiker, S. Hill, J.A. Hocking, L.J. Hofman, P. Hofmann, T.G. Höhfeld, J. Holyoake, T.L. Hong, M.-H. Hood, D.A. Hotamisligil, G.S. Houwerzijl, E.J. Høyer-Hansen, M. Hu, B. Hu, C.-A.A. Hu, H.-M. Hua, Y. Huang, C. Huang, J. Huang, S. Huang, W.-P. Huber, T.B. Huh, W.-K. Hung, T.-H. Hupp, T.R. Hur, G.M. Hurley, J.B. Hussain, S.N.A. Hussey, P.J. Hwang, J.J. Hwang, S. Ichihara, A. Ilkhanizadeh, S. Inoki, K. Into, T. Iovane, V. Iovanna, J.L. Ip, N.Y. Isaka, Y. Ishida, H. Isidoro, C. Isobe, K.-I. Iwasaki, A. Izquierdo, M. Izumi, Y. Jaakkola, P.M. Jäättelä, M. Jackson, G.R. Jackson, W.T. Janji, B. Jendrach, M. Jeon, J.-H. Jeung, E.-B. Jiang, H. Jiang, H. Jiang, J.X. Jiang, M. Jiang, Q. Jiang, X. Jiménez, A. Jin, M. Jin, S. Joe, C.O. Johansen, T. Johnson, D.E. Johnson, G.V.W. Jones, N.L. Joseph, B. Joseph, S.K. Joubert, A.M. Juhász, G. Juillerat-Jeanneret, L. Jung, C.H. Jung, Y.-K. Kaarniranta, K. Kaasik, A. Kabuta, T. Kadowaki, M. Kagedal, K. Kamada, Y. Kaminskyy, V.O. Kampinga, H.H. Kanamori, H. Kang, C. Kang, K.B. Il Kang, K. Kang, R. Kang, Y.-A. Kanki, T. Kanneganti, T.-D. Kanno, H. Kanthasamy, A.G. Kanthasamy, A. Karantza, V. Kaushal, G.P. Kaushik, S. Kawazoe, Y. Ke, P.-Y. Kehrl, J.H. Kelekar, A. Kerkhoff, C. Kessel, D.H. Khalil, H. Kiel, J.A.K.W. Kiger, A.A. Kihara, A. Kim, D.R. Kim, D.-H. Kim, D.-H. Kim, E.-K. Kim, H.-R. Kim, J.-S. Kim, J.H. Kim, J.C. Kim, J.K. Kim, P.K. Kim, S.W. Kim, Y.-S. Kim, Y. Kimchi, A. Kimmelman, A.C. King, J.S. Kinsella, T.J. Kirkin, V. Kirshenbaum, L.A. Kitamoto, K. Kitazato, K. Klein, L. Klimecki, W.T. Klucken, J. Knecht, E. Ko, B.C.B. Koch, J.C. Koga, H. Koh, J.-Y. Koh, Y.H. Koike, M. Komatsu, M. Kominami, E. Kong, H.J. Kong, W.-J. Korolchuk, V.I. Kotake, Y. Koukourakis, M.I. Kouri Flores, J.B. Kovács, A.L. Kraft, C. Krainc, D. Krämer, H. Kretz-Remy, C. Krichevsky, A.M. Kroemer, G. Krüger, R. Krut, O. Ktistakis, N.T. Kuan, C.-Y. Kucharczyk, R. Kumar, A. Kumar, R. Kumar, S. Kundu, M. Kung, H.-J. Kurz, T. Kwon, H.J. La Spada, A.R. Lafont, F. Lamark, T. Landry, J. Lane, J.D. Lapaquette, P. Laporte, J.F. László, L. Lavandero, S. Lavoie, J.N. Layfield, R. Lazo, P.A. Le, W. Le Cam, L. Ledbetter, D.J. Lee, A.J.X. Lee, B.-W. Lee, G.M. Lee, J. Lee, J.-H. Lee, M. Lee, M.-S. Lee, S.H. Leeuwenburgh, C. Legembre, P. Legouis, R. Lehmann, M. Lei, H.-Y. Lei, Q.-Y. Leib, D.A. Leiro, J. Lemasters, J.J. Lemoine, A. Lesniak, M.S. Lev, D. Levenson, V.V. Levine, B. Levy, E. Li, F. Li, J.-L. Li, L. Li, S. Li, W. Li, X.-J. Li, Y.-B. Li, Y.-P. Liang, C. Liang, Q. Liao, Y.-F. Liberski, P.P. Lieberman, A. Lim, H.J. Lim, K.-L. Lim, K. Lin, C.-F. Lin, F.-C. Lin, J. Lin, J.D. Lin, K. Lin, W.-W. Lin, W.-C. Lin, Y.-L. Linden, R. Lingor, P. Lippincott-Schwartz, J. Lisanti, M.P. Liton, P.B. Liu, B. Liu, C.-F. Liu, K. Liu, L. Liu, Q.A. Liu, W. Liu, Y.-C. Liu, Y. Lockshin, R.A. Lok, C.-N. Lonial, S. Loos, B. Lopez-Berestein, G. López-Otín, C. Lossi, L. Lotze, M.T. Lõw, P. Lu, B. Lu, B. Lu, B. Lu, Z. Luciano, F. Lukacs, N.W. Lund, A.H. Lynch-Day, M.A. Ma, Y. Macian, F. MacKeigan, J.P. Macleod, K.F. Madeo, F. Maiuri, L. Maiuri, M.C. Malagoli, D. Malicdan, M.C.V. Malorni, W. Man, N. Mandelkow, E.-M. Manon, S. Manov, I. Mao, K. Mao, X. Mao, Z. Marambaud, P. Marazziti, D. Marcel, Y.L. Marchbank, K. Marchetti, P. Marciniak, S.J. Marcondes, M. Mardi, M. Marfe, G. Mariño, G. Markaki, M. Marten, M.R. Martin, S.J. Martinand-Mari, C. Martinet, W. Martinez-Vicente, M. Masini, M. Matarrese, P. Matsuo, S. Matteoni, R. Mayer, A. Mazure, N.M. McConkey, D.J. McConnell, M.J. McDermott, C. McDonald, C. McInerney, G.M. McKenna, S.L. McLaughlin, B. McLean, P.J. McMaster, C.R. McQuibban, G.A. Meijer, A.J. Meisler, M.H. Meléndez, A. Melia, T.J. Melino, G. Mena, M.A. Menendez, J.A. Menna-Barreto, R.F.S. Menon, M.B. Menzies, F.M. Mercer, C.A. Merighi, A. Merry, D.E. Meschini, S. Meyer, C.G. Meyer, T.F. Miao, C.-Y. Miao, J.-Y. Michels, P.A.M. Michiels, C. Mijaljica, D. Milojkovic, A. Minucci, S. Miracco, C. Miranti, C.K. Mitroulis, I. Miyazawa, K. Mizushima, N. Mograbi, B. Mohseni, S. Molero, X. Mollereau, B. Mollinedo, F. Momoi, T. Monastyrska, I. Monick, M.M. Monteiro, M.J. Moore, M.N. Mora, R. Moreau, K. Moreira, P.I. Moriyasu, Y. Moscat, J. Mostowy, S. Mottram, J.C. Motyl, T. Moussa, C.E.-H. Müller, S. Muller, S. Münger, K. Münz, C. Murphy, L.O. Murphy, M.E. Musarò, A. Mysorekar, I. Nagata, E. Nagata, K. Nahimana, A. Nair, U. Nakagawa, T. Nakahira, K. Nakano, H. Nakatogawa, H. Nanjundan, M. Naqvi, N.I. Narendra, D.P. Narita, M. Navarro, M. Nawrocki, S.T. Nazarko, T.Y. Nemchenko, A. Netea, M.G. Neufeld, T.P. Ney, P.A. Nezis, I.P. Nguyen, H.P. Nie, D. Nishino, I. Nislow, C. Nixon, R.A. Noda, T. Noegel, A.A. Nogalska, A. Noguchi, S. Notterpek, L. Novak, I. Nozaki, T. Nukina, N. Nürnberger, T. Nyfeler, B. Obara, K. Oberley, T.D. Oddo, S. Ogawa, M. Ohashi, T. Okamoto, K. Oleinick, N.L. Oliver, F.J. Olsen, L.J. Olsson, S. Opota, O. Osborne, T.F. Ostrander, G.K. Otsu, K. Ou, J.-H.J. Ouimet, M. Overholtzer, M. Ozpolat, B. Paganetti, P. Pagnini, U. Pallet, N. Palmer, G.E. Palumbo, C. Pan, T. Panaretakis, T. Pandey, U.B. Papackova, Z. Papassideri, I. Paris, I. Park, J. Park, O.K. Parys, J.B. Parzych, K.R. Patschan, S. Patterson, C. Pattingre, S. Pawelek, J.M. Peng, J. Perlmutter, D.H. Perrotta, I. Perry, G. Pervaiz, S. Peter, M. Peters, G.J. Petersen, M. Petrovski, G. Phang, J.M. Piacentini, M. Pierre, P. Pierrefite-Carle, V. Pierron, G. Pinkas-Kramarski, R. Piras, A. Piri, N. Platanias, L.C. Pöggeler, S. Poirot, M. Poletti, A. Poüs, C. Pozuelo-Rubio, M. Prætorius-Ibba, M. Prasad, A. Prescott, M. Priault, M. Produit-Zengaffinen, N. Progulske-Fox, A. Proikas-Cezanne, T. Przedborski, S. Przyklenk, K. Puertollano, R. Puyal, J. Qian, S.-B. Qin, L. Qin, Z.-H. Quaggin, S.E. Raben, N. Rabinowich, H. Rabkin, S.W. Rahman, I. Rami, A. Ramm, G. Randall, G. Randow, F. Rao, V.A. Rathmell, J.C. Ravikumar, B. Ray, S.K. Reed, B.H. Reed, J.C. Reggiori, F. Régnier-Vigouroux, A. Reichert, A.S. Reiners Jr., J.J. Reiter, R.J. Ren, J. Revuelta, J.L. Rhodes, C.J. Ritis, K. Rizzo, E. Robbins, J. Roberge, M. Roca, H. Roccheri, M.C. Rocchi, S. Rodemann, H.P. De Córdoba, S.R. Rohrer, B. Roninson, I.B. Rosen, K. Rost-Roszkowska, M.M. Rouis, M. Rouschop, K.M.A. Rovetta, F. Rubin, B.P. Rubinsztein, D.C. Ruckdeschel, K. Rucker III, E.B. Rudich, A. Rudolf, E. Ruiz-Opazo, N. Russo, R. Rusten, T.E. Ryan, K.M. Ryter, S.W. Sabatini, D.M. Sadoshima, J. Saha, T. Saitoh, T. Sakagami, H. Sakai, Y. Salekdeh, G.H. Salomoni, P. Salvaterra, P.M. Salvesen, G. Salvioli, R. Sanchez, A.M.J. Sánchez-Alcázar, J.A. Sánchez-Prieto, R. Sandri, M. Sankar, U. Sansanwal, P. Santambrogio, L. Saran, S. Sarkar, S. Sarwal, M. Sasakawa, C. Sasnauskiene, A. Sass, M. Sato, K. Sato, M. Schapira, A.H.V. Scharl, M. Schätzl, H.M. Scheper, W. Schiaffino, S. Schneider, C. Schneider, M.E. Schneider-Stock, R. Schoenlein, P.V. Schorderet, D.F. Schüller, C. Schwartz, G.K. Scorrano, L. Sealy, L. Seglen, P.O. Segura-Aguilar, J. Seiliez, I. Seleverstov, O. Sell, C. Seo, J.B. Separovic, D. Setaluri, V. Setoguchi, T. Settembre, C. Shacka, J.J. Shanmugam, M. Shapiro, I.M. Shaulian, E. Shaw, R.J. Shelhamer, J.H. Shen, H.-M. Shen, W.-C. Sheng, Z.-H. Shi, Y. Shibuya, K. Shidoji, Y. Shieh, J.-J. Shih, C.-M. Shimada, Y. Shimizu, S. Shintani, T. Shirihai, O.S. Shore, G.C. Sibirny, A.A. Sidhu, S.B. Sikorska, B. Silva-Zacarin, E.C.M. Simmons, A. Simon, A.K. Simon, H.-U. Simone, C. Simonsen, A. Sinclair, D.A. Singh, R. Sinha, D. Sinicrope, F.A. Sirko, A. Siu, P.M. Sivridis, E. Skop, V. Skulachev, V.P. Slack, R.S. Smaili, S.S. Smith, D.R. Soengas, M.S. Soldati, T. Song, X. Sood, A.K. Soong, T.W. Sotgia, F. Spector, S.A. Spies, C.D. Springer, W. Srinivasula, S.M. Stefanis, L. Steffan, J.S. Stendel, R. Stenmark, H. Stephanou, A. Stern, S.T. Sternberg, C. Stork, B. Strålfors, P. Subauste, C.S. Sui, X. Sulzer, D. Sun, J. Sun, S.-Y. Sun, Z.-J. Sung, J.J.Y. Suzuki, K. Suzuki, T. Swanson, M.S. Swanton, C. Sweeney, S.T. Sy, L.-K. Szabadkai, G. Tabas, I. Taegtmeyer, H. Tafani, M. Takács-Vellai, K. Takano, Y. Takegawa, K. Takemura, G. Takeshita, F. Talbot, N.J. Tan, K.S.W. Tanaka, K. Tanaka, K. Tang, D. Tang, D. Tanida, I. Tannous, B.A. Tavernarakis, N. Taylor, G.S. Taylor, G.A. Taylor, J.P. Terada, A.S. Terman, A. Tettamanti, G. Thevissen, K. Thompson, C.B. Thorburn, A. Thumm, M. Tian, F. Tian, Y. Tocchini-Valentini, G. Tolkovsky, A.M. Tomino, Y. Tönges, L. Tooze, S.A. Tournier, C. Tower, J. Towns, R. Trajkovic, V. Travassos, L.H. Tsai, T.-F. Tschan, M.P. Tsubata, T. Tsung, A. Turk, B. Turner, L.S. Tyagi, S.C. Uchiyama, Y. Ueno, T. Umekawa, M. Umemiya-Shirafuji, R. Unni, V.K. Vaccaro, M.I. Valente, E.M. Van Den Berghe, G. Van Der Klei, I.J. Van Doorn, W.G. Van Dyk, L.F. Van Egmond, M. Van Grunsven, L.A. Vandenabeele, P. Vandenberghe, W.P. Vanhorebeek, I. Vaquero, E.C. Velasco, G. Vellai, T. Vicencio, J.M. Vierstra, R.D. Vila, M. Vindis, C. Viola, G. Viscomi, M.T. Voitsekhovskaja, O.V. Von Haefen, C. Votruba, M. Wada, K. Wade-Martins, R. Walker, C.L. Walsh, C.M. Walter, J. Wan, X.-B. Wang, A. Wang, C. Wang, D. Wang, F. Wang, F. Wang, G. Wang, H. Wang, H.-G. Wang, H.-D. Wang, J. Wang, K. Wang, M. Wang, R.C. Wang, X. Wang, X. Wang, Y.-J. Wang, Y. Wang, Z. Wang, Z.C. Wang, Z. Wansink, D.G. Ward, D.M. Watada, H. Waters, S.L. Webster, P. Wei, L. Weihl, C.C. Weiss, W.A. Welford, S.M. Wen, L.-P. Whitehouse, C.A. Whitton, J.L. Whitworth, A.J. Wileman, T. Wiley, J.W. Wilkinson, S. Willbold, D. Williams, R.L. Williamson, P.R. Wouters, B.G. Wu, C. Wu, D.-C. Wu, W.K.K. Wyttenbach, A. Xavier, R.J. Xi, Z. Xia, P. Xiao, G. Xie, Z. Xie, Z. Xu, D.-Z. Xu, J. Xu, L. Xu, X. Yamamoto, A. Yamamoto, A. Yamashina, S. Yamashita, M. Yan, X. Yanagida, M. Yang, D.-S. Yang, E. Yang, J.-M. Yang, S.Y. Yang, W. Yang, W.Y. Yang, Z. Yao, M.-C. Yao, T.-P. Yeganeh, B. Yen, W.-L. Yin, J.-J. Yin, X.-M. Yoo, O.-J. Yoon, G. Yoon, S.-Y. Yorimitsu, T. Yoshikawa, Y. Yoshimori, T. Yoshimoto, K. You, H.J. Youle, R.J. Younes, A. Yu, L. Yu, L. Yu, S.-W. Yu, W.H. Yuan, Z.-M. Yue, Z. Yun, C.-H. Yuzaki, M. Zabirnyk, O. Silva-Zacarin, E. David Zacks, E. Zacksenhaus, L. Zaffaroni, N. Zakeri, Z. Zeh III, H.J. Zeitlin, S.O. Zhang, H. Zhang, H.-L. Zhang, J. Zhang, J.-P. Zhang, L. Zhang, L. Zhang, M.-Y. Zhang, X.D. Zhao, M. Zhao, Y.-F. Zhao, Y. Zhao, Z.J. Zheng, X. Zhivotovsky, B. Zhong, Q. Zhou, C.-Z. Zhu, C. Zhu, W.-G. Zhu, X.-F. Zhu, X. Zhu, Y. Zoladek, T. Zong, W.-X. Zorzano, A. Zschocke, J. Zuckerbraun, B.
- Abstract
In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field. © 2012 Landes Bioscience.
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- 2012
26. Isolation and functional assessment of common, polymorphic variants of the B-MYB proto-oncogene associated with a reduced cancer risk (Oncogene (2008) 27, (2929-2933) DOI: 10.1038/sj.onc.1210947)
- Author
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Schwab, R., Bussolari, R., Corvetta, D., Chayka, O., Santilli, G., Kwok, J. M. -M., Ferrari-Amorotti, G., Tonini, G. P., Iacoviello, L., Bertorelle, R., Menin, C., Hubank, M., Calabretta, B., and Sala, A.
- Published
- 2008
27. Tumor induced by Moloney sarcoma virus causes periosteal osteogenesis engaging osteopontin, fibronectin, stromelysin-1 and tenascin
- Author
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Pawel Wlodarski, Sevignani, C., Fernandes, M. J., Calabretta, B., and Wlodarski, K. H.
- Subjects
Mice, Inbred BALB C ,MMP-3 ,osteopontin ,Moloney murine sarcoma virus ,Tenascin ,Blotting, Northern ,orthotopic osteogenesis ,stromelysin-1 ,fibronectin ,tenascin ,Murine Moloney sarcoma virus ,Mu-MSV ,Fibronectins ,Mice ,Osteogenesis ,Periosteum ,Animals ,Matrix Metalloproteinase 3 ,Osteopontin ,Sarcoma, Experimental - Abstract
Excessive bone formation occurring in such conditions as paravertebral ligamentous ossification, hallux osteophytes or some neoplastic tumors, presents a significant problem, both epidemiological and clinical. Since pathogenesis of this disorder is still unclear, we studied its mechanism in experimental model utilizing inducible orthotopic osteogenesis. Periosteal bone apposition stimulated by Moloney sarcoma is characterized by unusually high volume of new bone tissue appearing subperiosteally in the bone adjacent to the tumor. Genes engaged in this growth have not been characterized so far. Here we show the results of mRNA Representation Difference Analysis in Moloney sarcoma, which reveal high expression of four genes coding extracellular matrix proteins: osteopontin, fibronectin, stromelysin-1 and tenascin. These findings suggest that the uncommon dynamics of the Moloney sarcoma-induced osteogenesis depends on high expression of these extracellular matrix proteins.
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- 2007
28. Different Frequency Classes of Sequences in Heterogeneous Nuclear RNA of Normal Promyelocytes and Lymphoblasts and of Leukemic Blast Cells of Circulating Blood and of the HL60 Line
- Author
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Torelli, U., primary, Torelli, G., additional, Narni, F., additional, Donelli, A., additional, Ferrari, S., additional, Franchini, G., additional, and Calabretta, B., additional
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- 1981
- Full Text
- View/download PDF
29. Ricerca di markers diagnostici, prognostici e predittivi in carcinomi mammari attraverso analisi proteomica
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Pecorari, L, Silvestri, C, Candini, O, Rossi, E, Bellei, E, Bussolari, R, Iannone, A, Federico, M, Cortesi, L, and Calabretta, B.
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Markers ,proteomica ,carcinoma mammario ,Markers, proteomica, carcinoma mammario - Published
- 2006
30. C-Myb and Bcl-x overexpression predicts poor prognosis in colorectal cancer: Clinical and experimental findings
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Annamaria Biroccio, Benassi, B., D Agnano, I., D Angelo, C., Buglioni, S., Mottolese, M., Ricciotti, A., Citro, G., Cosimelli, M., Ramsay, R. G., Calabretta, B., and Zupi, G.
- Subjects
animal structures ,Rectal Neoplasms ,fungi ,Carcinoma ,bcl-X Protein ,Carcinoma/physiopathology ,Colonic Neoplasms/physiopathology ,Proto-Oncogene Proteins c-bcl-2/metabolism ,Rectal Neoplasms/physiopathology ,Prognosis ,Transfection ,Survival Analysis ,Proto-Oncogene Proteins c-myb ,Proto-Oncogene Proteins c-bcl-2 ,Colonic Neoplasms ,Humans ,RNA, Messenger ,Cell Division ,Regular Articles - Abstract
The aim of this study was twofold: to assess the relationship between c-Myb and Bcl-x expression and to evaluate the prognostic significance of their expression in colorectal carcinoma (CRC) patients. Analysis of tumors from 91 CRC patients for expression of c-Myb and Bcl-x revealed a significant relationship between these two proteins. Kaplan-Meier's analysis showed an increased risk of relapse and death in patients whose tumor specimens displayed high c-Myb levels and Bcl-x positivity. Similar results were also observed excluding Dukes' D patients. Molecular analysis using three c-Myb-overexpressing LoVo clones indicated that c-Myb overexpression was accompanied by up-regulation of Bcl-x(L) protein and mRNA. Tumors originating from these clones injected in nude mice were significantly larger than those formed in mice injected with parental or vector-transfected LoVo cells. Moreover, tumors derived from parental and control vector-transfected but not from c-Myb-overexpressing LoVo cells showed high frequency of apoptotic cells. These results provide direct evidence of an association between c-Myb and Bcl-x expression and suggest that expression of both molecules might be a useful prognostic marker in CRC.
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- 2001
31. Guidelines for the use and interpretation of assays for monitoring autophagy.
- Author
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Klionsky, Dj, Abdalla, Fc, Abeliovich, H, Abraham, Rt, Acevedo-Arozena, A, Adeli, K, Agholme, L, Agnello, M, Agostinis, P, Aguirre-Ghiso, Ja, Ahn, Hj, Ait-Mohamed, O, Ait-Si-Ali, S, Akematsu, T, Akira, S, Al-Younes, Hm, Al-Zeer, Ma, Albert, Ml, Albin, Rl, Alegre-Abarrategui, J, Aleo, Mf, Alirezaei, M, Almasan, A, Almonte-Becerril, M, Amano, A, Amaravadi, R, Amarnath, S, Amer, Ao, Andrieu-Abadie, N, Anantharam, V, Ann, Dk, Anoopkumar-Dukie, S, Aoki, H, Apostolova, N, Arancia, G, Aris, Jp, Asanuma, K, Asare, Ny, Ashida, H, Askanas, V, Askew, D, Auberger, P, Baba, M, Backues, Sk, Baehrecke, Eh, Bahr, Ba, Bai, Xy, Bailly, Y, Baiocchi, R, Baldini, G, Balduini, W, Ballabio, A, Bamber, Ba, Bampton, Et, Bánhegyi, G, Bartholomew, Cr, Bassham, Dc, Bast RC, Jr, Batoko, H, Bay, Bh, Beau, I, Béchet, Dm, Begley, Tj, Behl, C, Behrends, C, Bekri, S, Bellaire, B, Bendall, Lj, Benetti, L, Berliocchi, L, Bernardi, H, Bernassola, F, Besteiro, S, Bhatia-Kissova, I, Bi, X, Biard-Piechaczyk, M, Blum, J, 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T. (ORCID:0000-0002-9096-4967), Klionsky, Dj, Abdalla, Fc, Abeliovich, H, Abraham, Rt, Acevedo-Arozena, A, Adeli, K, Agholme, L, Agnello, M, Agostinis, P, Aguirre-Ghiso, Ja, Ahn, Hj, Ait-Mohamed, O, Ait-Si-Ali, S, Akematsu, T, Akira, S, Al-Younes, Hm, Al-Zeer, Ma, Albert, Ml, Albin, Rl, Alegre-Abarrategui, J, Aleo, Mf, Alirezaei, M, Almasan, A, Almonte-Becerril, M, Amano, A, Amaravadi, R, Amarnath, S, Amer, Ao, Andrieu-Abadie, N, Anantharam, V, Ann, Dk, Anoopkumar-Dukie, S, Aoki, H, Apostolova, N, Arancia, G, Aris, Jp, Asanuma, K, Asare, Ny, Ashida, H, Askanas, V, Askew, D, Auberger, P, Baba, M, Backues, Sk, Baehrecke, Eh, Bahr, Ba, Bai, Xy, Bailly, Y, Baiocchi, R, Baldini, G, Balduini, W, Ballabio, A, Bamber, Ba, Bampton, Et, Bánhegyi, G, Bartholomew, Cr, Bassham, Dc, Bast RC, Jr, Batoko, H, Bay, Bh, Beau, I, Béchet, Dm, Begley, Tj, Behl, C, Behrends, C, Bekri, S, Bellaire, B, Bendall, Lj, Benetti, L, Berliocchi, L, Bernardi, H, Bernassola, F, Besteiro, S, Bhatia-Kissova, I, Bi, X, Biard-Piechaczyk, M, Blum, J, Boise, Lh, Bonaldo, P, Boone, Dl, Bornhauser, Bc, Bortoluci, Kr, Bossis, I, Bost, F, Bourquin, Jp, Boya, P, Boyer-Guittaut, M, Bozhkov, Pv, Brady, Nr, Brancolini, C, Brech, A, Brenman, Je, Brennand, A, Bresnick, Eh, Brest, P, Bridges, D, Bristol, Ml, Brookes, P, Brown, Ej, Brumell, Jh, Brunetti-Pierri, N, Brunk, Ut, Bulman, De, Bultman, Sj, Bultynck, G, Burbulla, Lf, Bursch, W, Butchar, Jp, Buzgariu, W, Bydlowski, Sp, Cadwell, K, Cahová, M, Cai, D, Cai, J, Cai, Q, Calabretta, B, Calvo-Garrido, J, Camougrand, N, Campanella, M, Campos-Salinas, J, Candi, E, Cao, L, Caplan, Ab, Carding, Sr, Cardoso, Sm, Carew, J, Carlin, Cr, Carmignac, V, Carneiro, La, Carra, S, Caruso, Ra, Casari, G, Casas, C, Castino, R, Cebollero, E, Cecconi, F, Celli, J, Chaachouay, H, Chae, Hj, Chai, Cy, Chan, Dc, Chan, Ey, Chang, Rc, Che, Cm, Chen, Cc, Chen, Gc, Chen, Gq, Chen, M, Chen, Q, Chen, S, Chen, W, Chen, X, Chen, Yg, Chen, Y, Chen, Yj, Chen, Z, Cheng, A, Cheng, Ch, Cheng, Y, Cheong, H, Cheong, Jh, Cherry, S, Chess-Williams, R, Cheung, Zh, Chevet, E, Chiang, Hl, Chiarelli, R, Chiba, T, Chin, L, Chiou, Sh, Chisari, Fv, Cho, Ch, Cho, Dh, Choi, Am, Choi, D, Choi, K, Choi, Me, Chouaib, S, Choubey, D, Choubey, V, Chu, Ct, Chuang, Th, Chueh, Sh, Chun, T, Chwae, Yj, Chye, Ml, Ciarcia, R, Ciriolo, Mr, Clague, Mj, Clark, R, Clarke, Pg, Clarke, R, Codogno, P, Coller, Ha, Colombo, Mi, Comincini, S, Condello, M, Condorelli, F, Cookson, Mr, Coombs, Gh, Coppens, I, Corbalan, R, Cossart, P, Costelli, P, Costes, S, Coto-Montes, A, Couve, E, Coxon, Fp, Cregg, Jm, Crespo, Jl, Cronjé, Mj, Cuervo, Am, Cullen, Jj, Czaja, Mj, D'Amelio, M, Darfeuille-Michaud, A, Davids, Lm, Davies, Fe, De Felici, M, de Groot, Jf, de Haan, Ca, De Martino, L, De Milito, A, De Tata, V, Debnath, J, Degterev, A, Dehay, B, Delbridge, Lm, Demarchi, F, Deng, Yz, Dengjel, J, Dent, P, Denton, D, Deretic, V, Desai, Sd, Devenish, Rj, Di Gioacchino, M, Di Paolo, G, Di Pietro, C, Díaz-Araya, G, Díaz-Laviada, I, Diaz-Meco, Mt, Diaz-Nido, J, Dikic, I, Dinesh-Kumar, Sp, Ding, Wx, Distelhorst, Cw, Diwan, A, Djavaheri-Mergny, M, Dokudovskaya, S, Dong, Z, Dorsey, Fc, Dosenko, V, Dowling, Jj, Doxsey, S, Dreux, M, Drew, Me, Duan, Q, Duchosal, Ma, Duff, K, Dugail, I, Durbeej, M, Duszenko, M, Edelstein, Cl, Edinger, Al, Egea, G, Eichinger, L, Eissa, Nt, Ekmekcioglu, S, El-Deiry, W, Elazar, Z, Elgendy, M, Ellerby, Lm, Eng, Ke, Engelbrecht, Am, Engelender, S, Erenpreisa, J, Escalante, R, Esclatine, A, Eskelinen, El, Espert, L, Espina, V, Fan, H, Fan, J, Fan, Qw, Fan, Z, Fang, S, Fang, Y, Fanto, M, Fanzani, A, Farkas, T, Farré, Jc, Faure, M, Fechheimer, M, Feng, Cg, Feng, J, Feng, Q, Feng, Y, Fésüs, L, Feuer, R, Figueiredo-Pereira, Me, Fimia, Gm, Fingar, Dc, Finkbeiner, S, Finkel, T, Finley, Kd, Fiorito, F, Fisher, Ea, Fisher, Pb, Flajolet, M, Florez-McClure, Ml, Florio, S, Fon, Ea, Fornai, F, Fortunato, F, Fotedar, R, Fowler, Dh, Fox, H, Franco, R, Frankel, Lb, Fransen, M, Fuentes, Jm, Fueyo, J, 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Harris, J, Harris, Sd, Hashimoto, M, Haspel, Ja, Hayashi, S, Hazelhurst, La, He, C, He, Yw, Hébert, Mj, Heidenreich, Ka, Helfrich, Mh, Helgason, Gv, Henske, Ep, Herman, B, Herman, Pk, Hetz, C, Hilfiker, S, Hill, Ja, Hocking, Lj, Hofman, P, Hofmann, Tg, Höhfeld, J, Holyoake, Tl, Hong, Mh, Hood, Da, Hotamisligil, G, Houwerzijl, Ej, Høyer-Hansen, M, Hu, B, Hu, Ca, Hu, Hm, Hua, Y, Huang, C, Huang, J, Huang, S, Huang, Wp, Huber, Tb, Huh, Wk, Hung, Th, Hupp, Tr, Hur, Gm, Hurley, Jb, Hussain, Sn, Hussey, Pj, Hwang, Jj, Hwang, S, Ichihara, A, Ilkhanizadeh, S, Inoki, K, Into, T, Iovane, V, Iovanna, Jl, Ip, Ny, Isaka, Y, Ishida, H, Isidoro, C, Isobe, K, Iwasaki, A, Izquierdo, M, Izumi, Y, Jaakkola, Pm, Jäättelä, M, Jackson, Gr, Jackson, Wt, Janji, B, Jendrach, M, Jeon, Jh, Jeung, Eb, Jiang, H, Jiang, Jx, Jiang, M, Jiang, Q, Jiang, X, Jiménez, A, Jin, M, Jin, S, Joe, Co, Johansen, T, Johnson, De, Johnson, Gv, Jones, Nl, Joseph, B, Joseph, Sk, Joubert, Am, Juhász, G, Juillerat-Jeanneret, L, Jung, 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Kurz, T, Kwon, Hj, La Spada, Ar, Lafont, F, Lamark, T, Landry, J, Lane, Jd, Lapaquette, P, Laporte, Jf, László, L, Lavandero, S, Lavoie, Jn, Layfield, R, Lazo, Pa, Le, W, Le Cam, L, Ledbetter, Dj, Lee, Aj, Lee, Bw, Lee, Gm, Lee, J, Lee, Jh, Lee, M, Lee, Sh, Leeuwenburgh, C, Legembre, P, Legouis, R, Lehmann, M, Lei, Hy, Lei, Qy, Leib, Da, Leiro, J, Lemasters, Jj, Lemoine, A, Lesniak, M, Lev, D, Levenson, Vv, Levine, B, Levy, E, Li, F, Li, Jl, Li, L, Li, S, Li, W, Li, Xj, Li, Yb, Li, Yp, Liang, C, Liang, Q, Liao, Yf, Liberski, Pp, Lieberman, A, Lim, Hj, Lim, Kl, Lim, K, Lin, Cf, Lin, Fc, Lin, J, Lin, Jd, Lin, K, Lin, Ww, Lin, Wc, Lin, Yl, Linden, R, Lingor, P, Lippincott-Schwartz, J, Lisanti, Mp, Liton, Pb, Liu, B, Liu, Cf, Liu, K, Liu, L, Liu, Qa, Liu, W, Liu, Yc, Liu, Y, Lockshin, Ra, Lok, Cn, Lonial, S, Loos, B, Lopez-Berestein, G, López-Otín, C, Lossi, L, Lotze, Mt, Lőw, P, Lu, B, Lu, Z, Luciano, F, Lukacs, Nw, Lund, Ah, Lynch-Day, Ma, Ma, Y, Macian, F, Mackeigan, Jp, Macleod, Kf, Madeo, F, Maiuri, L, Maiuri, Mc, Malagoli, D, Malicdan, Mc, Malorni, W, Man, N, Mandelkow, Em, Manon, S, Manov, I, Mao, K, Mao, X, Mao, Z, Marambaud, P, Marazziti, D, Marcel, Yl, Marchbank, K, Marchetti, P, Marciniak, Sj, Marcondes, M, Mardi, M, Marfe, G, Mariño, G, Markaki, M, Marten, Mr, Martin, Sj, Martinand-Mari, C, Martinet, W, Martinez-Vicente, M, Masini, M, Matarrese, P, Matsuo, S, Matteoni, R, Mayer, A, Mazure, Nm, Mcconkey, Dj, Mcconnell, Mj, Mcdermott, C, Mcdonald, C, Mcinerney, Gm, Mckenna, Sl, Mclaughlin, B, Mclean, Pj, Mcmaster, Cr, Mcquibban, Ga, Meijer, Aj, Meisler, Mh, Meléndez, A, Melia, Tj, Melino, G, Mena, Ma, Menendez, Ja, Menna-Barreto, Rf, Menon, Mb, Menzies, Fm, Mercer, Ca, Merighi, A, Merry, De, Meschini, S, Meyer, Cg, Meyer, Tf, Miao, Cy, Miao, Jy, Michels, Pa, Michiels, C, Mijaljica, D, Milojkovic, A, Minucci, S, Miracco, C, Miranti, Ck, Mitroulis, I, Miyazawa, K, Mizushima, N, Mograbi, B, Mohseni, S, Molero, X, Mollereau, B, Mollinedo, F, Momoi, T, 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Zuckerbraun, B., and Viscomi M. T. (ORCID:0000-0002-9096-4967)
- Abstract
In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused o
- Published
- 2012
32. Bcl-2 expression restores the leukemogenic potential of a BCR/ABL mutant defective in transformation
- Author
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Cirinna, M., Rossana Trotta, Salomoni, P., Kossev, P., Wasik, M., Perrotti, D., and Calabretta, B.
- Subjects
Leukemia, Experimental ,Immunology ,Fusion Proteins, bcr-abl ,Apoptosis ,Cell Biology ,Hematology ,Mice, SCID ,Transfection ,Biochemistry ,Cell Line ,Mice ,Cell Transformation, Neoplastic ,Proto-Oncogene Proteins c-bcl-2 ,hemic and lymphatic diseases ,Mutation ,Animals ,Humans ,Proto-Oncogene Proteins c-bcl-2/pharmacology ,bcl-Associated Death Protein ,Phosphorylation ,Carrier Proteins ,Neoplasm Transplantation - Abstract
Growth factor–dependent hematopoietic cell lines expressing the BCR/ABL oncoprotein of the Ph chromosome show growth factor–independent proliferation and resistance to apoptosis. Apoptosis resistance of BCR/ABL-expressing cells may depend on enhanced expression of anti-apoptotic proteins as well as reduced expression and/or inactivation of pro-apoptotic proteins. Compared to myeloid precursor 32Dcl3 cells expressing wild type BCR/ABL, cells expressing a BCR/ABL mutant lacking amino acids 176-426 in the BCR domain (p185ΔBCR) are susceptible to apoptosis induced by interleukin-3 (IL-3) deprivation. These cells exhibited the hypophosphorylated apoptotic BAD and markedly reduced levels of Bcl-2. Upon ectopic expression of Bcl-2, these cells showed no changes in BAD phosphorylation, but they became apoptosis-resistant and proliferated in the absence of IL-3, albeit more slowly than cells expressing wild type BCR/ABL. Moreover, the p185ΔBCR/Bcl-2 double transfectants were leukemogenic when injected into immunodeficient mice, but Bcl-2 expression did not restore the leukemia-inducing effects of p185ΔBCR to the levels of wild type BCR/ABL. Leukemic cells recovered from the spleen of mice injected with p185ΔBCR/Bcl-2 cells did not show rearrangements in the Bcl-2 genomic locus, but they exhibited enhanced proliferation in culture and induced a rapidly fatal disease process when inoculated in secondary recipient mice. Together, these data support the importance of anti-apoptotic pathways for BCR/ABL-dependent leukemogenesis and suggest that Bcl-2 expression promotes secondary changes leading to a more aggressive tumor phenotype.
- Published
- 2000
33. Activation of mitochondrial Raf-1 is involved in the antiapoptotic effects of Akt
- Author
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Majewski, M., Nieborowska-Skorska, M., Salomoni, P., Slupianek, A., Reiss, K., Rossana Trotta, Calabretta, B., and Skorski, T.
- Subjects
Enzyme Activation ,Oncogene Protein v-akt ,Proto-Oncogene Proteins c-raf ,Mice ,Apoptosis ,Retroviridae Proteins, Oncogenic ,Animals ,Cell Line ,Mitochondria - Abstract
The Akt serine/threonine kinase is required for the survival of many cell types and for transformation of hematopoietic cells by the BCR/ABL oncogenic tyrosine kinase. Analysis of the potential mechanisms whereby Akt promotes survival of hematopoietic cells revealed that it induced the activity of plasma membrane and mitochondrial Raf-1 in a Ras-independent, but PKC-dependent manner. Inhibition of plasma membrane Raf-1-dependent mitogen-activated protein kinase activity had no effect on the enhanced survival of cells expressing Akt. By contrast, suppression of mitochondrial Raf-1 enzymatic activity by expression of a mitochondria-targeted Raf-1 dominant-negative mutant rendered Akt-expressing cells susceptible to apoptosis induced by growth factor deprivation and was accompanied by inhibition of BAD, but not mitogen-activated protein kinase, phosphorylation. Together, these data indicate that PKC-dependent activation of Raf-1 plays an important role in Akt-dependent antiapoptotic effects.
- Published
- 1999
34. Double knockout of the ALL-1 gene blocks hematopoietic differentiation in vitro
- Author
-
Fidanza V, Melotti P, Yano T, Nakamura T, Allan Bradley, Canaani E, Calabretta B, and Cm, Croce
- Subjects
Genetic Markers ,Genes Tumor Suppressor/physiology ,Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ,Precursor Cell Lymphoblastic Leukemia-Lymphoma ,Hematopoietic Stem Cells ,Translocation, Genetic ,Globins ,Colony-Forming Units Assay ,Mice ,Phenotype ,Tumor Cells, Cultured ,Animals ,Genes, Tumor Suppressor ,Biomarkers ,Peroxidase - Abstract
The ALL-1 gene is involved in translocations with many partner genes in different types of the acute leukemias, but it is not clear whether it acts as an oncogene or whether the fusion proteins resulting from the translocations have dominant negative effects. To distinguish between these two possibilities, we analyzed the ability of wild-type AB2.1 embryonal stem (ES) cells and of single or double ALL-1 gene knockout cells derived from them to differentiate along hematopoietic lineages after withdrawal of leukemia inhibitory factor, using in vitro colony formation assays. All-1 double knockout ES cells formed a significantly greater number of colonies with faster kinetics than wild-type and ALL-1 single knockout ES cells. Parental ES cells formed lineage-restricted colonies, whereas single and double knockout ES cells developed, at high frequency, immature and/or "biphenotypic" colonies, mimicking the aberrant hematopoiesis typical of leukemic patients. These data are consistent with the possibility that loss of function of the ALL-1 gene is important in leukemogenesis.
- Published
- 1996
35. The influence of phosphorothioate oligodeoxynucleotides on various organs in vivo
- Author
-
Nieborowska-Skórska M, Ap, Białek, Nicholas Nicolaides, Rv, Iozzo, Kawalec M, Calabretta B, Kawiak J, Marlicz K, and Skórski T
- Subjects
Male ,Mice ,Leukemia, Myelogenous, Chronic, BCR-ABL Positive ,Tumor Cells, Cultured ,Animals ,Humans ,Tissue Distribution ,Mice, SCID ,Oligonucleotides, Antisense ,Thionucleotides ,Blast Crisis ,Oligonucleotides Antisense/pharmacology ,Thionucleotides/pharmacokinetics ,Neoplasm Transplantation - Abstract
To characterize the distribution and toxicity of phosphorothioate antisense oligodeoxynucleotides ([S]ODNs) in vivo, the mice, previously injected with BV173 leukemic cells (Philadelphia chromosome-positive chronic myeloid leukemia blast-crisis), received intravenously 26-mer BCR-ABL antisense oligodeoxynucleotides (1 mg/mouse/day) for 9 consecutive days. Our investigation revealed that [S]ODNs were distributed to almost all organs except the brain with the highest level in the liver, spleen and kidneys. They were also detected in CD10+ leukemic cells isolated from spleen and bone marrow. Intracellular distribution assay showed the presence of [S]ODNs most prominently in nuclear and cytoplasmic fractions. Our data demonstrated no significant toxicity of [S]ODNs except the increase in spleen weight.
- Published
- 1996
36. Antisense strategies in the treatment of leukemias
- Author
-
Calabretta, B., Skorski, T., Mariusz Z. Ratajczak, and Gewirtz, A. M.
- Subjects
Mice ,Leukemia ,Leukemia, Myelogenous, Chronic, BCR-ABL Positive ,Leukemia/drug therapy ,Oligonucleotides ,Antisense/therapeutic use ,Animals ,Humans ,Mice, SCID ,Oncogenes ,Oligonucleotides, Antisense - Abstract
Oligodeoxynucleotides are short nucleotide sequences of DNA synthesized as reverse complements of the desired mRNA target's nucleotide sequence. On formation of the RNA-DNA duplex, gene expression is prevented. Delivery of oligodeoxynucleotides targeting oncogene-encoded mRNAs to human cells in culture is associated with inhibition of cell proliferation and, in some circumstances, cell death. Oligodeoxynucleotides chemically modified to survive nuclease attack have been used systemically in murine models of human hematologic malignancies. In some studies, a measurable antileukemia effect has been observed. On the basis of these preclinical investigations, phase 1 clinical trials involving ex vivo and systemic administration of such compounds are now in progress at different institutions. Despite the remarkable progress of the past few years, much remains to be addressed on uptake, cellular distribution, mechanism(s) of action, and metabolism of such compounds. Furthermore, the "antisense effects" of the oligodeoxynucleotides might also be associated with nonspecific effects. In conclusion, time, a great deal of effort, and patience will tell whether such compounds will have a role as novel antileukemia therapeutic agents.
- Published
- 1996
37. miRNA let-7c promotes granulocytic differentiation in acute myeloid leukemia
- Author
-
Pelosi, A, primary, Careccia, S, additional, Lulli, V, additional, Romania, P, additional, Marziali, G, additional, Testa, U, additional, Lavorgna, S, additional, Lo-Coco, F, additional, Petti, M C, additional, Calabretta, B, additional, Levrero, M, additional, Piaggio, G, additional, and Rizzo, M G, additional
- Published
- 2012
- Full Text
- View/download PDF
38. Expression of p89c-Mybex9b, an alternatively spliced form of c-Myb, is required for proliferation and survival of p210BCR/ABL-expressing cells
- Author
-
Manzotti, G, primary, Mariani, S A, additional, Corradini, F, additional, Bussolari, R, additional, Cesi, V, additional, Vergalli, J, additional, Ferrari-Amorotti, G, additional, Fragliasso, V, additional, Soliera, A R, additional, Cattelani, S, additional, Raschellà, G, additional, Holyoake, T L, additional, and Calabretta, B, additional
- Published
- 2012
- Full Text
- View/download PDF
39. Inhibition of erythro-myeloid differentiation by constitutive expression of a DNA binding-deficient c-myb mutant: implication for c-myb function
- Author
-
Arturo Sala, Bellon, T., Melotti, P., Peschle, C., and Calabretta, B.
- Subjects
Transcriptional Activation ,Binding Sites ,Recombinant Fusion Proteins ,Cell Differentiation ,DNA ,Proto-Oncogene Mas ,Hematopoiesis ,Protein Structure, Tertiary ,Mice ,Proto-Oncogene Proteins c-myb ,Cricetinae ,Proto-Oncogene Proteins ,Granulocyte Colony-Stimulating Factor ,Mutagenesis, Site-Directed ,Tumor Cells, Cultured ,Animals ,Humans ,Dimethyl Sulfoxide ,Erythropoiesis ,Leukemia, Erythroblastic, Acute ,Promoter Regions, Genetic ,Protein Binding ,DNA/metabolism ,Hematopoiesis/physiology ,Proto-Oncogene Proteins/physiology - Abstract
The c-myb proto-oncogene encodes a nuclear protein involved in the regulation of cell proliferation, differentiation, and development. Myb protein contains a DNA binding and a transactivating domain thought to mediate its biologic properties. The DNA binding domain consists of three repeats (R1, R2, and R3), each containing a highly conserved motif of tryptophan residues. A c-myb mutant (DR1-myb) lacking the last 46 amino acids of R1 and 23 amino terminal residues of R2, a region homologous to the ADA-2 yeast transcriptional adaptor, lost DNA binding ability, but remained able to transactivate the human heat-shock promoter. Transfection of murine 32D and murine erythroleukemia (MEL) cell lines with DR1-myb caused inhibition of cellular differentiation induced by granulocyte colony-stimulating factor (G-CSF) and dimethyl sulfoxide (DMSO), respectively. A second c-myb mutant (D-ADA2-myb) lacking the first 23 amino acids of R2, also lost DNA binding and transactivation activity, but did not inhibit DMSO-induced differentiation of MEL transfected cells. These findings suggest that deletion of R1 activates a DNA binding-independent mechanism of c-myb function, which may involve interaction of Myb with cellular factors.
- Published
- 1995
40. Antisense oligodeoxynucleotides for the treatment of chronic myelogenous leukemia: are they still a promise?
- Author
-
Paolo de Fabritiis and Calabretta, B.
- Subjects
CML ,Oligonucleotides Antisense/therapeutic use - Published
- 1995
41. c-Myb and its target Bmi1 are required for p190BCR/ABL leukemogenesis in mouse and human cells
- Author
-
Waldron, T, primary, De Dominici, M, additional, Soliera, A R, additional, Audia, A, additional, Iacobucci, I, additional, Lonetti, A, additional, Martinelli, G, additional, Zhang, Y, additional, Martinez, R, additional, Hyslop, T, additional, Bender, T P, additional, and Calabretta, B, additional
- Published
- 2011
- Full Text
- View/download PDF
42. Lack of correlation between N-myc and MAX expression in neuroblastoma tumors and in cell lines: implication for N-myc-MAX complex formation
- Author
-
Raschella, G., Romeo, A., Negroni, A., Sabina Pucci, Dominici, C., Castello, M. A., Bevilacqua, P., Felsani, A., and Calabretta, B.
- Subjects
Transcription, Genetic ,Molecular Sequence Data ,Genes, myc ,Gene Expression ,Polymerase Chain Reaction ,Cell Line ,Proto-Oncogene Proteins c-myc ,Neuroblastoma ,Oligodeoxyribonucleotides ,DNA-Binding Proteins ,Humans ,Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ,Amino Acid Sequence ,Molecular Weight ,Basic-Leucine Zipper Transcription Factors ,DNA, Neoplasm ,Base Sequence ,Tumor Cells, Cultured ,Transcription Factors ,Blotting, Southern ,DNA ,Consensus Sequence ,Genetic ,Southern ,Cultured ,Blotting ,myc ,Tumor Cells ,Genes ,Settore MED/03 - Genetica Medica ,Neoplasm ,Neuroblastoma/genetics ,Neuroblastoma/metabolism ,Proto-Oncogene Proteins c-myc/metabolism ,Transcription - Abstract
Detectable levels of MAX messenger RNA were found in a set of human neuroblastoma tumors and established cell lines. MAX mRNA levels were independent of tumor stage and N-myc genomic amplification. By contrast, N-myc mRNA transcripts were detectable only in tumors with amplification of N-myc gene and in cell lines. Analysis by reverse transcriptase polymerase chain reaction and hybridization to specific oligodeoxynucleotide probes revealed approximately equal amounts of two MAX transcripts in all cases analyzed. Immunoprecipitations with a specific antibody to MAX detected two proteins of M(r) 21,000 and 22,000 in approximately equal amounts in all neuroblastoma lines regardless of N-myc amplification and/or expression. On the other hand, protein binding to the myc DNA consensus sequence correlated with N-myc expression in neuroblastoma cells. Thus, N-myc expression might be a limiting factor in the formation of the N-myc-MAX heterodimer in neuroblastomas.
- Published
- 1994
43. Elimination of clonogenic Philadelphia-positive cells using BCR-ABL antisense oligodeoxynucleotides
- Author
-
Fabritiis, P., Sergio Amadori, Calabretta, B., and Mandelli, F.
- Subjects
Base Sequence ,Bone Marrow Purging ,Molecular Sequence Data ,Fusion Proteins, bcr-abl ,Bone Marrow Cells ,Oligonucleotides, Antisense ,Oligodeoxyribonucleotides ,Bone Marrow Purging/methods ,Fusion Proteins ,bcr-abl/genetics ,Neoplastic Stem Cells/drug effects ,Oligonucleotides Antisense/pharmacology ,Leukemia, Myelogenous, Chronic, BCR-ABL Positive ,Neoplastic Stem Cells ,Tumor Cells, Cultured ,Humans ,Blast Crisis ,Tumor Stem Cell Assay - Abstract
Synthetic BCR-ABL antisense oligodeoxynucleotides are known to suppress in vitro clonogenic growth of primary cells from patients with CML. To evaluate the use of BCR-ABL antisense oligodeoxynucleotides as in vitro purging agents before autografting, we studied their effect on the clonogenic BV-173 cell line. At a concentration of 80 micrograms/ml, antisense oligodeoxynucleotides suppressed 85%, 95.5% and 95% of leukaemic cell growth after 24, 48 and 72 h of incubation, respectively. A correlation was observed between the concentration of oligomers and cell inhibition; however, concentrations higher than 80 micrograms/ml did not produce significant increase of BV-173 cell elimination. When the antisense treatment was performed on a wide range of target cell concentrations (from 1 x 10(5) to 5 x 10(6)/ml), the efficacy of purging was similar in all the groups. Addition of antisense oligodeoxynucleotides every 24 h produced, after 3 days, a cell growth inhibition superior to any single treatment; in particular, three treatments for 24 h at a concentration of 80 micrograms/ml were more effective than a single treatment at the same concentration or a single treatment at a concentration of 160 micrograms/ml. Incubation of normal human BM cells with the same doses which were very effective at inhibiting BV-173 cell proliferation, did not affect the growth of normal CFU-GM and of more immature progenitors.
- Published
- 1993
44. Regulation of proliferation and cytokine expression of bone marrow fibroblasts: role of c-myb
- Author
-
Szczylik, C, Skorski, T, Ku, Dh, Nicolaides, Nc, Wen, Sc, Rudnicka, L, Bonati, A, Malaguarnera, Lucia, Calabretta, B, and Sep
- Published
- 1993
45. SUCCESSFUL MAFOSFAMIDE PURGING OF BONE MARROW FROM CHRONIC MYELOGENOUS LEUKEMIA (CML) CELLS
- Author
-
Nieborowska-Skórska, M., Skórski, T., Mariusz Z. Ratajczak, Szczylik, C., Malaguarnera, L., and Calabretta, B.
- Subjects
Antineoplastic Agents/therapeutic use ,Blast Crisis/therapy ,Cyclophosphamide/analogs & derivatives ,Bone Marrow Purging ,Antineoplastic Agents ,Polymerase Chain Reaction ,Colony-Forming Units Assay ,Bone Marrow ,Leukemia, Myeloid, Chronic-Phase ,Tumor Cells, Cultured ,Humans ,Drug Screening Assays, Antitumor ,Blast Crisis ,Oligonucleotide Probes ,Cyclophosphamide - Abstract
The in vitro sensitivity of human chronic myeloid leukemia-blast crisis and chronic phase (CML-BC and CML-CP, respectively) cells as well as adherent cell-depleted, T lymphocyte-depleted normal bone marrow cells (A-T-NBMC) to various concentrations of mafosfamide (ASTA Z7654), was examined by colony formation assay in the presence of IL-3 and GM-CSF, to test the possibility of purging of BMC from CML cells. Colony formation by CML cells was inhibited more efficiently than by NBMC. After the incubation with 50 micrograms/ml or 100 micrograms/ml of mafosfamide, the growth of leukemic CFU-GM was totally abrogated in 2/11 or 9/11 cases of CML-BC and in 1/7 or 6/7 cases of CML-CP, respectively. At the same time the CFU-GM arising from normal BMC were not inhibited totally with 50 or 100 micrograms/ml of the drug in any of five experiments. CML cells were still unable to form secondary colonies, while normal BMC were capable of regrowth. The CD34+ cells isolated form CML-BC and CML-CP patients were also more susceptible to mafosfamide cytotoxicity in comparison to CD34+ cells derived from NBMC. To confirm the possibility of purging, CML-BC cells were mixed with NBMC (1:1) and incubated with mafosfamide. Finally, the growing colonies were examined for the presence of bcr/abl hybrid gene by reverse transcriptase-Taq polymerase chain reaction (RT-PCR) and specific hybridization. The bcr/abl gene was not detected in the colonies growing after 100 micrograms/ml, and the signal was diminished after incubation with 50 micrograms/ml of mafosfamide, as compared to control. These results strongly suggest that high concentrations of mafosfamide may be useful for the purging of autologous BMC from CML cells.
- Published
- 1993
46. Inhibition of in vitro proliferation of chronic myelogenous leukemia progenitor cells by c-myb antisense oligonucleotides
- Author
-
Szczylik, C., Skorski, T., Malaguarnera, Lucia, Chen, S. T., and Calabretta, B.
- Published
- 1992
47. Isolation and functional assessment of common, polymorphic variants of the B-MYB proto-oncogene associated with a reduced cancer risk
- Author
-
Schwab, R, primary, Bussolari, R, additional, Corvetta, D, additional, Chayka, O, additional, Santilli, G, additional, Kwok, J M-M, additional, Amorotti, G F, additional, Tonini, G P, additional, Iacoviello, L, additional, Bertorelle, R, additional, Menin, C, additional, Hubank, M, additional, Calabretta, B, additional, and Sala, A, additional
- Published
- 2007
- Full Text
- View/download PDF
48. Gene-targeted specific inhibition of chronic myeloid leukemia cell growth by BCR-ABL antisense oligodeoxynucleotides. 1991;29(3):85-9
- Author
-
Skorski, T, Szczylik, C, Malaguarnera, Lucia, Calabretta, B, GENE TARGETED SPECIFIC INHIBITION OF CHRONIC MYELOID LEUKEMIA CELL GROWTH BY, BCR ABL ANTISENSE OLIGODEOXYNUCLEOTIDES, and FOLIA HISTOCHEM CYTOBIOL
- Published
- 1991
49. Inhibition of proliferation by c-myb antisense oligodeoxynucleotides in colon adenocarcinoma cell lines that express c-myb
- Author
-
Melani, C., Rivoltini, L., Parmiani, G., Calabretta, B., and Mario Paolo Colombo
- Subjects
Gene Expression Regulation, Neoplastic ,Adenocarcinoma/genetics ,Gene Expression Regulation ,Neoplastic/genetics ,Oligonucleotides Antisense/pharmacology ,Colonic Neoplasms ,Tumor Cells, Cultured ,Humans ,Dimethylformamide ,Oncogenes ,RNA, Messenger ,RNA, Neoplasm ,Adenocarcinoma ,Oligonucleotides, Antisense ,Polymerase Chain Reaction ,Cell Division - Abstract
Steady-state mRNA levels of the protooncogene c-myb were measured by Northern blot analysis in the human colon carcinoma cell lines LoVo, the doxorubicin-resistant derivative LoVo/Dx, Colo 205, and HT 29. Overexpression of c-myb mRNA was detected in the Colo 205 cell line, probably because of gene amplification, while in human HT 29 cells c-myb was not expressed at a detectable level. Comparison between LoVo and LoVo/Dx cell lines showed that c-myb mRNA levels were much higher in the doxorubicin-resistant derivative than in the parental line. c-myb antisense oligodeoxynucleotides inhibited cell proliferation only in the cell lines with detectable mRNA c-myb (LoVo, LoVo/DX, and Colo 205). The dose of antisense exerting inhibitory effect was related to the levels of c-myb mRNA expression. Inhibition of c-myb expression in antisense-treated LoVo/DX cells was demonstrated by the reverse transcriptase polymerase chain reaction technique. LoVo/Dx cells were induced to differentiate by treatment with dimethylformamide to determine whether down-regulation of c-myb expression would accompany the process of differentiation. During the treatment with dimethylformamide the expression of c-myb decreased in parallel with the reduction of cell growth, while terminal differentiation of these cells was associated with changes in the expression of carcinoembryonic antigen and laminin receptor genes. Our findings demonstrate that the expression of c-myb is important for the proliferation of colon carcinoma cell lines and suggest that the role of this protooncogene is not restricted to cells of hematopoietic origin but is more general than previously thought.
- Published
- 1991
50. Signal transducer and activator of transcription (STAT)5 activation by BCR/ABL is dependent on intact Src homology (SH)3 and SH2 domains of BCR/ABL and is required for leukemogenesis.
- Author
-
Nieborowska-Skorska, M, Wasik, M A, Slupianek, A, Salomoni, P, Kitamura, T, Calabretta, B, Skorski, T, Nieborowska-Skorska, M, Wasik, M A, Slupianek, A, Salomoni, P, Kitamura, T, Calabretta, B, and Skorski, T
- Abstract
Signal transducer and activator of transcription (STAT)5 is constitutively activated in BCR/ ABL-expressing cells, but the mechanisms and functional consequences of such activation are unknown. We show here that BCR/ABL induces phosphorylation and activation of STAT5 by a mechanism that requires the BCR/ABL Src homology (SH)2 domain and the proline-rich binding site of the SH3 domain. Upon expression in 32Dcl3 growth factor-dependent myeloid precursor cells, STAT5 activation-deficient BCR/ABL SH3+SH2 domain mutants functioned as tyrosine kinase and activated Ras, but failed to protect from apoptosis induced by withdrawal of interleukin 3 and/or serum and did not induce leukemia in severe combined immunodeficiency mice. In complementation assays, expression of a dominant-active STAT5B mutant (STAT5B-DAM), but not wild-type STAT5B (STAT5B-WT), in 32Dcl3 cells transfected with STAT5 activation-deficient BCR/ABL SH3+SH2 mutants restored protection from apoptosis, stimulated growth factor-independent cell cycle progression, and rescued the leukemogenic potential in mice. Moreover, expression of a dominant-negative STAT5B mutant (STAT5B-DNM) in 32Dcl3 cells transfected with wild-type BCR/ABL inhibited apoptosis resistance, growth factor-independent proliferation, and the leukemogenic potential of these cells. In retrovirally infected mouse bone marrow cells, expression of STAT5B-DNM inhibited BCR/ABL-dependent transformation. Moreover, STAT5B-DAM, but not STAT5B-WT, markedly enhanced the ability of STAT5 activation-defective BCR/ABL SH3+SH2 mutants to induce growth factor-independent colony formation of primary mouse bone marrow progenitor cells. However, STAT5B-DAM did not rescue the growth factor-independent colony formation of kinase-deficient K1172R BCR/ABL or the triple mutant Y177F+R522L+ Y793F BCR/ABL, both of which also fail to activate STAT5. Together, these data demonstrate that STAT5 activation by BCR/ABL is dependent on signaling from more than one domain and
- Published
- 1999
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