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Pathological interactions between hematopoietic stem cells and their niche revealed by mouse models of primary myelofibrosis.

Expert review of hematology

Varricchio L, Mancini A, Migliaccio AR.
PMID: 20352017
Expert Rev Hematol. 2009 Jun 01;2(3):315-334. doi: 10.1586/ehm.09.17.

Primary myelofibrosis (PMF) belongs to the Philadelphia-negative myeloproliferative neoplasms and is a hematological disorder caused by abnormal function of the hematopoietic stem cells. The disease manifests itself with a plethora of alterations, including anemia, splenomegaly and extramedullary hematopoiesis. Its...

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Varricchio L, Mancini A, Migliaccio AR. Pathological interactions between hematopoietic stem cells and their niche revealed by mouse models of primary myelofibrosis. Expert Rev Hematol. 2009;2(3):315-334doi: 10.1586/ehm.09.17.
Varricchio, L., Mancini, A., & Migliaccio, A. R. (2009). Pathological interactions between hematopoietic stem cells and their niche revealed by mouse models of primary myelofibrosis. Expert review of hematology, 2(3), 315-334. https://doi.org/10.1586/ehm.09.17
Varricchio, Lilian, et al. "Pathological interactions between hematopoietic stem cells and their niche revealed by mouse models of primary myelofibrosis." Expert review of hematology vol. 2,3 (2009): 315-334. doi: https://doi.org/10.1586/ehm.09.17
Varricchio L, Mancini A, Migliaccio AR. Pathological interactions between hematopoietic stem cells and their niche revealed by mouse models of primary myelofibrosis. Expert Rev Hematol. 2009 Jun 01;2(3):315-334. doi: 10.1586/ehm.09.17. PMID: 20352017; PMCID: PMC2845468.
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Dual Targeting of Oncogenic Activation and Inflammatory Signaling Increases Therapeutic Efficacy in Myeloproliferative Neoplasms.

Cancer cell

Kleppe M, Koche R, Zou L, van Galen P, Hill CE, Dong L, De Groote S, Papalexi E, Hanasoge Somasundara AV, Cordner K, Keller M, Farnoud N, Medina J, McGovern E, Reyes J, Roberts J, Witkin M, Rapaport F, Teruya-Feldstein J, Qi J, Rampal R, Bernstein BE, Bradner JE, Levine RL.
PMID: 29634952
Cancer Cell. 2018 Apr 09;33(4):785-787. doi: 10.1016/j.ccell.2018.03.024.

No abstract available.

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Kleppe M, Koche R, Zou L, et al. Dual Targeting of Oncogenic Activation and Inflammatory Signaling Increases Therapeutic Efficacy in Myeloproliferative Neoplasms. Cancer Cell. 2018;33(4):785-787doi: 10.1016/j.ccell.2018.03.024.
Kleppe, M., Koche, R., Zou, L., van Galen, P., Hill, C. E., Dong, L., De Groote, S., Papalexi, E., Hanasoge Somasundara, A. V., Cordner, K., Keller, M., Farnoud, N., Medina, J., McGovern, E., Reyes, J., Roberts, J., Witkin, M., Rapaport, F., Teruya-Feldstein, J., Qi, J., Rampal, R., Bernstein, B. E., Bradner, J. E., & Levine, R. L. (2018). Dual Targeting of Oncogenic Activation and Inflammatory Signaling Increases Therapeutic Efficacy in Myeloproliferative Neoplasms. Cancer cell, 33(4), 785-787. https://doi.org/10.1016/j.ccell.2018.03.024
Kleppe, Maria, et al. "Dual Targeting of Oncogenic Activation and Inflammatory Signaling Increases Therapeutic Efficacy in Myeloproliferative Neoplasms." Cancer cell vol. 33,4 (2018): 785-787. doi: https://doi.org/10.1016/j.ccell.2018.03.024
Kleppe M, Koche R, Zou L, van Galen P, Hill CE, Dong L, De Groote S, Papalexi E, Hanasoge Somasundara AV, Cordner K, Keller M, Farnoud N, Medina J, McGovern E, Reyes J, Roberts J, Witkin M, Rapaport F, Teruya-Feldstein J, Qi J, Rampal R, Bernstein BE, Bradner JE, Levine RL. Dual Targeting of Oncogenic Activation and Inflammatory Signaling Increases Therapeutic Efficacy in Myeloproliferative Neoplasms. Cancer Cell. 2018 Apr 09;33(4):785-787. doi: 10.1016/j.ccell.2018.03.024. PMID: 29634952; PMCID: PMC5908465.
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PRMT5 Inhibition Modulates E2F1 Methylation and Gene-Regulatory Networks Leading to Therapeutic Efficacy in JAK2.

Cancer discovery

Pastore F, Bhagwat N, Pastore A, Radzisheuskaya A, Karzai A, Krishnan A, Li B, Bowman RL, Xiao W, Viny AD, Zouak A, Park YC, Cordner KB, Braunstein S, Maag JL, Grego A, Mehta J, Wang M, Lin H, Durham BH, Koche RP, Rampal RK, Helin K, Scherle P, Vaddi K, Levine RL.
PMID: 32669286
Cancer Discov. 2020 Nov;10(11):1742-1757. doi: 10.1158/2159-8290.CD-20-0026. Epub 2020 Jul 15.

We investigated the role of PRMT5 in myeloproliferative neoplasm (MPN) pathogenesis and aimed to elucidate key PRMT5 targets contributing to MPN maintenance. PRMT5 is overexpressed in primary MPN cells, and PRMT5 inhibition potently reduced MPN cell proliferation

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Pastore F, Bhagwat N, Pastore A, et al. PRMT5 Inhibition Modulates E2F1 Methylation and Gene-Regulatory Networks Leading to Therapeutic Efficacy in JAK2. Cancer Discov. 2020;10(11):1742-1757doi: 10.1158/2159-8290.CD-20-0026.
Pastore, F., Bhagwat, N., Pastore, A., Radzisheuskaya, A., Karzai, A., Krishnan, A., Li, B., Bowman, R. L., Xiao, W., Viny, A. D., Zouak, A., Park, Y. C., Cordner, K. B., Braunstein, S., Maag, J. L., Grego, A., Mehta, J., Wang, M., Lin, H., Durham, B. H., Koche, R. P., Rampal, R. K., Helin, K., Scherle, P., Vaddi, K., & Levine, R. L. (2020). PRMT5 Inhibition Modulates E2F1 Methylation and Gene-Regulatory Networks Leading to Therapeutic Efficacy in JAK2. Cancer discovery, 10(11), 1742-1757. https://doi.org/10.1158/2159-8290.CD-20-0026
Pastore, Friederike, et al. "PRMT5 Inhibition Modulates E2F1 Methylation and Gene-Regulatory Networks Leading to Therapeutic Efficacy in JAK2." Cancer discovery vol. 10,11 (2020): 1742-1757. doi: https://doi.org/10.1158/2159-8290.CD-20-0026
Pastore F, Bhagwat N, Pastore A, Radzisheuskaya A, Karzai A, Krishnan A, Li B, Bowman RL, Xiao W, Viny AD, Zouak A, Park YC, Cordner KB, Braunstein S, Maag JL, Grego A, Mehta J, Wang M, Lin H, Durham BH, Koche RP, Rampal RK, Helin K, Scherle P, Vaddi K, Levine RL. PRMT5 Inhibition Modulates E2F1 Methylation and Gene-Regulatory Networks Leading to Therapeutic Efficacy in JAK2. Cancer Discov. 2020 Nov;10(11):1742-1757. doi: 10.1158/2159-8290.CD-20-0026. Epub 2020 Jul 15. PMID: 32669286; PMCID: PMC7642059.
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LKB1/.

Cancer discovery

Marinaccio C, Suraneni P, Celik H, Volk A, Wen QJ, Ling T, Bulic M, Lasho T, Koche RP, Famulare CA, Farnoud N, Stein B, Schieber M, Gurbuxani S, Root DE, Younger ST, Hoffman R, Gangat N, Ntziachristos P, Chandel NS, Levine RL, Rampal RK, Challen GA, Tefferi A, Crispino JD.
PMID: 33579786
Cancer Discov. 2021 Jun;11(6):1398-1410. doi: 10.1158/2159-8290.CD-20-1353. Epub 2021 Feb 12.

The myeloproliferative neoplasms (MPN) frequently progress to blast phase disease, an aggressive form of acute myeloid leukemia. To identify genes that suppress disease progression, we performed a focused CRISPR/Cas9 screen and discovered that depletion of LKB1/

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Marinaccio C, Suraneni P, Celik H, et al. LKB1/. Cancer Discov. 2021;11(6):1398-1410doi: 10.1158/2159-8290.CD-20-1353.
Marinaccio, C., Suraneni, P., Celik, H., Volk, A., Wen, Q. J., Ling, T., Bulic, M., Lasho, T., Koche, R. P., Famulare, C. A., Farnoud, N., Stein, B., Schieber, M., Gurbuxani, S., Root, D. E., Younger, S. T., Hoffman, R., Gangat, N., Ntziachristos, P., Chandel, N. S., Levine, R. L., Rampal, R. K., Challen, G. A., Tefferi, A., & Crispino, J. D. (2021). LKB1/. Cancer discovery, 11(6), 1398-1410. https://doi.org/10.1158/2159-8290.CD-20-1353
Marinaccio, Christian, et al. "LKB1/." Cancer discovery vol. 11,6 (2021): 1398-1410. doi: https://doi.org/10.1158/2159-8290.CD-20-1353
Marinaccio C, Suraneni P, Celik H, Volk A, Wen QJ, Ling T, Bulic M, Lasho T, Koche RP, Famulare CA, Farnoud N, Stein B, Schieber M, Gurbuxani S, Root DE, Younger ST, Hoffman R, Gangat N, Ntziachristos P, Chandel NS, Levine RL, Rampal RK, Challen GA, Tefferi A, Crispino JD. LKB1/. Cancer Discov. 2021 Jun;11(6):1398-1410. doi: 10.1158/2159-8290.CD-20-1353. Epub 2021 Feb 12. PMID: 33579786; PMCID: PMC8178182.
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Gender and Vascular Complications in the JAK2 V617F-Positive Myeloproliferative Neoplasms.

Thrombosis

Stein BL, Rademaker A, Spivak JL, Moliterno AR.
PMID: 22084670
Thrombosis. 2011;2011:874146. doi: 10.1155/2011/874146. Epub 2011 Jul 24.

We previously found that gender influenced the JAK2 V617F allele burden, but it is unknown whether this gender difference in molecular epidemiology influences complications in the myeloproliferative neoplasms (MPNs). Historically, vascular complications represented the most common cause of mortality...

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Stein BL, Rademaker A, Spivak JL, et al. Gender and Vascular Complications in the JAK2 V617F-Positive Myeloproliferative Neoplasms. Thrombosis. 2011;2011:874146doi: 10.1155/2011/874146.
Stein, B. L., Rademaker, A., Spivak, J. L., & Moliterno, A. R. (2011). Gender and Vascular Complications in the JAK2 V617F-Positive Myeloproliferative Neoplasms. Thrombosis, 2011874146. https://doi.org/10.1155/2011/874146
Stein, Brady L, et al. "Gender and Vascular Complications in the JAK2 V617F-Positive Myeloproliferative Neoplasms." Thrombosis vol. 2011 (2011): 874146. doi: https://doi.org/10.1155/2011/874146
Stein BL, Rademaker A, Spivak JL, Moliterno AR. Gender and Vascular Complications in the JAK2 V617F-Positive Myeloproliferative Neoplasms. Thrombosis. 2011;2011:874146. doi: 10.1155/2011/874146. Epub 2011 Jul 24. PMID: 22084670; PMCID: PMC3200304.
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The possible role of mutated endothelial cells in myeloproliferative neoplasms.

Haematologica

Farina M, Russo D, Hoffman R.
PMID: 34320782
Haematologica. 2021 Nov 01;106(11):2813-2823. doi: 10.3324/haematol.2021.278499.

Myeloproliferative neoplasms (MPN) are chronic, clonal hematologic malignancies characterized by myeloproliferation and a high incidence of vascular complications (thrombotic and bleeding). Although MPN-specific driver mutations have been identified, the underlying events that culminate in these clinical manifestations require further...

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Farina M, Russo D, Hoffman R. The possible role of mutated endothelial cells in myeloproliferative neoplasms. Haematologica. 2021;106(11):2813-2823doi: 10.3324/haematol.2021.278499.
Farina, M., Russo, D., & Hoffman, R. (2021). The possible role of mutated endothelial cells in myeloproliferative neoplasms. Haematologica, 106(11), 2813-2823. https://doi.org/10.3324/haematol.2021.278499
Farina, Mirko, et al. "The possible role of mutated endothelial cells in myeloproliferative neoplasms." Haematologica vol. 106,11 (2021): 2813-2823. doi: https://doi.org/10.3324/haematol.2021.278499
Farina M, Russo D, Hoffman R. The possible role of mutated endothelial cells in myeloproliferative neoplasms. Haematologica. 2021 Nov 01;106(11):2813-2823. doi: 10.3324/haematol.2021.278499. PMID: 34320782; PMCID: PMC8561279.
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Calreticulin: Challenges Posed by the Intrinsically Disordered Nature of Calreticulin to the Study of Its Function.

Frontiers in cell and developmental biology

Varricchio L, Falchi M, Dall'Ora M, De Benedittis C, Ruggeri A, Uversky VN, Migliaccio AR.
PMID: 29218307
Front Cell Dev Biol. 2017 Nov 23;5:96. doi: 10.3389/fcell.2017.00096. eCollection 2017.

Calreticulin is a Ca

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Varricchio L, Falchi M, Dall'Ora M, et al. Calreticulin: Challenges Posed by the Intrinsically Disordered Nature of Calreticulin to the Study of Its Function. Front Cell Dev Biol. 2017;5:96doi: 10.3389/fcell.2017.00096.
Varricchio, L., Falchi, M., Dall'Ora, M., De Benedittis, C., Ruggeri, A., Uversky, V. N., & Migliaccio, A. R. (2017). Calreticulin: Challenges Posed by the Intrinsically Disordered Nature of Calreticulin to the Study of Its Function. Frontiers in cell and developmental biology, 596. https://doi.org/10.3389/fcell.2017.00096
Varricchio, Lilian, et al. "Calreticulin: Challenges Posed by the Intrinsically Disordered Nature of Calreticulin to the Study of Its Function." Frontiers in cell and developmental biology vol. 5 (2017): 96. doi: https://doi.org/10.3389/fcell.2017.00096
Varricchio L, Falchi M, Dall'Ora M, De Benedittis C, Ruggeri A, Uversky VN, Migliaccio AR. Calreticulin: Challenges Posed by the Intrinsically Disordered Nature of Calreticulin to the Study of Its Function. Front Cell Dev Biol. 2017 Nov 23;5:96. doi: 10.3389/fcell.2017.00096. eCollection 2017. PMID: 29218307; PMCID: PMC5703715.
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Phosphoproteomic Landscaping Identifies Non-canonical cKIT Signaling in Polycythemia Vera Erythroid Progenitors.

Frontiers in oncology

Federici G, Varricchio L, Martelli F, Falchi M, Picconi O, Francescangeli F, Contavalli P, Girelli G, Tafuri A, Petricoin EF, Mazzarini M, Zeuner A, Migliaccio AR.
PMID: 31824842
Front Oncol. 2019 Nov 22;9:1245. doi: 10.3389/fonc.2019.01245. eCollection 2019.

Although stem cell factor (SCF)/cKIT interaction plays key functions in erythropoiesis, cKIT signaling in human erythroid cells is still poorly defined. To provide new insights into cKIT-mediated erythroid expansion in development and disease, we performed phosphoproteomic profiling of primary...

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Federici G, Varricchio L, Martelli F, et al. Phosphoproteomic Landscaping Identifies Non-canonical cKIT Signaling in Polycythemia Vera Erythroid Progenitors. Front Oncol. 2019;9:1245doi: 10.3389/fonc.2019.01245.
Federici, G., Varricchio, L., Martelli, F., Falchi, M., Picconi, O., Francescangeli, F., Contavalli, P., Girelli, G., Tafuri, A., Petricoin, E. F., Mazzarini, M., Zeuner, A., & Migliaccio, A. R. (2019). Phosphoproteomic Landscaping Identifies Non-canonical cKIT Signaling in Polycythemia Vera Erythroid Progenitors. Frontiers in oncology, 91245. https://doi.org/10.3389/fonc.2019.01245
Federici, Giulia, et al. "Phosphoproteomic Landscaping Identifies Non-canonical cKIT Signaling in Polycythemia Vera Erythroid Progenitors." Frontiers in oncology vol. 9 (2019): 1245. doi: https://doi.org/10.3389/fonc.2019.01245
Federici G, Varricchio L, Martelli F, Falchi M, Picconi O, Francescangeli F, Contavalli P, Girelli G, Tafuri A, Petricoin EF, Mazzarini M, Zeuner A, Migliaccio AR. Phosphoproteomic Landscaping Identifies Non-canonical cKIT Signaling in Polycythemia Vera Erythroid Progenitors. Front Oncol. 2019 Nov 22;9:1245. doi: 10.3389/fonc.2019.01245. eCollection 2019. PMID: 31824842; PMCID: PMC6883719.
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Transfusion-independent β(0)-thalassemia after bone marrow transplantation failure: proposed involvement of high parental HbF and an epigenetic mechanism.

American journal of blood research

Paciaroni K, Lucarelli G, Martelli F, Migliaccio AR, von Lindern M, Borg J, Gillemans N, van Dijk TB, Philipsen S.
PMID: 25232502
Am J Blood Res. 2014 Sep 05;4(1):27-32. eCollection 2014.

Currently, bone marrow transplantation is the only curative treatment for β-thalassemia and sickle cell disease. In rare cases, sustained and full fetal hemoglobin production was observed in patients after failure of bone marrow transplantation. This rendered the patients transfusion-free,...

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Paciaroni K, Lucarelli G, Martelli F, et al. Transfusion-independent β(0)-thalassemia after bone marrow transplantation failure: proposed involvement of high parental HbF and an epigenetic mechanism. Am J Blood Res. 2014;4(1):27-32
Paciaroni, K., Lucarelli, G., Martelli, F., Migliaccio, A. R., von Lindern, M., Borg, J., Gillemans, N., van Dijk, T. B., & Philipsen, S. (2014). Transfusion-independent β(0)-thalassemia after bone marrow transplantation failure: proposed involvement of high parental HbF and an epigenetic mechanism. American journal of blood research, 4(1), 27-32.
Paciaroni, Katia, et al. "Transfusion-independent β(0)-thalassemia after bone marrow transplantation failure: proposed involvement of high parental HbF and an epigenetic mechanism." American journal of blood research vol. 4,1 (2014): 27-32.
Paciaroni K, Lucarelli G, Martelli F, Migliaccio AR, von Lindern M, Borg J, Gillemans N, van Dijk TB, Philipsen S. Transfusion-independent β(0)-thalassemia after bone marrow transplantation failure: proposed involvement of high parental HbF and an epigenetic mechanism. Am J Blood Res. 2014 Sep 05;4(1):27-32. eCollection 2014. PMID: 25232502; PMCID: PMC4165118.
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Getting personal with B19 parvovirus.

Blood

Migliaccio G, Migliaccio AR.
PMID: 20133475
Blood. 2010 Feb 04;115(5):922-3. doi: 10.1182/blood-2009-11-252593.

No abstract available.

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Migliaccio G, Migliaccio AR. Getting personal with B19 parvovirus. Blood. 2010;115(5):922-3doi: 10.1182/blood-2009-11-252593.
Migliaccio, G., & Migliaccio, A. R. (2010). Getting personal with B19 parvovirus. Blood, 115(5), 922-3. https://doi.org/10.1182/blood-2009-11-252593
Migliaccio, Giovanni, and Migliaccio, Anna Rita. "Getting personal with B19 parvovirus." Blood vol. 115,5 (2010): 922-3. doi: https://doi.org/10.1182/blood-2009-11-252593
Migliaccio G, Migliaccio AR. Getting personal with B19 parvovirus. Blood. 2010 Feb 04;115(5):922-3. doi: 10.1182/blood-2009-11-252593. PMID: 20133475.
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The role of glucocorticoid receptor (GR) polymorphisms in human erythropoiesis.

American journal of blood research

Varricchio L, Migliaccio AR.
PMID: 25755906
Am J Blood Res. 2014 Dec 15;4(2):53-72. eCollection 2014.

Glucocorticoids are endogenous steroid hormones that regulate several biological functions including proliferation, differentiation and apoptosis in numerous cell types in response to stress. Synthetic glucocorticoids, such as dexamethasone (Dex) are used to treat a variety of diseases ranging from...

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Varricchio L, Migliaccio AR. The role of glucocorticoid receptor (GR) polymorphisms in human erythropoiesis. Am J Blood Res. 2014;4(2):53-72
Varricchio, L., & Migliaccio, A. R. (2014). The role of glucocorticoid receptor (GR) polymorphisms in human erythropoiesis. American journal of blood research, 4(2), 53-72.
Varricchio, Lilian, and Migliaccio, Anna Rita. "The role of glucocorticoid receptor (GR) polymorphisms in human erythropoiesis." American journal of blood research vol. 4,2 (2014): 53-72.
Varricchio L, Migliaccio AR. The role of glucocorticoid receptor (GR) polymorphisms in human erythropoiesis. Am J Blood Res. 2014 Dec 15;4(2):53-72. eCollection 2014. PMID: 25755906; PMCID: PMC4348794.
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Histone acetyltransferase inhibitors block neuroblastoma cell growth in vivo.

Oncogenesis

Gajer JM, Furdas SD, Gründer A, Gothwal M, Heinicke U, Keller K, Colland F, Fulda S, Pahl HL, Fichtner I, Sippl W, Jung M.
PMID: 25664930
Oncogenesis. 2015 Feb 09;4:e137. doi: 10.1038/oncsis.2014.51.

We have previously described novel histone acetyltransferase (HAT) inhibitors that block neuroblastoma cell growth in vitro. Here we show that two selected pyridoisothiazolone HAT inhibitors, PU139 and PU141, induce cellular histone hypoacetylation and inhibit growth of several neoplastic cell...

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Gajer JM, Furdas SD, Gründer A, et al. Histone acetyltransferase inhibitors block neuroblastoma cell growth in vivo. Oncogenesis. 2015;4:e137doi: 10.1038/oncsis.2014.51.
Gajer, J. M., Furdas, S. D., Gründer, A., Gothwal, M., Heinicke, U., Keller, K., Colland, F., Fulda, S., Pahl, H. L., Fichtner, I., Sippl, W., & Jung, M. (2015). Histone acetyltransferase inhibitors block neuroblastoma cell growth in vivo. Oncogenesis, 4e137. https://doi.org/10.1038/oncsis.2014.51
Gajer, J M, et al. "Histone acetyltransferase inhibitors block neuroblastoma cell growth in vivo." Oncogenesis vol. 4 (2015): e137. doi: https://doi.org/10.1038/oncsis.2014.51
Gajer JM, Furdas SD, Gründer A, Gothwal M, Heinicke U, Keller K, Colland F, Fulda S, Pahl HL, Fichtner I, Sippl W, Jung M. Histone acetyltransferase inhibitors block neuroblastoma cell growth in vivo. Oncogenesis. 2015 Feb 09;4:e137. doi: 10.1038/oncsis.2014.51. PMID: 25664930; PMCID: PMC4338425.
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