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Successful treatment of a Caucasian case of multifocal Castleman's disease with TAFRO syndrome with a pathophysiology targeted therapy - a case report.

Experimental hematology & oncology

Tedesco S, Postacchini L, Manfredi L, Goteri G, Luchetti MM, Festa A, Gabrielli A, Pomponio G.
PMID: 25671135
Exp Hematol Oncol. 2015 Jan 14;4(1):3. doi: 10.1186/2162-3619-4-3. eCollection 2015.

BACKGROUND: Castleman-Kojima disease (TAFRO Syndrome) is characterized by Thrombocytopenia, Anasarca, myeloFibrosis, Renal dysfunction, Organomegaly, multiple lymphadenopathy and histopathology pattern of atypical Castleman's disease (CD). Only few cases of this recently identified unique variant of Multicentric CD (MCD) are described...

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Tedesco S, Postacchini L, Manfredi L, et al. Successful treatment of a Caucasian case of multifocal Castleman's disease with TAFRO syndrome with a pathophysiology targeted therapy - a case report. Exp Hematol Oncol. 2015;4(1):3doi: 10.1186/2162-3619-4-3.
Tedesco, S., Postacchini, L., Manfredi, L., Goteri, G., Luchetti, M. M., Festa, A., Gabrielli, A., & Pomponio, G. (2015). Successful treatment of a Caucasian case of multifocal Castleman's disease with TAFRO syndrome with a pathophysiology targeted therapy - a case report. Experimental hematology & oncology, 4(1), 3. https://doi.org/10.1186/2162-3619-4-3
Tedesco, Silvia, et al. "Successful treatment of a Caucasian case of multifocal Castleman's disease with TAFRO syndrome with a pathophysiology targeted therapy - a case report." Experimental hematology & oncology vol. 4,1 (2015): 3. doi: https://doi.org/10.1186/2162-3619-4-3
Tedesco S, Postacchini L, Manfredi L, Goteri G, Luchetti MM, Festa A, Gabrielli A, Pomponio G. Successful treatment of a Caucasian case of multifocal Castleman's disease with TAFRO syndrome with a pathophysiology targeted therapy - a case report. Exp Hematol Oncol. 2015 Jan 14;4(1):3. doi: 10.1186/2162-3619-4-3. eCollection 2015. PMID: 25671135; PMCID: PMC4322808.
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[No title available]

Experimental hematology & oncology

Brufsky A.
PMID: 28344858
Exp Hematol Oncol. 2017 Mar 22;6:7. doi: 10.1186/s40164-017-0066-5. eCollection 2017.

No abstract available.

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Brufsky A. . Exp Hematol Oncol. 2017;6:7doi: 10.1186/s40164-017-0066-5.
Brufsky, A. (2017). . Experimental hematology & oncology, 67. https://doi.org/10.1186/s40164-017-0066-5
Brufsky, Adam. "." Experimental hematology & oncology vol. 6 (2017): 7. doi: https://doi.org/10.1186/s40164-017-0066-5
Brufsky A. . Exp Hematol Oncol. 2017 Mar 22;6:7. doi: 10.1186/s40164-017-0066-5. eCollection 2017. PMID: 28344858; PMCID: PMC5361712.
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Long-term survival in a patient with progressive multifocal leukoencephalopathy after therapy with rituximab, fludarabine and cyclophosphamide for chronic lymphocytic leukemia.

Experimental hematology & oncology

Garrote H, de la Fuente A, Oña R, Rodríguez I, Echevarría JE, Sepúlveda JM, García JF.
PMID: 25767742
Exp Hematol Oncol. 2015 Mar 01;4:8. doi: 10.1186/s40164-015-0003-4. eCollection 2015.

A 50-year-old male with chronic lymphocytic leukemia (CLL) was treated with fludarabine, cyclophosphamide and rituximab, which produced a complete remission. Eight months after the last dose of rituximab he had visual disturbance, diminished muscular strength in the right arm...

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Garrote H, de la Fuente A, Oña R, et al. Long-term survival in a patient with progressive multifocal leukoencephalopathy after therapy with rituximab, fludarabine and cyclophosphamide for chronic lymphocytic leukemia. Exp Hematol Oncol. 2015;4:8doi: 10.1186/s40164-015-0003-4.
Garrote, H., de la Fuente, A., Oña, R., Rodríguez, I., Echevarría, J. E., Sepúlveda, J. M., & García, J. F. (2015). Long-term survival in a patient with progressive multifocal leukoencephalopathy after therapy with rituximab, fludarabine and cyclophosphamide for chronic lymphocytic leukemia. Experimental hematology & oncology, 48. https://doi.org/10.1186/s40164-015-0003-4
Garrote, Heidys, et al. "Long-term survival in a patient with progressive multifocal leukoencephalopathy after therapy with rituximab, fludarabine and cyclophosphamide for chronic lymphocytic leukemia." Experimental hematology & oncology vol. 4 (2015): 8. doi: https://doi.org/10.1186/s40164-015-0003-4
Garrote H, de la Fuente A, Oña R, Rodríguez I, Echevarría JE, Sepúlveda JM, García JF. Long-term survival in a patient with progressive multifocal leukoencephalopathy after therapy with rituximab, fludarabine and cyclophosphamide for chronic lymphocytic leukemia. Exp Hematol Oncol. 2015 Mar 01;4:8. doi: 10.1186/s40164-015-0003-4. eCollection 2015. PMID: 25767742; PMCID: PMC4357158.
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Acquired factor VIII deficiency: two case reports and a review of literature.

Experimental hematology & oncology

Mo L, Bao GC.
PMID: 28352491
Exp Hematol Oncol. 2017 Mar 24;6:8. doi: 10.1186/s40164-017-0068-3. eCollection 2017.

BACKGROUND: Acquired factor VIII (FVIII) deficiency, or acquired hemophilia A (AHA), is a rare autoimmune disorder involving antibody-mediated depletion of coagulation FVIII, leading to severe, life-threatening bleeding. The condition is often associated with other autoimmune disorders, and its treatment...

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Mo L, Bao GC. Acquired factor VIII deficiency: two case reports and a review of literature. Exp Hematol Oncol. 2017;6:8doi: 10.1186/s40164-017-0068-3.
Mo, L., & Bao, G. C. (2017). Acquired factor VIII deficiency: two case reports and a review of literature. Experimental hematology & oncology, 68. https://doi.org/10.1186/s40164-017-0068-3
Mo, Lan, and Bao, George C. "Acquired factor VIII deficiency: two case reports and a review of literature." Experimental hematology & oncology vol. 6 (2017): 8. doi: https://doi.org/10.1186/s40164-017-0068-3
Mo L, Bao GC. Acquired factor VIII deficiency: two case reports and a review of literature. Exp Hematol Oncol. 2017 Mar 24;6:8. doi: 10.1186/s40164-017-0068-3. eCollection 2017. PMID: 28352491; PMCID: PMC5366150.
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Selective inhibitors of nuclear export (SINE) in hematological malignancies.

Experimental hematology & oncology

Das A, Wei G, Parikh K, Liu D.
PMID: 25745591
Exp Hematol Oncol. 2015 Mar 01;4:7. doi: 10.1186/s40164-015-0002-5. eCollection 2015.

Regulated nucleo-cytoplasmic transport plays a major role in maintaining cellular homeostasis. CRM1 (chromosome region maintenance 1 or exportin 1 or XPO 1) is responsible for the nucleo-cytoplasmic transport of more than 200 proteins, including most of the tumor suppressor...

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Das A, Wei G, Parikh K, et al. Selective inhibitors of nuclear export (SINE) in hematological malignancies. Exp Hematol Oncol. 2015;4:7doi: 10.1186/s40164-015-0002-5.
Das, A., Wei, G., Parikh, K., & Liu, D. (2015). Selective inhibitors of nuclear export (SINE) in hematological malignancies. Experimental hematology & oncology, 47. https://doi.org/10.1186/s40164-015-0002-5
Das, Arundhati, et al. "Selective inhibitors of nuclear export (SINE) in hematological malignancies." Experimental hematology & oncology vol. 4 (2015): 7. doi: https://doi.org/10.1186/s40164-015-0002-5
Das A, Wei G, Parikh K, Liu D. Selective inhibitors of nuclear export (SINE) in hematological malignancies. Exp Hematol Oncol. 2015 Mar 01;4:7. doi: 10.1186/s40164-015-0002-5. eCollection 2015. PMID: 25745591; PMCID: PMC4350974.
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Histomorphological responses after therapy with pegylated interferon α-2a in patients with essential thrombocythemia (ET) and polycythemia vera (PV).

Experimental hematology & oncology

Masarova L, Yin CC, Cortes JE, Konopleva M, Borthakur G, Newberry KJ, Kantarjian HM, Bueso-Ramos CE, Verstovsek S.
PMID: 29152412
Exp Hematol Oncol. 2017 Nov 09;6:30. doi: 10.1186/s40164-017-0090-5. eCollection 2017.

BACKGROUND: Pegylated interferon alfa-2a (PEG-IFN-α-2a) is a potent immunomodulating agent capable of inducing high rate of hematologic and even complete molecular remission in patients with essential thrombocythemia (ET) and polycythemia vera (PV). We recently reported results of a phase...

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Masarova L, Yin CC, Cortes JE, et al. Histomorphological responses after therapy with pegylated interferon α-2a in patients with essential thrombocythemia (ET) and polycythemia vera (PV). Exp Hematol Oncol. 2017;6:30doi: 10.1186/s40164-017-0090-5.
Masarova, L., Yin, C. C., Cortes, J. E., Konopleva, M., Borthakur, G., Newberry, K. J., Kantarjian, H. M., Bueso-Ramos, C. E., & Verstovsek, S. (2017). Histomorphological responses after therapy with pegylated interferon α-2a in patients with essential thrombocythemia (ET) and polycythemia vera (PV). Experimental hematology & oncology, 630. https://doi.org/10.1186/s40164-017-0090-5
Masarova, Lucia, et al. "Histomorphological responses after therapy with pegylated interferon α-2a in patients with essential thrombocythemia (ET) and polycythemia vera (PV)." Experimental hematology & oncology vol. 6 (2017): 30. doi: https://doi.org/10.1186/s40164-017-0090-5
Masarova L, Yin CC, Cortes JE, Konopleva M, Borthakur G, Newberry KJ, Kantarjian HM, Bueso-Ramos CE, Verstovsek S. Histomorphological responses after therapy with pegylated interferon α-2a in patients with essential thrombocythemia (ET) and polycythemia vera (PV). Exp Hematol Oncol. 2017 Nov 09;6:30. doi: 10.1186/s40164-017-0090-5. eCollection 2017. PMID: 29152412; PMCID: PMC5679503.
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Dabrafenib and trametinib activity in a patient with BRAF V600E mutated and microsatellite instability high (MSI-H) metastatic endometrial cancer.

Experimental hematology & oncology

Moschetta M, Mak G, Hauser J, Davies C, Uccello M, Arkenau HT.
PMID: 28078189
Exp Hematol Oncol. 2017 Jan 10;6:1. doi: 10.1186/s40164-016-0061-2. eCollection 2017.

BACKGROUND: Targeting BRAF V600E mutation has been proven effective in the treatment of several types of cancer. In endometrial adenocarcinoma, the BRAF V600E mutation has been rarely reported. Whether targeting BRAF oncogene may represent a plausible therapeutic strategy for...

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Moschetta M, Mak G, Hauser J, et al. Dabrafenib and trametinib activity in a patient with BRAF V600E mutated and microsatellite instability high (MSI-H) metastatic endometrial cancer. Exp Hematol Oncol. 2017;6:1doi: 10.1186/s40164-016-0061-2.
Moschetta, M., Mak, G., Hauser, J., Davies, C., Uccello, M., & Arkenau, H. T. (2017). Dabrafenib and trametinib activity in a patient with BRAF V600E mutated and microsatellite instability high (MSI-H) metastatic endometrial cancer. Experimental hematology & oncology, 61. https://doi.org/10.1186/s40164-016-0061-2
Moschetta, Michele, et al. "Dabrafenib and trametinib activity in a patient with BRAF V600E mutated and microsatellite instability high (MSI-H) metastatic endometrial cancer." Experimental hematology & oncology vol. 6 (2017): 1. doi: https://doi.org/10.1186/s40164-016-0061-2
Moschetta M, Mak G, Hauser J, Davies C, Uccello M, Arkenau HT. Dabrafenib and trametinib activity in a patient with BRAF V600E mutated and microsatellite instability high (MSI-H) metastatic endometrial cancer. Exp Hematol Oncol. 2017 Jan 10;6:1. doi: 10.1186/s40164-016-0061-2. eCollection 2017. PMID: 28078189; PMCID: PMC5223353.
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Breast cancer brain metastases: the last frontier.

Experimental hematology & oncology

Leone JP, Leone BA.
PMID: 26605131
Exp Hematol Oncol. 2015 Nov 24;4:33. doi: 10.1186/s40164-015-0028-8. eCollection 2015.

Breast cancer is a common cause of brain metastases, with metastases occurring in at least 10-16 % of patients. Longer survival of patients with metastatic breast cancer and the use of better imaging techniques are associated with an increased...

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Leone JP, Leone BA. Breast cancer brain metastases: the last frontier. Exp Hematol Oncol. 2015;4:33doi: 10.1186/s40164-015-0028-8.
Leone, J. P., & Leone, B. A. (2015). Breast cancer brain metastases: the last frontier. Experimental hematology & oncology, 433. https://doi.org/10.1186/s40164-015-0028-8
Leone, José Pablo, and Leone, Bernardo Amadeo. "Breast cancer brain metastases: the last frontier." Experimental hematology & oncology vol. 4 (2015): 33. doi: https://doi.org/10.1186/s40164-015-0028-8
Leone JP, Leone BA. Breast cancer brain metastases: the last frontier. Exp Hematol Oncol. 2015 Nov 24;4:33. doi: 10.1186/s40164-015-0028-8. eCollection 2015. PMID: 26605131; PMCID: PMC4657380.
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Extranodal diffuse large B-cell lymphoma with monoclonal gammopathy: an aggressive and primary refractory disease responding to an immunomodulatory agent.

Experimental hematology & oncology

Mondello P, Pitini V, Barresi V, Brea EJ, Di Mirto C, Arrigo C, Cuzzocrea S, Mian M.
PMID: 26740908
Exp Hematol Oncol. 2016 Jan 06;5:1. doi: 10.1186/s40164-015-0030-1. eCollection 2015.

BACKGROUND: Although the clinical outcome of patients with diffuse large B cell lymphoma (DLBCL) has been improved by the addition of rituximab to standard chemotherapy, almost one-third fails or relapses after first line treatment. The presence of monoclonal gammopathy...

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Mondello P, Pitini V, Barresi V, et al. Extranodal diffuse large B-cell lymphoma with monoclonal gammopathy: an aggressive and primary refractory disease responding to an immunomodulatory agent. Exp Hematol Oncol. 2016;5:1doi: 10.1186/s40164-015-0030-1.
Mondello, P., Pitini, V., Barresi, V., Brea, E. J., Di Mirto, C., Arrigo, C., Cuzzocrea, S., & Mian, M. (2015). Extranodal diffuse large B-cell lymphoma with monoclonal gammopathy: an aggressive and primary refractory disease responding to an immunomodulatory agent. Experimental hematology & oncology, 51. https://doi.org/10.1186/s40164-015-0030-1
Mondello, Patrizia, et al. "Extranodal diffuse large B-cell lymphoma with monoclonal gammopathy: an aggressive and primary refractory disease responding to an immunomodulatory agent." Experimental hematology & oncology vol. 5 (2015): 1. doi: https://doi.org/10.1186/s40164-015-0030-1
Mondello P, Pitini V, Barresi V, Brea EJ, Di Mirto C, Arrigo C, Cuzzocrea S, Mian M. Extranodal diffuse large B-cell lymphoma with monoclonal gammopathy: an aggressive and primary refractory disease responding to an immunomodulatory agent. Exp Hematol Oncol. 2016 Jan 06;5:1. doi: 10.1186/s40164-015-0030-1. eCollection 2015. PMID: 26740908; PMCID: PMC4702294.
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CD57+ T-cells are a subpopulation of T-follicular helper cells in nodular lymphocyte predominant Hodgkin lymphoma.

Experimental hematology & oncology

Sattarzadeh A, Diepstra A, Rutgers B, van den Berg A, Visser L.
PMID: 26380151
Exp Hematol Oncol. 2015 Sep 15;4:27. doi: 10.1186/s40164-015-0022-1. eCollection 2015.

BACKGROUND: Nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) is characterized by lymphocyte-predominant (LP) cells in a background of CD4+ CD57+ T-cells. These cells are normally present in the germinal center of lymphoid tissues. The cells rosetting LP cells are described...

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Sattarzadeh A, Diepstra A, Rutgers B, et al. CD57+ T-cells are a subpopulation of T-follicular helper cells in nodular lymphocyte predominant Hodgkin lymphoma. Exp Hematol Oncol. 2015;4:27doi: 10.1186/s40164-015-0022-1.
Sattarzadeh, A., Diepstra, A., Rutgers, B., van den Berg, A., & Visser, L. (2015). CD57+ T-cells are a subpopulation of T-follicular helper cells in nodular lymphocyte predominant Hodgkin lymphoma. Experimental hematology & oncology, 427. https://doi.org/10.1186/s40164-015-0022-1
Sattarzadeh, Ahmad, et al. "CD57+ T-cells are a subpopulation of T-follicular helper cells in nodular lymphocyte predominant Hodgkin lymphoma." Experimental hematology & oncology vol. 4 (2015): 27. doi: https://doi.org/10.1186/s40164-015-0022-1
Sattarzadeh A, Diepstra A, Rutgers B, van den Berg A, Visser L. CD57+ T-cells are a subpopulation of T-follicular helper cells in nodular lymphocyte predominant Hodgkin lymphoma. Exp Hematol Oncol. 2015 Sep 15;4:27. doi: 10.1186/s40164-015-0022-1. eCollection 2015. PMID: 26380151; PMCID: PMC4570656.
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Nucleotide excision repair deficiency in melanoma in response to UVA.

Experimental hematology & oncology

Murray HC, Maltby VE, Smith DW, Bowden NA.
PMID: 26913219
Exp Hematol Oncol. 2016 Feb 24;5:6. doi: 10.1186/s40164-016-0035-4. eCollection 2015.

BACKGROUND: The causative link between UV exposure and melanoma development is well known, however the mechanistic relationship remains incompletely characterised. UVA and UVB components of sunlight are implicated in melanomagenesis; however the majority of studies have focused on the...

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Murray HC, Maltby VE, Smith DW, et al. Nucleotide excision repair deficiency in melanoma in response to UVA. Exp Hematol Oncol. 2016;5:6doi: 10.1186/s40164-016-0035-4.
Murray, H. C., Maltby, V. E., Smith, D. W., & Bowden, N. A. (2015). Nucleotide excision repair deficiency in melanoma in response to UVA. Experimental hematology & oncology, 56. https://doi.org/10.1186/s40164-016-0035-4
Murray, Heather C, et al. "Nucleotide excision repair deficiency in melanoma in response to UVA." Experimental hematology & oncology vol. 5 (2015): 6. doi: https://doi.org/10.1186/s40164-016-0035-4
Murray HC, Maltby VE, Smith DW, Bowden NA. Nucleotide excision repair deficiency in melanoma in response to UVA. Exp Hematol Oncol. 2016 Feb 24;5:6. doi: 10.1186/s40164-016-0035-4. eCollection 2015. PMID: 26913219; PMCID: PMC4765239.
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Identification of AIM2 as a downstream target of JAK2V617F.

Experimental hematology & oncology

Liew EL, Araki M, Hironaka Y, Mori S, Tan TZ, Morishita S, Edahiro Y, Ohsaka A, Komatsu N.
PMID: 26823993
Exp Hematol Oncol. 2016 Jan 28;5:2. doi: 10.1186/s40164-016-0032-7. eCollection 2015.

BACKGROUND: The gain-of-function mutation JAK2V617F is frequently found in Philadelphia-chromosome-negative myeloproliferative neoplasm (MPN) patients. However, the tumorigenic properties of JAK2V617F have mostly been characterized in in vivo and in vitro murine models due to the lack of appropriate human...

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Liew EL, Araki M, Hironaka Y, et al. Identification of AIM2 as a downstream target of JAK2V617F. Exp Hematol Oncol. 2016;5:2doi: 10.1186/s40164-016-0032-7.
Liew, E. L., Araki, M., Hironaka, Y., Mori, S., Tan, T. Z., Morishita, S., Edahiro, Y., Ohsaka, A., & Komatsu, N. (2015). Identification of AIM2 as a downstream target of JAK2V617F. Experimental hematology & oncology, 52. https://doi.org/10.1186/s40164-016-0032-7
Liew, Ei Leen, et al. "Identification of AIM2 as a downstream target of JAK2V617F." Experimental hematology & oncology vol. 5 (2015): 2. doi: https://doi.org/10.1186/s40164-016-0032-7
Liew EL, Araki M, Hironaka Y, Mori S, Tan TZ, Morishita S, Edahiro Y, Ohsaka A, Komatsu N. Identification of AIM2 as a downstream target of JAK2V617F. Exp Hematol Oncol. 2016 Jan 28;5:2. doi: 10.1186/s40164-016-0032-7. eCollection 2015. PMID: 26823993; PMCID: PMC4730608.
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Showing 1 to 12 of 503 entries