Expansion of circulating CD56brightnatural killer cells in patients with JAK2-positive chronic myeloproliferative neoplasms during treatment with interferon-α

2014 ◽  
Vol 94 (3) ◽  
pp. 227-234 ◽  
Author(s):  
Caroline H. Riley ◽  
Morten Hansen ◽  
Marie K. Brimnes ◽  
Hans C. Hasselbalch ◽  
Ole W. Bjerrum ◽  
...  
Keyword(s):  
Myeloproliferative Neoplasms ◽  
Interferon Α ◽  
Killer Cells ◽  
Chronic Myeloproliferative Neoplasms

scholarly journals What are the current treatment approaches for patients with polycythemia vera and essential thrombocythemia?

Hematology ◽  
2017 ◽  
Vol 2017 (1) ◽  
pp. 480-488 ◽  
Author(s):  
Alessandro M. Vannucchi ◽  
Paola Guglielmelli
Keyword(s):  
Polycythemia Vera ◽  
Essential Thrombocythemia ◽  
State Of The Art ◽  
Myeloproliferative Neoplasms ◽  
Symptom Burden ◽  
Current Treatment ◽  
Interferon Α ◽  
Jak2 Inhibitor ◽  
Chronic Myeloproliferative Neoplasms

Abstract Polycythemia vera (PV) and essential thrombocythemia (ET) are chronic myeloproliferative neoplasms that are characterized by thrombohemorrhagic complications, symptom burden, and impaired survival mainly due to thrombosis, progression to myelofibrosis, and transformation to acute leukemia. In this manuscript, we will review the most recent changes in diagnostic criteria, the improvements in risk stratification, and the “state of the art” in the daily management of these disorders. The role of conventional therapies and novel agents, interferon α and the JAK2 inhibitor ruxolitinib, is critically discussed based on the results of a few basic randomized clinical studies. Several unmet needs remain, above all, the lack of a curative approach that might overcome the still burdensome morbidity and mortality of these hematologic neoplasms, as well as the toxicities associated with therapeutic agents.

scholarly journals Cancer Immune Therapy for Philadelphia Chromosome-Negative Chronic Myeloproliferative Neoplasms

Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1763 ◽  
Author(s):  
Morten Orebo Holmström ◽  
Hans Carl Hasselbalch ◽  
Mads Hald Andersen
Keyword(s):  
Cancer Immunotherapy ◽  
Myeloproliferative Neoplasms ◽  
Immune Therapy ◽  
Philadelphia Chromosome ◽  
Driver Mutations ◽  
Interferon Α ◽  
Therapeutic Vaccination ◽  
Hematopoietic Stem ◽  
Chronic Myeloproliferative Neoplasms ◽  
Anti Cancer

Philadelphia chromosome-negative chronic myeloproliferative neoplasms (MPN) are neoplastic diseases of the hematopoietic stem cells in the bone marrow. MPN are characterized by chronic inflammation and immune dysregulation. Of interest, the potent immunostimulatory cytokine interferon-α has been used to treat MPN for decades. A deeper understanding of the anti-cancer immune response and of the different immune regulatory mechanisms in patients with MPN has paved the way for an increased perception of the potential of cancer immunotherapy in MPN. Therapeutic vaccination targeting the driver mutations in MPN is one recently described potential new treatment modality. Furthermore, T cells can directly react against regulatory immune cells because they recognize proteins like arginase and programmed death ligand 1 (PD-L1). Therapeutic vaccination with arginase or PD-L1 therefore offers a novel way to directly affect immune inhibitory pathways, potentially altering tolerance to tumor antigens like mutant CALR and mutant JAK2. Other therapeutic options that could be used in concert with therapeutic cancer vaccines are immune checkpoint–blocking antibodies and interferon-α. For more advanced MPN, adoptive cellular therapy is a potential option that needs more preclinical investigation. In this review, we summarize current knowledge about the immune system in MPN and discuss the many opportunities for anti-cancer immunotherapy in patients with MPN.

Interferon-Alpha in the Treatment of Philadelphia-Negative Chronic Myeloproliferative Neoplasms. Status and Perspectives

2011 ◽  
Vol 12 (3) ◽  
pp. 392-419 ◽  
Author(s):  
Hans Carl Hasselbalch ◽  
Thomas Stauffer Larsen ◽  
Caroline Hasselbalch Riley ◽  
Morten Krogh Jensen ◽  
Jean-Jacques Kiladjian
Keyword(s):  
Interferon Alpha ◽  
Myeloproliferative Neoplasms ◽  
Chronic Myeloproliferative Neoplasms

scholarly journals Methylation status of SOCS1 and SOCS3 in BCR-ABL negative and JAK2V617F negative chronic myeloproliferative neoplasms

2008 ◽  
Vol 32 (10) ◽  
pp. 1638-1640 ◽  
Author(s):  
Marta Fernández-Mercado ◽  
Virginia Cebrián ◽  
Begoña Euba ◽  
Marta García-Granero ◽  
María J. Calasanz ◽  
...  
Keyword(s):  
Myeloproliferative Neoplasms ◽  
Methylation Status ◽  
Chronic Myeloproliferative Neoplasms

scholarly journals Neutrophil extracellular trap formation and circulating nucleosomes in patients with chronic myeloproliferative neoplasms

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Cecilia P. Marin Oyarzún ◽  
Agostina Carestia ◽  
Paola R. Lev ◽  
Ana C. Glembotsky ◽  
Miguel A. Castro Ríos ◽  
...  
Keyword(s):  
Myeloproliferative Neoplasms ◽  
Neutrophil Extracellular Trap ◽  
Chronic Myeloproliferative Neoplasms ◽  
Trap Formation ◽  
Extracellular Trap

scholarly journals THE JAK2V617F POINT MUTATION INCREASES THE OSTEOCLAST FORMING ABILITY OF MONOCYTES IN PATIENTS WITH CHRONIC MYELOPROLIFERATIVE NEOPLASMS AND MAKES THEIR OSTEOCLASTS MORE SUSCEPTIBLE TO JAK2 INHIBITION

2018 ◽  
Vol 10 ◽  
pp. e2018058
Author(s):  
Emmanouil Spanoudakis ◽  
Menelaos Papoutselis ◽  
Ioanna Bazntiara ◽  
Eleftheria Lamprianidou ◽  
Xrisa Kordella ◽  
...  
Keyword(s):  
Point Mutation ◽  
Genomic Dna ◽  
Myeloproliferative Neoplasms ◽  
Myeloproliferative Neoplasm ◽  
Cellular Level ◽  
Hemopoietic Stem Cell ◽  
Jak2 Inhibitor ◽  
Chronic Myeloproliferative Neoplasms ◽  
Cell Niche ◽  
Jak2 Inhibition

JAK2V617F is a gain of function point mutation that occurs in Myeloproliferative Neoplasm (MPN) patients and deranges their hemopoiesis at cellular level. We speculate that hyperfunctioning JAK2 can modify osteoclast (OCL) homeostasis in MPN patients. We studied 18 newly diagnosed MPN patients and four age-matched normal donors (ND). Osteoclast forming assays started from selected monocytes also and under titrated concentrations of the JAK2 Inhibitor AG-490 (Tyrphostin). Genomic DNA was extracted from the formed osteoclasts, and the JAK2V617F/JAK2WT genomic DNA ratio was calculated. OCLs formed from monocytes derived from heterozygous (Het) for the JAK2V617F mutation MPN patients, were three times more compared to those from JAK2 wild type (WT) MPN patients (p=0,05) and from ND as well (p=0,03). The ratio of JAK2V617F/JAK2WT genomic DNA was increased in OCLs compared to the input monocyte cells showing a survival advantage of the mutated clone. In comparison to ND and JAK2 WT MPN patients, OCLs from patients JAK2V617F (Het) were more susceptible to JAK2 inhibition. These alterations in osteoclast homeostasis, attributed to mutated JAK2, can deregulate the hemopoietic stem cell niche in MPN patients.

Chronic kidney disease in patients with the Philadelphia-negative chronic myeloproliferative neoplasms

2014 ◽  
Vol 38 (4) ◽  
pp. 490-495 ◽  
Author(s):  
Alexander Sidelmann Christensen ◽  
Jonas Bech Møller ◽  
Hans Carl Hasselbalch
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Myeloproliferative Neoplasms ◽  
Chronic Myeloproliferative Neoplasms
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