Advertisement

Topics

PubMed Journals Articles About "Ruxolitinib Primary Myelofibrosis" RSS

16:11 EST 20th January 2019 | BioPortfolio

Ruxolitinib Primary Myelofibrosis PubMed articles on BioPortfolio. Our PubMed references draw on over 21 million records from the medical literature. Here you can see the latest Ruxolitinib Primary Myelofibrosis articles that have been published worldwide.

More Information about "Ruxolitinib Primary Myelofibrosis" on BioPortfolio

We have published hundreds of Ruxolitinib Primary Myelofibrosis news stories on BioPortfolio along with dozens of Ruxolitinib Primary Myelofibrosis Clinical Trials and PubMed Articles about Ruxolitinib Primary Myelofibrosis for you to read. In addition to the medical data, news and clinical trials, BioPortfolio also has a large collection of Ruxolitinib Primary Myelofibrosis Companies in our database. You can also find out about relevant Ruxolitinib Primary Myelofibrosis Drugs and Medications on this site too.

Showing "Ruxolitinib Primary Myelofibrosis" PubMed Articles 1–25 of 9,000+

IL-6 stimulation of DNA replication is JAK1/2 mediated in cross-talk with hyperactivated ERK1/2 signaling.

Myeloproliferative neoplasms (MPNs) are developing resistance to therapy by JAK1/2 inhibitor ruxolitinib. To explore the mechanism of ruxolitinib's limited effect, we examined the JAK1/2 mediated induction of proliferation related ERK1/2 and AKT signaling by proinflammatory interleukin-6 (IL-6) in MPN granulocytes and JAK2V617F mutated human erythroleukemia (HEL) cells. We found that JAK1/2 or JAK2 inhibition prevented the IL-6 activation of STAT3 and AKT pathways in polycythemia vera and HEL cells. Further...


Distinguishing autoimmune myelofibrosis from primary myelofibrosis.

Bone marrow fibrosis (BMF) is a histologic finding in a wide range of diseases, including malignancies, endocrine disorders, autoimmune diseases, and infections. Autoimmune myelofibrosis (AIMF) is an uncommon etiology of BMF; it can be secondary to a defined autoimmune disease, or it can be primary in the absence of a clinically diagnosed autoimmune disease but the presence of serologic evidence of autoantibodies. Distinguishing between primary myelofibrosis (PMF) and non-neoplastic AIMF is of the utmost im...

Captopril mitigates splenomegaly and myelofibrosis in the Gata1 murine model of myelofibrosis.

Allogeneic stem cell transplantation is currently the only curative therapy for primary myelofibrosis (MF), while the JAK2 inhibitor, ruxolitinib. Has been approved only for palliation. Other therapies are desperately needed to reverse life-threatening MF. However, the cell(s) and cytokine(s) that promote MF remain unclear. Several reports have demonstrated that captopril, an inhibitor of angiotensin-converting enzyme that blocks the production of angiotensin II (Ang II), mitigates fibrosis in heart, lung, ...


Durability of spleen response affects the outcome of ruxolitinib-treated patients with myelofibrosis: Results from a multicentre study on 284 patients.

Ruxolitinib Therapy Followed by Reduced Intensity Conditioning for Hematopoietic Cell Transplantation for Myelofibrosis - Myeloproliferative Disorders Research Consortium 114 study.

We evaluated the feasibility of ruxolitinib therapy followed by a reduced intensity conditioning (RIC) regimen for myelofibrosis (MF) patients undergoing transplant in a two stage Simon phase II trial. The aims were to decrease the incidence of graft failure (GF) and non-relapse mortality (NRM) in comparison to previous Myeloproliferative Disorders Research consortium 101 study. The plan was to enrol 11 patients each in related donor (RD), and unrelated donor (URD) arms, with trial termination if ≥3 failu...

Gaucher Disease and Myelofibrosis: A Combined Disease or a Misdiagnosis?

Gaucher disease (GD) and primary myelofibrosis (PMF) share similar clinical and laboratory features, such as cytopenia, hepatosplenomegaly, and marrow fibrosis, often resulting in a misdiagnosis.

WT1 gene is overexpressed in myeloproliferative neoplasms, especially in myelofibrosis.

Classical Philadelphia-negative myeloproliferative neoplasms include Polycythemia Vera (PV), Essential Thrombocythemia (ET) and Primary Myelofibrosis (PMF). They are characterized by the presence of driver mutations of JAK2, CALR or MPL genes. Overexpression of WT1 is used as a marker of minimal residual disease in acute myeloid leukemia, especially after allogeneic stem cell transplantation (SCT). We investigated WT1 expression at diagnosis in 152 MPN patients and showed that the WT1 transcript was overexp...

Ruxolitinib treatment for steroid refractory acute and chronic graft versus host disease in children: Clinical and immunological results.

Ruxolitinib is a promising treatment for steroid refractory graft-versus-host disease (GvHD). However, data concerning effects on T cells are probably involved in increased risk of opportunistic infections. We analyzed clinical and immunological changes in children with GvHD taking ruxolitinib. Twenty-two children that underwent transplantation and received ruxolitinib were included. Ruxolitinib indication was acute and chronic GvHD in 13 and 9 patients, respectively. Overall response rate in acute GvHD and...

Characterization of a human induced Pluripotent Stem (iPS) cell line (INCABRi002-A) derived from a primary myelofibrosis patient harboring the 5-bp insertion in CALR and the p.W146X mutation in TP53.

Primary myelofibrosis (PMF) is a hematological malignancy characterized by activation of the JAK/STAT pathway and risk of leukemic transformation. In this study, we generated an induced Pluripotent Stem (iPS) cell line derived from a 65-year old male PMF patient carrying the 5-pb insertion in the CALR gene (CALR) and the c.437 G > A mutation in the TP53 gene (p.W146X). The newly derived PMF3.17 iPS cell line harbors the original mutations and was characterized as bona fide iPS. Resource table.

Mechanisms for mTORC1 activation and synergistic induction of apoptosis by ruxolitinib and BH3 mimetics or autophagy inhibitors in JAK2-V617F-expressing leukemic cells including newly established PVTL-2.

The activated JAK2-V617F mutant is very frequently found in myeloproliferative neoplasms (MPNs), and its inhibitor ruxolitinib has been in clinical use, albeit with limited efficacies. Here, we examine the signaling mechanisms from JAK2-V617F and responses to ruxolitinib in JAK2-V617F-positive leukemic cell lines, including PVTL-2, newly established from a patient with post-MPN secondary acute myeloid leukemia, and the widely used model cell line HEL. We have found that ruxolitinib downregulated the mTORC1/...

A case of gout secondary to primary myelofibrosis.

A 52-year-old man was referred to our department with a 2-year history of polyarthritis. He was diagnosed as gout due to acute arthritis of bilateral feet dorsum 2 years ago,but he didn't receive any standard treatment. 1 year ago,there were more and more joints evolved during the gout attack, and many subcutaneous nodules occurred. When he presented to our clinic 1 month ago,the urate acid level was as high as 715 μmol/L. Moreover, we could find bone erosion in the X rays of his hand and foot,as well as s...

A phase I clinical trial of ruxolitinib in combination with nilotinib in chronic myeloid leukemia patients with molecular evidence of disease.

Preclinical evidence indicates that the bone marrow microenvironment provides a protective niche for leukemic stem cells, allowing them to evade the effects of BCR-ABL tyrosine kinase inhibitors (TKIs), but that targeting of the JAK-STAT pathway with the JAK2 inhibitor ruxolitinib increases TKI-induced apoptosis. A phase I clinical trial (NCT01702064) investigated the tolerability and safety of treating chronic-phase chronic myeloid leukemia patients with ruxolitinib in combination with the BCR-ABL TKI nilo...

Intraoral granulocytic sarcoma as a manifestation of myelofibrosis: A case report and review of the literature.

Granulocytic sarcoma (GS) is an extramedullary tumor associated with myelodysplastic syndromes or myeloproliferative diseases. Intraoral manifestations are considered uncommon, with a reasonable number of cases, and are mostly related to leukemia. The association of oral GS and myelofibrosis is very rare and only three cases have been published. In this paper, we report the fourth case of oral lesion in a patient with a diagnosis of myelofibrosis. The aim of this study was to present a review of the literat...

Inflammatory functional iron deficiency common in myelofibrosis, contributes to anaemia and impairs quality of life. From the Nordic MPN study Group.

The study investigates the hypothesis that inflammation in myelofibrosis (MF) like in myeloma and lymphoma, may disturb iron distribution and contribute to anaemia.

Thrombin Generation Testing in Patients with Myelofibrosis.

Primary myelofibrosis (PMF) is a chronic clonal myeloid disorder. Together with essential thrombocythemia (ET) and polycythemia vera (PV), it belongs to a group of Philadelphia chromosome-negative myeloproliferative neoplasms. Thrombotic events are serious complications negatively influencing the quality and length of these patients' lives. The confirmed risk factors for venous thromboembolism are age over 60 years, a positive history of thromboembolism, presence of common cardiovascular risks, JAK2 V617F m...

Aggressive B-cell lymphomas in patients with myelofibrosis receiving JAK1/2 inhibitor therapy.

Inhibition of Janus-kinase 1/2 (JAK1/2) is a mainstay to treat myeloproliferative neoplasms (MPN). Sporadic observations reported the co-incidence of B-cell non-Hodgkin lymphomas during treatment of MPN with JAK1/2 inhibitors. We assessed 626 MPN patients including 69 with myelofibrosis receiving JAK1/2 inhibitors for lymphoma development. B-cell lymphomas evolved in 4/69 patients (5.8%) upon JAK1/2 inhibition compared to 2/557 (0.36%) with conventional treatment (16-fold increased risk). A similar 15-fold ...

Utility of Ruxolitinib in a Child with Chronic Mucocutaneous Candidiasis Caused by a Novel STAT1 Gain-of-Function Mutation.

Signal transducer and activator of transcription 1 gain-of-function (STAT1 GOF) mutations are the most common cause of chronic mucocutaneous candidiasis (CMC). We aim to report the effect of oral ruxolitinib, the Janus kinase (JAK) family tyrosine kinase inhibitor, on clinical and immune status of a 12-year-old boy with severe CMC due to a novel STAT1 GOF mutation.

Utility of JAK2 V617F allelic burden in distinguishing chronic Myelomonocytic leukemia from primary myelofibrosis with Monocytosis.

The concurrent presence of JAK2 V617F, monocytosis and bone marrow fibrosis can be observed in both chronic myelomonocytic leukemia (CMML) and primary myelofibrosis (PMF). It can be challenging to distinguish CMML with JAK2 mutation and fibrosis from other myeloid neoplasms, particularly PMF. To identify key features that may help distinguish these two entities, we retrospectively studied 21 cases diagnosed as "CMML" with JAK2 V617F and bone marrow fibrosis that were identified from a cohort of 610 cases of...

Patient Perspectives Regarding Allogeneic Bone Marrow Transplant in Myelofibrosis.

Hematopoietic stem cell transplant (HCT) is a curative treatment for patients with myelofibrosis (MF), however many eligible patients decline this potentially life-saving procedure. The reasons behind this decision are not clear. We sought to survey patients with MF to understand their perspective on HCT.

Recurrent ischemic cerebrovascular events as presenting manifestations of myeloproliferative neoplasms.

Myeloproliferative neoplasms (MPN) - polycythemia vera, essential thrombocythemia and primary myelofibrosis - are associated with increased risk for ischemic cerebrovascular events (ICVE). Due to their low prevalence, MPN often remain undiagnosed as the cause of ICVE.

Efficacy of Ruxolitinib Therapy in a Patient with Severe Enterocolitis Associated with a STAT3 Gain of Function Mutation.

A triplex probe-based TaqMan qPCR assay for Calreticulin type I and II mutation detection.

Calreticulin (CALR) exon 9 frameshift mutations have recently been identified in 30-40% of patients with essential thrombocythemia (ET) and primary myelofibrosis (PMF) without JAK2 or MPL mutations. We aimed to develop a qPCR assay to screen type I and II mutations of CALR.

Myeloproliferative neoplasms in the young: Mayo Clinic experience with 361 patients age 40 years or younger.

Between 1967 and 2017, 361 patients with myeloproliferative neoplasms (MPN), age ≤40 years, were seen at our institution, constituting 12% of all MPN patients (n=3,023) seen during the same time period; disease-specific incidences were 12% in polycythemia vera (PV; n=79), 20% in essential thrombocythemia (ET; n=219) and 5% in primary myelofibrosis (PMF; n=63). Compared to their older counterparts, younger patients were more likely to present with low risk disease (P

A t(3;8)(q26.2;q24) involving the EVI1 (MECOM) Gene.

Polycythemia vera (PV) is a Philadelphia chromosome-negative myeloproliferative neoplasm (MPN) primarily characterized by increased red blood cell production. We report a case of a 68-year-old male with a history of PV. About four years later, the patient developed myelofibrosis. A bone marrow biopsy confirmed the presence of myelofibrosis confirmed by a hypercellular bone marrow (80%) with increased reticulin fibrosis (MF2-3), 5% blasts, and a normal 46,XY karyotype. A follow-up bone marrow biopsy document...

Busulfan or thiotepa based conditioning in myelofibrosis: a phase II multicenter randomized study from the GITMO group.

We are reporting a randomized study comparing fludarabine in combination with busulfan (FB) or thiotepa (FT), as conditioning regimen for hematopoietic stem cell transplantation (HSCT) in patients with myelofibrosis. The primary study endpoint was progression-free survival (PFS). Sixty patients were enrolled with a median age of 56 years and an intermediate-2 or high-risk score in 65%, according to the Dynamic International Prognostic Staging System (DIPSS). Donors were HLA-identical sibling (n=25), matched...


Advertisement
Quick Search
Advertisement
Advertisement