- Third COVID-19 mRNA vaccine booster dose indicated for myelofibrosis patients
The results showed that three out of four MF patients developed immunoglobulin G (IgG) antibodies after two doses of the vaccine. However, the rate of antibody development was slower than that which was detected in healthy individuals, which may indicate that these patients had an impairment of their immune response when stimulated by the vaccine.
- SARS-CoV-2: Einige Krebstherapeutika machen Impfung unwirksam
Auch die 16 Patienten, die mit dem Januskinase-Hemmer Ruxolitinib behandelt wurden, produzierten kaum IgG-Antikörper gegen das Spikeprotein: Die mittlere Konzentration betrug 10 AU/ml im Vergleich zu 6.961 AU/ml bei unbehandelten Leukämie/Lymphom-Patienten und 21.395 AU/ml bei den gesunden Klinikmitarbeitern.
- Side Effects of Jakafi (Ruxolitinib), Warnings, Uses
Common side effects of Jakafi include:bruising,dizziness,headache,urinary tract infections,weight gain,bloating,gas,low blood platelet levels (thrombocytopenia),anemia,fatigue,diarrhea,shortness of breath, and nausea. Some side effects of Jakafi may be similar to the symptoms of myelofibrosis. Tell your doctor if you have serious side effects of Jakafi including: pale skin,lightheadedness,shortness of breath,rapid heart rate,trouble concentrating,easy bruising,unusual bleeding (nose, mouth, vagina, or rectum),purple or red pinpoint spots under your skin,fever,chills,body aches,flu symptoms,vomiting,sores in your mouth and throat,pain or burning when you urinate, or blisters or painful skin rash
- FDA requires warnings about increased risk of serious heart-related events, cancer, blood clots, and death for JAK inhibitors that treat certain chronic inflammatory conditions | FDA
- Janus Kinase Inhibitors and Coronavirus Disease (COVID)-19: Rationale, Clinical Evidence and Safety Issues
We are witnessing a paradigm shift in drug development and clinical practice to fight the novel coronavirus disease (COVID-19), and a number of clinical trials have been or are being testing various pharmacological approaches to counteract viral load and its complications such as cytokine storm.
- EU-Zulassung für Fedratinib: Neuer Wirkstoff bei Myelofibrose | PZ – Pharmazeutische Zeitung
Celgene, ein Tochterunternehmen von Bristol-Myers-Squibb (BMS), hat die EU-Zulassung für den neuen Kinasehemmer Fedratinib (Inrebic®) erhalten. Es sei die erste neue Therapieoption für Patienten mit Myelofibrose seit fast zehn Jahren.
- Trying to Find the Cause for a JAK2 Genetic Mutation | The Mighty
It basically reaffirmed that my rare blood cancer was environmentally derived, and raised the premise that certain heritable precursors needed to be present in order for the specific genetic mutation to take place.
- Combination therapy with interferon and ruxolitinib for polycythemia vera and myelofibrosis: are two drugs better than one?
Combination treatment seemed to speed the time to remission, improve blood counts, reduce marrow cellularity and fibrosis and decrease the JAK2 allele burden, all with acceptable toxicity. The dropout rate at the end of 2 years was 6% for PV patients and 32% for MF patients. These results are most interesting and encouraging, but require confirmation, because it was a single-arm study.
- Ruxolitinib and interferon-α2 combination therapy for patients with polycythemia vera or myelofibrosis: a phase II study
In conclusion, combination treatment with ruxolitinib and low-dose PEG-IFNa2 improved peripheral blood cell counts, bone marrow cellularity and fibrosis along with symptom burden with acceptable toxicity in some patients with PV and proliferative MF. Most patients in the study were intolerant of or refractory to standard PEGIFNa2 treatment, and more than half had discontinued previous treatment with hydroxyurea, highlighting that this combination treatment is a viable choice for patients with few treatment options left.
- Krebspatient erkrankt an Covid-19 - dann sind fast all seine Tumore verschwunden - FOCUS Online
Der Fall eines 61 Jahre alten Krebspatienten geht um die Welt. Erst erkrankt er an Covid-19, dann sind fast alle seine Tumore verschwunden. Mediziner vermuten, die Corona-Infektion könnte zur Heilung beigetragen haben - sprechen aber auch von einer "Rarität".
- Recent insights regarding the molecular basis of myeloproliferative neoplasms
The discovery of the molecular features of MPN has revealed novel diagnostic and prognostic markers, provided insight into MPN pathobiology, and prompted new research questions. However, there is much that remain unknown. For example, although several heterogeneous noncanonical mutations in MPL and JAK2 have been identified [51,52], studies have not determined which mutations drive the disease in a significant proportion of triple-negative MPN cases. The hereditary basis of MPNs are poorly understood and future studies should seek to identify novel disease-related germline mutations. In addition, the functional disease outcomes of known germline mutations should be clearly defined.
- Sustained major molecular response on interferon alpha-2b in two patients with polycythemia vera - PubMed
We report here the first profound and sustained molecular responses with a JAK2 V617F allele burden below 1.0% in two patients with polycythemia vera treated with interferon alpha-2b (IFN-2b). Discontinuation of IFN-2b in one of the patients was followed by a sustained long-lasting (12 months of follow-up) major molecular response.
- Chronic inflammation as a promotor of mutagenesis in essential thrombocythemia, polycythemia vera and myelofibrosis. A human inflammation model for cancer development? - ScienceDirect
Recently chronic inflammation has been proposed as a trigger and driver of clonal evolution in MPNs. Herein, it is hypothesized that sustained inflammation may elicit the stem cell insult by inducing a state of chronic oxidative stress with elevated levels of reactive oxygen species (ROS) in the bone marrow, thereby creating a high-risk microenvironment for induction of mutations due to the persistent inflammation-induced oxidative damage to DNA in hematopoietic cells.
- The role of cytokines in the initiation and progression of myelofibrosis - ScienceDirect
The discovery of the Janus kinase 2 (JAK2) V617F mutation has led to the development of a number of JAK1/2 inhibitors in the treatment of MF and similar neoplasms. Here, the role of cytokines in MF initiation and progression is discussed, the impact of current therapies is reviewed, and new combination therapies are proposed, such as JAK1/2 inhibitors with interferons, statins, and epigenetic modifiers for patients with MF and related neoplasms.
- Perspectives on interferon-alpha in the treatment of polycythemia vera and related myeloproliferative neoplasms: minimal residual disease and cure?
In this review, we tell the IFN story in MPNs from the very beginning in the 1980s up to 2018 and describe the perspectives for IFN-alpha2 treatment of MPNs in the future. The mechanisms of actions are discussed and the impact of chronic inflammation as the driving force for clonal expansion and disease progression in MPNs is discussed in the context of combination therapies with potent anti-inflammatory agents, such as the JAK1–2 inhibitors (licensed only ruxolitinib) and statins as well. Interferon-alpha2 being the cornerstone treatment in MPNs and having the potential of inducing minimal residual disease (MRD) with normalization of the bone marrow and low-JAK2V617F allele burden, we believe that combination therapy with ruxolitinib may be even more efficacious and hopefully revert disease progression in many more patients to enter the path towards MRD.