ReviewExpert opinion on therapeutic targets2012
Targeting JAK2 in the therapy of myeloproliferative neoplasms.
Review in Expert opinion on therapeutic targets, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- The JAK2 46/1 haplotype is a risk factor for myeloproliferative neoplasms in Chinese patients.International journal of hematology · 2012Trial
- A comprehensive molecular analysis of 113 primary ovarian clear cell carcinomas reveals common therapeutically significant aberrations.Diagnostic pathology · 2023Article
- Shared Genetic Risk Factors Between Cancer and Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2022Article
- Value Proposition of Untapped Wet Wastes: Carboxylic Acid Production through Anaerobic Digestion.iScience · 2020Review
- Stat3 as a potential therapeutic target for rheumatoid arthritis.Scientific reports · 2017Article
- Review
- Pharmacologic suppression of JAK1/2 by JAK1/2 inhibitor AZD1480 potently inhibits IL-6-induced experimental prostate cancer metastases formation.Molecular cancer therapeutics · 2014Article
- Myelofibrosis, JAK2 inhibitors and erythropoiesis.Leukemia · 2013Article
- Quantitative threefold allele-specific PCR (QuanTAS-PCR) for highly sensitive JAK2 V617F mutant allele detection.BMC cancer · 2013Article
- CD169⁺ macrophages provide a niche promoting erythropoiesis under homeostasis and stress.Nature medicine · 2013Article
- Heterozygous and homozygous JAK2(V617F) states modeled by induced pluripotent stem cells from myeloproliferative neoplasm patients.PloS one · 2013Article
- Ruxolitinib: in the treatment of myelofibrosis.Drugs · 2012Article
- Hsp90 inhibitors and the reduction of anti-cancer drug resistance by non-genetic and genetic mechanisms.Pharmaceuticals (Basel, Switzerland) · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
introductionMyeloproliferative neoplasms (MPNs) are a group of stem cell diseases, including polycythemia vera, essential thrombocythemia and primary myelofibrosis. Currently, there is no curative therapy for these diseases other than bone marrow transplant; therefore there is an apparent need for palliative treatment. MPNs are frequently associated with activating mutations in JAK2; small-molecule drugs targeting this molecule have entered clinical trials. AREAS COVERED: In this review novel JAK2 inhibitors are discussed and alternative approaches to inhibiting their transforming potential are highlighted. Current clinical approaches do not only aim at blocking JAK2 activity, but also at reducing its stability and expression are highlighted, including inhibition of heat shock protein 90 (HSP90) and deacetylases (DAC) have the potential to significantly enhance the efficacy of JAK2 inhibitors. EXPERT OPINION: Preliminary results from clinical trials indicate the feasibility and efficacy of JAK2-targeted approaches. However, JAK2 inhibitor treatment is limited by dose-dependent toxicity and combination treatment might be required. The discovery of JAK2 mutations that cause secondary resistance in vitro would further highlight the need for the development of next-generation JAK2 inhibitors and novel synergistic approaches.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.