Trial reportLeukemia2007
A phase II trial of tipifarnib in myelofibrosis: primary, post-polycythemia vera and post-essential thrombocythemia.
Trial report in Leukemia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Janus kinase-1 and Janus kinase-2 inhibitors for treating myelofibrosis.The Cochrane database of systematic reviews · 2015Pooled it
- Phase II study of the farnesyltransferase inhibitor R115777 in advanced melanoma (CALGB 500104).Journal of translational medicine · 2012Trial
- Trial
- Trial
- Phase I trial of a combination of the multikinase inhibitor sorafenib and the farnesyltransferase inhibitor tipifarnib in advanced malignancies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Trial
- Phase II trial of tipifarnib as maintenance therapy in first complete remission in adults with acute myelogenous leukemia and poor-risk features.Clinical cancer research : an official journal of the American Association for Cancer Research · 2008Trial
- Research trends in essential thrombocythemia from 2001 to 2024: a bibliometric analysis.Discover oncology · 2025Article
- Therapeutic benefit of decitabine, a hypomethylating agent, in patients with high-risk primary myelofibrosis and myeloproliferative neoplasm in accelerated or blastic/acute myeloid leukemia phase.Leukemia research · 2015Article
- Targeting mutant KRAS for anticancer therapeutics: a review of novel small molecule modulators.Journal of medicinal chemistry · 2013Review
- Inhibition of the Ras/Raf/MEK/ERK and RET kinase pathways with the combination of the multikinase inhibitor sorafenib and the farnesyltransferase inhibitor tipifarnib in medullary and differentiated thyroid malignancies.The Journal of clinical endocrinology and metabolism · 2011Article
- Deactylase inhibition in myeloproliferative neoplasms.Investigational new drugs · 2010Review
- Therapy of myelofibrosis (excluding JAK2 inhibitors).International journal of hematology · 2010Review
- Recent advances in diagnosis and treatment of chronic myeloproliferative neoplasms.F1000 medicine reports · 2010Article
- Article
- Novel strategies for patients with chronic myeloproliferative disorders.Current opinion in hematology · 2009Review
- Article
- Tipifarnib in the treatment of newly diagnosed acute myelogenous leukemia.Biologics : targets & therapy · 2008Article
- Ceramide signaling in cancer and stem cells.Future lipidology · 2008Article
- Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
Patients with primary myelofibrosis (PMF) or post-polycythemia vera or post-essential thrombocythemia myelofibrosis (post-PV/ET MF) have limited therapeutic options. The farnesyltransferase-inhibitor tipifarnib inhibits in vitro proliferation of myeloid progenitors from such patients. In the current phase II clinical trial, single-agent oral tipifarnib (300 mg twice daily x 21 of 28 days) was given to 34 symptomatic patients with either PMF (n=28) or post-PV/ET MF (n=6). Median time to discontinuation of protocol therapy was 4.6 months; reasons for early termination (n=19; 56%) included disease progression (21%) and adverse drug effects (18%). Toxicities (>/=grade 3) included myelosuppression (n=16), neuropathy (n=2), fatigue (n=1), rash (n=1) and hyponatremia (n=1). Response rate was 33% for hepatosplenomegaly and 38% for transfusion-requiring anemia. No favorable changes occurred in bone marrow fibrosis, angiogenesis or cytogenetic status. Pre- and post-treatment patient sample analysis for in vitro myeloid colony growth revealed substantial reduction in the latter. Clinical response did not correlate with either degree of colony growth, measurable decrease in quantitative JAK2(V617F) levels or tipifarnib IC(50) values (median 11.8 nM) seen in pretreatment samples. The current study indicates both in vitro and in vivo tipifarnib activity in PMF and post-PV/ET MF.
Indexed as
Identifiers
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.