ReviewDrugs2001
Farnesyltransferase inhibitors: potential role in the treatment of cancer.
Review in Drugs, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 70 citations in OpenAlex.
- The Persistent Power of the Taxane/Platin Chemotherapy.Cancers · 2025Review
- Targeting K-Ras-mediated DNA damage response in radiation oncology: Current status, challenges and future perspectives.Clinical and translational radiation oncology · 2023Review
- Insights into the mechanistic dichotomy of the protein farnesyltransferase peptide substrates CVIM and CVLS.Journal of the American Chemical Society · 2012Article
- Identification of a novel class of farnesylation targets by structure-based modeling of binding specificity.PLoS computational biology · 2011Article
- [Cutaneous malignant peripheral nerve sheath tumor in neurofibromatosis type 1].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2009Article
- Inactivation of Icmt inhibits transformation by oncogenic K-Ras and B-Raf.The Journal of clinical investigation · 2004Article
- Article
- Transformation-selective apoptotic program triggered by farnesyltransferase inhibitors requires Bin1.Oncogene · 2003Article
- Role for RhoB and PRK in the suppression of epithelial cell transformation by farnesyltransferase inhibitors.Oncogene · 2003Article
- The potential role of bisphosphonates in prostate cancer.Prostate cancer and prostatic diseases · 2002Review
- The farnesyl transferase inhibitor RPR-130401 does not alter radiation susceptibility in human tumor cells with a K-Ras mutation in spite of large changes in ploidy and lamin B distribution.BMC pharmacology · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
New targets for drug discovery have been identified rapidly as a result of the many recent and rapid advances in the understanding of signal transduction pathways that contribute to oncogenesis. In particular, oncogenic Ras proteins have been seen as an important target for novel anti-cancer drugs. Since the decade-old identification and cloning of farnesyltransferase (FTase), a critical enzyme that post-translationally modifies Ras and other farnesylated proteins, FTase inhibitors (FTIs) have been under intense investigation designed to bring them to clinical practice for cancer therapy. FTIs can inhibit the growth of tumour cells in culture and in animal models, and are now in clinical trials. Interestingly, their mechanism of action is not as simple as originally envisioned, and Ras is probably not the most important farnesylated protein whose modification is inhibited as a result of FTI treatment. Although K-Ras can escape inhibition of processing by FTIs, tumours with oncogenically mutated K-Ras proteins can still be inhibited by FTI treatment. Indeed, Ras mutation status does not correlate with FTI sensitivity or resistance. Instead, it now appears likely that inhibition of the processing of other farnesylated proteins such as RhoB and the centromere-binding proteins CENP-E and CENP-F can explain the ability of FTIs to cause cell cycle arrest and apoptosis in preclinical studies, and even to cause regression in animal tumour models. Preclinical studies suggest the likelihood that FTIs will be useful in combination therapies with conventional treatment modalities including cytotoxics (especially paclitaxel) and radiation. Phase I combination trials are underway, and early phase II/III trials using FTIs as monotherapy are open for patients with a wide variety of cancers. Early preclinical results also suggest the possibility of using FTIs as chemopreventive agents. Studies to be completed over the next 2 or 3 years should define the appropriate patient populations, administration and scheduling necessary to optimise the use of these novel anticancer agents.
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.