Evidence map›Paper›PMID 11398905›Full record

ReviewDrugs2001

Farnesyltransferase inhibitors: potential role in the treatment of cancer.

A D Cox

Abstract readReview
PubMed Publisher
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.7field-weighted citation impact, top 4% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. [Cutaneous malignant peripheral nerve sheath tumor in neurofibromatosis type 1].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2009
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. The potential role of bisphosphonates in prostate cancer.Prostate cancer and prostatic diseases · 2002
    Review
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

A D CoxDepartment of Radiation Oncology, Lineberger Cancer Center, School of Medicine, University of North Carolina at Chapel Hill, 27599-7512, USA. cox@radonc.unc.edu
University of North Carolina at Chapel Hill · US

Funding

VALIDATION OF INHIBITORS OF RHO GTPASES FOR CANCER TREATMENTU19CA067771 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI LAWRENCE, NICOLAS · 1995 to 2009
$8.9M
MECHANISM OF FTI ACTION AND K-RAS INHIBITIONR01CA076092 · NCI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI COX, ADRIENNE D · 1998 to 2000
$170k
NCI NIH HHS CA67771NCI NIH HHS CA 76092
6 · The paper itself

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

Alkyl and Aryl TransferasesAnimalsApoptosisClinical Trials as TopicEnzyme InhibitorsFarnesyltranstransferaseGenes, rasHumansMutationNeoplasmsRadiation-Sensitizing AgentsAlkyl and Aryl TransferasesEnzyme InhibitorsFarnesyltranstransferaseRadiation-Sensitizing Agents

Identifiers

PMID11398905
OpenAlexW1991930569

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.