Evidence map›Paper›PMID 17137401›Full record

ReviewDrugs2006

Targeted anti-cancer therapies for renal cancer.

Robert J Amato, Jaroslaw Jac

Abstract readReview
PubMed Publisher
In one paragraph

Review in Drugs, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Inhibition of mTOR in kidney cancer.Current oncology (Toronto, Ont.) · 2009
    Article
  3. 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

2 authors at 2 institutions in 1 country.

Robert J AmatoGenitourinary Oncology Program, The Methodist Hospital Research Institute, Houston, Texas 77030, USA. ramato@tmh.tmc.edu
Jaroslaw Jac
Houston Methodist · USMethodist Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the past several years, significant advances in the underlying biological mechanisms of renal cell cancer, particularly the role of tumour angiogenesis, have permitted the design of molecularly targeted therapeutics. For this review, single-agent therapies inhibiting the following different targets were identified in the published literature: epithelial growth factor receptor, vascular endothelial growth factor receptor, basic fibroblast growth factor receptor, platelet-derived growth factor, nuclear factor-kappabeta, the mammalian target of rapamycin (mTOR) pathway, raf kinase pathway and tyrosine kinase pathway. Distinct fields of clinical research have emerged--monoclonal antibodies, small molecules, nanopeptides and immunomodulators. All therapies demonstrated acceptable toxicity profiles. Clinical benefit was assessed on the basis of the reported criteria for each study, and antitumour response (regression or delay in progression-free survival) ranged from 5% to 71%. On the basis of the limited studies to date, targeted therapies offer the greatest clinical benefit in the management of this malignancy, although additional basic research is still warranted to further improve clinical outcome.

Indexed as

Antineoplastic AgentsCarcinoma, Renal CellForecastingHumansKidney NeoplasmsNeovascularization, PathologicProtein-Tyrosine KinasesReceptor Protein-Tyrosine KinasesAntineoplastic AgentsProtein-Tyrosine KinasesReceptor Protein-Tyrosine Kinases

Identifiers

PMID17137401
OpenAlexW1973142451

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.