Evidence map›Paper›PMID 11122821›Full record

ReviewCurrent oncology reports2000

Antisense cancer therapy: the state of the science.

D M Kushner, R H Silverman

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current oncology reports, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
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.

D M KushnerDepartment of Gynecology and Obstetrics, The Cleveland Clinic Foundation, Cleveeland OH 44195, USA.
R H Silverman

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the last few years, antisense technology has emerged as an exciting and promising strategy in the fight against cancer. The antisense concept is to selectively bind short, modified DNA or RNA molecules to messenger RNA in cells and prevent the synthesis of the encoded protein. As anticancer agents, these molecules can be targeted against a myriad of genes involved in cell transformation, cell survival, metastasis, and angiogenesis. Indeed, the list of possible antisense targets increases as the knowledge of the genetic basis of oncogenesis expands. One aim of this review is to focus on those antisense cancer drugs that have entered human clinical trials. At least four of these compounds are currently in phase II trials, including those targeting protein kinase C-alpha, bcl-2, c-raf, and the R1-alpha subunit of protein kinase A. A new development in antisense chemistry (peptide nucleic acids) is discussed, along with alternative antisense-related strategies (ribozymes and 2-5A-antisense) designed to overcome some of the challenges of this already encouraging technology.

Indexed as

Clinical Trials as TopicGenes, ablGenes, bcl-2Genes, mybGenes, p53Genes, rasHumansIsoenzymesNeoplasmsOligoribonucleotides, AntisensePeptide Nucleic AcidsProtein Kinase CProtein Kinase C-alphaProto-Oncogene Proteins c-rafRNA, CatalyticIsoenzymesOligoribonucleotides, AntisensePeptide Nucleic AcidsPRKCA protein, humanProtein Kinase CProtein Kinase C-alphaProto-Oncogene Proteins c-rafRNA, Catalytic

Identifiers

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.