Evidence map›Paper›PMID 10720125›Full record

ReviewLeukemia2000

Antisense therapeutics in chronic myeloid leukaemia: the promise, the progress and the problems.

R E Clark

Abstract readReview
PubMed Publisher
In one paragraph

Review in Leukemia, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

9 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
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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.

R E ClarkUniversity Department of Haematology, Royal Liverpool University Hospital, UK.
University of Liverpool · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA sequences which are complementary or 'antisense' to a target mRNA can inhibit expression of that mRNA's protein product. Antisense therapeutics has therefore received attention for inhibiting oncogenes in haematological malignancy, in particular in chronic myeloid leukaemia. However, it is now becoming clear that antisense therapeutics is considerably more problematic than was naively initially assumed. In this article, some of these difficulties are discussed, together with the achievements in CML so far. Considerable further research is required in order to define an optimal antisense therapeutics strategy for clinical use.

Indexed as

AnimalsAntisense Elements (Genetics)Bone Marrow PurgingDeoxyribonucleasesForecastingFusion Proteins, bcr-ablGene Expression Regulation, NeoplasticGenes, mycHematopoietic Stem CellsHumansLeukemiaLeukemia, Myelogenous, Chronic, BCR-ABL PositiveLymphomaMiceMice, SCIDNeoplasm ProteinsAntisense Elements (Genetics)DeoxyribonucleasesFusion Proteins, bcr-ablNeoplasm ProteinsProto-Oncogene Proteins c-mycRNA, MessengerRNA, Neoplasm

Identifiers

PMID10720125
OpenAlexW2327432287

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.