Evidence map›Paper›PMID 17484128›Full record

ReviewSub-cellular biochemistry2007

Chromatin as a target for the DNA-binding anticancer drugs.

Parijat Majumder, Suman K Pradhan, Pukhrambam Grihanjali Devi, Sudipta Pal, Dipak Dasgupta

Open access · greenAbstract readReview
In one paragraph

Review in Sub-cellular biochemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

1 citing paper in PubMed, 11 citations in OpenAlex.

  1. 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

5 authors at 1 institution in 1 country.

Parijat MajumderBiophysics Division, Saha Institute of Nuclear Physics, Block-AF, Sector-I, Bidhannagar, Kolkata-700 064, India.
Suman K Pradhan
Pukhrambam Grihanjali Devi
Sudipta Pal
Dipak Dasgupta
Saha Institute of Nuclear Physics · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy has been a major approach to treat cancer. Both constituents of chromatin, chromosomal DNA and the associated chromosomal histone proteins are the molecular targets of the anticancer drugs. Small DNA binding ligands, which inhibit enzymatic processes with DNA substrate, are well known in cancer chemotherapy. These drugs inhibit the polymerase and topoisomerase activity. With the advent in the knowledge of chromatin chemistry and biology, attempts have shifted from studies of the structural basis of the association of these drugs or small ligands (with the potential of drugs) with DNA to their association with chromatin and nucleosome. These drugs often inhibit the expression of specific genes leading to a series of biochemical events. An overview will be given about the latest understanding of the molecular basis of their action. We shall restrict to those drugs, synthetic or natural, whose prime cellular targets are so far known to be chromosomal DNA.

Indexed as

AnimalsAntibiotics, AntineoplasticAntineoplastic AgentsAntineoplastic Agents, AlkylatingChromatinChromatin Assembly and DisassemblyCross-Linking ReagentsCrystallographyDNADNA AdductsDNA, CruciformDNA MethylationDNA Modification MethylasesEnzyme InhibitorsEpigenesis, GeneticGene Expression Regulation, NeoplasticAntibiotics, AntineoplasticAntineoplastic AgentsAntineoplastic Agents, AlkylatingChromatinCross-Linking ReagentsDNADNA AdductsDNA, CruciformDNA Modification MethylasesEnzyme InhibitorsIntercalating AgentsNucleic Acid Synthesis InhibitorsTopoisomerase Inhibitorstriplex DNA

Identifiers

PMID17484128
PMCPMC7121056
OpenAlexW1838208543

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.