Evidence map›Paper›PMID 25485184›Full record

ArticleMolecular cancer biology2013

Computational and synthetic studies towards improving rescinnamine as an inducer of MSH2-dependent apoptosis in cancer treatment.

ElShimaa M N AbdelHafez, Andrew Diamanduros, Lacramioara Negureanu, Yan Luy, J Hayley Bean, Katherine Zielke, Brittany Crowe, Aksana Vasilyeva, Jill E Clodfelter, Omar M Aly and 4 more

Open access · greenAbstract read
PubMed Full text at PMC
In one paragraph

Article in Molecular cancer biology, 2013. 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
–field-weighted citation impact, top 79% 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, 2 citations in OpenAlex.

  1. All-atom molecular dynamics comparison of disease-associated zinc fingers.Journal of biomolecular structure & dynamics · 2018
    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

14 authors at 3 institutions in 2 countries.

ElShimaa M N AbdelHafezDepartment of Chemistry, Wake Forest University, Winston-Salem, NC.
Andrew DiamandurosDepartment of Biology, Georgia Southern University, Statesboro, GA.
Lacramioara NegureanuDepartment of Physics, Wake Forest University, Winston-Salem, NC.
Yan LuyDepartment of Physics, Wake Forest University, Winston-Salem, NC.
J Hayley BeanDepartment of Biology, Georgia Southern University, Statesboro, GA.
Katherine ZielkeDepartment of Biology, Georgia Southern University, Statesboro, GA.
Brittany CroweDepartment of Biology, Georgia Southern University, Statesboro, GA.
Aksana VasilyevaDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC; now: St. Jude Hospital, Memphis, TN.
Jill E ClodfelterDepartment of Biochemistry, Wake Forest University School of Medicine, Winston-Salem, NC.
Omar M AlyDepartment of Medicinal Chemistry, Faculty of Pharmacy, Minia University, Minia , Egypt.
Gamal El-Din A A Abuo-RahmaDepartment of Medicinal Chemistry, Faculty of Pharmacy, Minia University, Minia , Egypt.
Karin D ScarpinatoDepartment of Biology, Georgia Southern University, Statesboro, GA.
Freddie R SalsburyDepartment of Physics, Wake Forest University, Winston-Salem, NC.
S Bruce KingDepartment of Chemistry, Wake Forest University, Winston-Salem, NC.
Wake Forest University · USGeorgia Southern University · USMinia University · EG

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
Targeting the MSH2-dependent Apoptotic PathwayR01CA129373 · NCI · WAKE FOREST UNIVERSITY · PI SALSBURY, FREDDIE R. · 2009 to 2013
$1.6M
NCI NIH HHS P30 CA012197NCI NIH HHS R01 CA129373
6 · The paper itself

Abstract

We, and others, have previously shown that mismatch repair proteins, in addition to their repair function, contribute to cell death initiation. In response to some drugs, this cell death activity is independent of the repair function of the proteins. Rescinnamine, a derivative of the indole alkaloid reserpine, a drug used to treat hypertension several decades ago, was shown to target the cell death-initiating activity of mismatch repair proteins. When used in animals, the hypotensive action of this drug prevents applying appropriate concentrations for statistically significant tumor reduction. Using a combination of computational modeling, chemical synthesis and cell assays, we determine how rescinnamine can be structurally modified and what effect these modifications have on cell survival. These results inform further computational modeling to suggest new synthetic lead molecules to move toward further biological testing.

Identifiers

PMID25485184
PMCPMC4254817
OpenAlexW2332712530

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.