Evidence map›Paper›PMID 26463706›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2015

Molecular Pathways: New Signaling Considerations When Targeting Cytoskeletal Balance to Reduce Tumor Growth.

Kristi R Chakrabarti, Lindsay Hessler, Lekhana Bhandary, Stuart S Martin

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. The Pro-Metastatic Roles of ROS.Antioxidants (Basel, Switzerland) · 2026
    Review
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  12. Estramustine Phosphate Inhibits TGF-Analytical cellular pathology (Amsterdam) · 2018
    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

4 authors at 1 institution in 1 country.

Kristi R Chakrabarti *Marlene and Stewart Greenebaum NCI Cancer Center, University of Maryland School of Medicine, 22 S. Greene Street, Baltimore, MD 21201, USA.
Lindsay Hessler *Marlene and Stewart Greenebaum NCI Cancer Center, University of Maryland School of Medicine, 22 S. Greene Street, Baltimore, MD 21201, USA.
Lekhana BhandaryMarlene and Stewart Greenebaum NCI Cancer Center, University of Maryland School of Medicine, 22 S. Greene Street, Baltimore, MD 21201, USA.
Stuart S MartinMarlene and Stewart Greenebaum NCI Cancer Center, University of Maryland School of Medicine, 22 S. Greene Street, Baltimore, MD 21201, USA.
University of Maryland, Baltimore · US

Funding

Training Grant in Cancer BiologyT32CA154274 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI Toni M Antalis, CURT I CIVIN · 2011 to 2026
$6.8M
Tubulin microtentacles in detached mammary epithelial cellsR01CA124704 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI MARTIN, STUART S · 2007 to 2025
$5.7M
Targeting microtubule stabilization to reduce breast tumor metastasisR01CA154624 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI MARTIN, STUART S · 2012 to 2023
$3.4M
AMPK Regulation of Microtubule Dynamics in Breast Cancer MetastasisF30CA196075 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI BRIGGS, KRISTI CHAKRABARTI · 2015 to 2018
$121k
NCI NIH HHS F30 CA196075NCI NIH HHS F30CA196075NCI NIH HHS R01 CA124704NCI NIH HHS R01CA124704NCI NIH HHS R01 CA154624NCI NIH HHS R01CA154624NCI NIH HHS T32 CA154274NCI NIH HHS T32CA154274
6 · The paper itself

Abstract

The dynamic balance between microtubule extension and actin contraction regulates mammalian cell shape, division, and motility, which has made the cytoskeleton an attractive and very successful target for cancer drugs. Numerous compounds in clinical use to reduce tumor growth cause microtubule breakdown (vinca alkaloids, colchicine-site, and halichondrins) or hyperstabilization of microtubules (taxanes and epothilones). However, both of these strategies indiscriminately alter the assembly and dynamics of all microtubules, which causes significant dose-limiting toxicities on normal tissues. Emerging data are revealing that posttranslational modifications of tubulin (detyrosination, acetylation) or microtubule-associated proteins (Tau, Aurora kinase) may allow for more specific targeting of microtubule subsets, thereby avoiding the broad disruption of all microtubule polymerization. Developing approaches to reduce tumor cell migration and invasion focus on disrupting actin regulation by the kinases SRC and ROCK. Because the dynamic balance between microtubule extension and actin contraction also regulates cell fate decisions and stem cell characteristics, disrupting this cytoskeletal balance could yield unexpected effects beyond tumor growth. This review will examine recent data demonstrating that cytoskeletal cancer drugs affect wound-healing responses, microtentacle-dependent reattachment efficiency, and stem cell characteristics in ways that could affect the metastatic potential of tumor cells, both beneficially and detrimentally.

Indexed as

Signal TransductionAnimalsAntineoplastic AgentsCytoskeletonHumansMicrotubulesMolecular Targeted TherapyNeoplasmsTranslational Research, BiomedicalAntineoplastic Agents

Identifiers

PMID26463706
PMCPMC4905577
OpenAlexW2174925742

What OpenQuestion holds

Textmetadata
LicenceTDM
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.