Evidence map›Paper›PMID 23597703›Full record

ReviewCancer letters2013

ACK1 tyrosine kinase: targeted inhibition to block cancer cell proliferation.

Kiran Mahajan, Nupam P Mahajan

Abstract readReview
In one paragraph

Review in Cancer letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing 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

33 citing papers in PubMed.

  1. Review
  2. Article
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  9. Review
  10. Article
  11. Progress in the therapeutic inhibition of Cdc42 signalling.Biochemical Society transactions · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Article
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  19. Review
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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

2 authors.

Kiran MahajanDrug Discovery Department, Moffitt Cancer Center, 12902 Magnolia Drive, Tampa, FL 33612, USA. kiran.mahajan@moffitt.org
Nupam P Mahajan

Funding

Ack1: A Critical Regulator of Hormone-Refractory Prostate CancerR01CA135328 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI MAHAJAN, NUPAM P · 2010 to 2014
$1.6M
NCI NIH HHS 1R01CA135328NCI NIH HHS R01 CA135328
6 · The paper itself

Abstract

ACK1 tyrosine kinase, located on chromosome 3q29, is aberrantly activated, amplified or mutated in a wide variety of human cancers. While the deregulated kinase is oncogenic and its activation correlates with progression to metastatic stage, its inhibition causes cell cycle arrest, sensitizes cells to ionizing radiation and induces apoptosis. Oncogenicity of ACK1 is not only due to its ability to promote activation of critical pro-survival kinases and harmone receptors by phosphorylating at distinct tyrosine residues, but also by employing a similar mechanism to eliminate a tumor suppressor from cancer cells. Despite the substantial data supporting the oncogenic role of ACK1, and the potential clinical benefit of blocking ACK1 in metastatic disease, to date ACK1-specific small molecule inhibitors have not been exploited for cancer therapy. This review highlights recent advances that elucidate how cancer cells employ ACK1 kinase to their advantage and discusses some of the novel ACK1 inhibitors that have shown promise in pre-clinical studies.

Indexed as

Cell Growth ProcessesCell Line, TumorHumansMolecular Targeted TherapyNeoplasmsProtein Kinase InhibitorsProtein-Tyrosine KinasesProtein Kinase InhibitorsProtein-Tyrosine KinasesTNK2 protein, humanACK1AKTDrug resistanceSmall molecule inhibitorTNK2Tyrosine kinase

Identifiers

PMID23597703
PMCPMC3750075

What OpenQuestion holds

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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.