Evidence map›Paper›PMID 39614261›Full record

ReviewJournal of experimental & clinical cancer research : CR2024

AKT kinases as therapeutic targets.

Dalal Hassan, Craig W Menges, Joseph R Testa, Alfonso Bellacosa

Abstract readReview
In one paragraph

Review in Journal of experimental & clinical cancer research : CR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. A renaissance in targeting the PI3K/AKT/mTOR pathway.Nature reviews. Drug discovery · 2026
    Review
  6. Review
  7. Article
  8. International journal of molecular sciences · 2026
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Neuroprotective effects ofFrontiers in molecular biosciences · 2026
    Article
  15. The structural heterogeneity of AKT autoinhibition.Protein science : a publication of the Protein Society · 2026
    Article
  16. Frontiers in nutrition · 2026
    Article
  17. Review
  18. Review
  19. Article
  20. 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

4 authors.

Dalal HassanNuclear Dynamics and Cancer Program, Cancer Epigenetics Institute, Institute for Cancer Research, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA, 19111, USA.
Craig W MengesCancer Prevention and Control Program, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA, 19111, USA.
Joseph R TestaCancer Prevention and Control Program, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA, 19111, USA.
Alfonso BellacosaNuclear Dynamics and Cancer Program, Cancer Epigenetics Institute, Institute for Cancer Research, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA, 19111, USA. Alfonso.Bellacosa@fccc.edu.ORCID http://orcid.org/0000-0001-6278-6801

Funding

PATHOLOGY, VIROLOGY, AND ANIMAL COREP01CA114047 · NCI · UNIVERSITY OF HAWAII AT MANOA · PI CARBONE, MICHELE · 2006 to 2010
$8.0M
Basis for Lymphomagenesis in Akt2 Transgenic MiceR01CA077429 · NCI · RESEARCH INST OF FOX CHASE CAN CTR · PI TESTA, JOSEPH R. · 1998 to 2013
$4.7M
NCI NIH HHS P01 CA114047NCI NIH HHS R01 CA077429
6 · The paper itself

Abstract

AKT, or protein kinase B, is a central node of the PI3K signaling pathway that is pivotal for a range of normal cellular physiologies that also underlie several pathological conditions, including inflammatory and autoimmune diseases, overgrowth syndromes, and neoplastic transformation. These pathologies, notably cancer, arise if either the activity of AKT or its positive or negative upstream or downstream regulators or effectors goes unchecked, superimposed on by its intersection with a slew of other pathways. Targeting the PI3K/AKT pathway is, therefore, a prudent countermeasure. AKT inhibitors have been tested in many clinical trials, primarily in combination with other drugs. While some have recently garnered attention for their favorable profile, concern over resistance and off-target effects have continued to hinder their widespread adoption in the clinic, mandating a discussion on alternative modes of targeting. In this review, we discuss isoform-centric targeting that may be more effective and less toxic than traditional pan-AKT inhibitors and its significance for disease prevention and treatment, including immunotherapy. We also touch on the emerging mutant- or allele-selective covalent allosteric AKT inhibitors (CAAIs), as well as indirect, novel AKT-targeting approaches, and end with a briefing on the ongoing quest for more reliable biomarkers predicting sensitivity and response to AKT inhibitors, and their current state of affairs.

Indexed as

Protein Kinase InhibitorsProto-Oncogene Proteins c-aktAnimalsHumansMolecular Targeted TherapyNeoplasmsSignal TransductionProtein Kinase InhibitorsProto-Oncogene Proteins c-aktAKT kinasesCancerInflammationOvergrowth syndromesTherapy

Identifiers

PMID39614261
PMCPMC11606119

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.