Evidence map›Paper›PMID 36243855›Full record

ArticleCurrent topics in microbiology and immunology2022

AKT Isoforms as a Target in Cancer and Immunotherapy.

Daniel J Smit, Manfred Jücker

Abstract read
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In one paragraph

Article in Current topics in microbiology and immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Trial
  2. Article
  3. 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

2 authors at 1 institution in 1 country.

Daniel J SmitInstitute of Biochemistry and Signal Transduction, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.ORCID http://orcid.org/0000-0002-3190-9511
Manfred JückerInstitute of Biochemistry and Signal Transduction, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany. juecker@uke.de.ORCID http://orcid.org/0000-0003-2176-6526
Universität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the past years, targeted therapies have received tremendous attention in cancer therapy. One of the most frequently targeted pathways is the PI3K/AKT/mTOR signaling pathway that regulates crucial cellular processes including proliferation, survival, and migration. In a wide variety of cancer entities, the PI3K/AKT/mTOR signaling pathway was found to be a critical driver of disease progression, indicating a noteworthy target in cancer therapy. This chapter focuses on targeted therapies against AKT, which is a key enzyme within the PI3K/AKT/mTOR pathway. Although the three different isoforms of AKT, namely AKT1, AKT2, and AKT3, have a high homology, the isoforms exhibit different biological functions. Recently, direct inhibitors against all AKT isoforms as well as selective inhibitors against specific AKT isoforms have been extensively investigated in preclinical work as well as in clinical trials to attenuate proliferation of cancer cells. While no AKT inhibitor has been approved by the FDA for cancer therapy to date, AKT still plays a crucial role in a variety of treatment strategies including immune checkpoint inhibition. In this chapter, we summarize the status of AKT inhibitors either targeting all or specific AKT isoforms. Furthermore, we explain the role of AKT signaling in direct inhibition of tumor cell growth as well as in immune cells and immune checkpoint inhibition.

Indexed as

NeoplasmsPhosphatidylinositol 3-KinasesHumansImmune Checkpoint InhibitorsImmunotherapyProtein IsoformsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesImmune Checkpoint InhibitorsPhosphatidylinositol 3-KinasesProtein IsoformsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAKTCancer therapyCTLA-4Immune checkpoint inhibitionImmune escapePD1 signalingPI3K/AKT/mTOR signaling pathwayTargeted therapy

Identifiers

PMID36243855
OpenAlexW4306362033

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.