Evidence map›Paper›PMID 24811392›Full record

ReviewNeuro-oncology2014

Role of AKT signaling in DNA repair and clinical response to cancer therapy.

Qun Liu, Kristen M Turner, W K Alfred Yung, Kexin Chen, Wei Zhang

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neuro-oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

98 citing papers in PubMed, 137 citations in OpenAlex.

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38 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 2 countries.

Qun LiuDepartment of Neuro-Oncology, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China (Q.L.); Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas (K.M.T., W.Z.); Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas (W.K.A.Y.); Department of Epidemiology and Biostatistics, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China (K.C.).
Kristen M TurnerDepartment of Neuro-Oncology, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China (Q.L.); Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas (K.M.T., W.Z.); Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas (W.K.A.Y.); Department of Epidemiology and Biostatistics, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China (K.C.).
W K Alfred YungDepartment of Neuro-Oncology, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China (Q.L.); Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas (K.M.T., W.Z.); Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas (W.K.A.Y.); Department of Epidemiology and Biostatistics, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China (K.C.).
Kexin ChenDepartment of Neuro-Oncology, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China (Q.L.); Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas (K.M.T., W.Z.); Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas (W.K.A.Y.); Department of Epidemiology and Biostatistics, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China (K.C.).
Wei ZhangDepartment of Neuro-Oncology, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China (Q.L.); Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas (K.M.T., W.Z.); Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas (W.K.A.Y.); Department of Epidemiology and Biostatistics, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China (K.C.).
The University of Texas MD Anderson Cancer Center · USTianjin Medical University Cancer Institute and Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Effective cancer treatment has been limited by the emergence of resistant cancer cells. The results of many studies indicate that AKT activation plays an important role in the acquisition of resistance to anticancer therapy. AKT is a critical effector serine/threonine kinase in the receptor tyrosine kinase/phosphatase and tensin homolog/phospho-inositide 3-kinase pathway and controls a myriad of cellular functions. Activation of AKT not only supports tumor growth and progression but also contributes to tumor-cell evasion of the cytotoxic effects of cancer therapy through many avenues including the promotion of anti-apoptosis, proliferation, and migration and regulation of the cell cycle. Accumulating evidence has implicated AKT as a direct participant in the DNA damage response and repair induced by commonly used genotoxic agents. In this review, we discuss the molecular mechanisms by which genotoxic agents activate AKT and therefore contribute to resistance to cancer therapeutics, with particular emphasis on DNA repair.

Indexed as

DNA RepairDrug Resistance, NeoplasmAnimalsDNA DamageHumansMiceNeoplasmsProto-Oncogene Proteins c-aktSignal TransductionProto-Oncogene Proteins c-aktcancerDNA damageDNA repair: AKTtreatment resistance

Identifiers

PMID24811392
PMCPMC4165418
OpenAlexW2026732233

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.