Evidence map›Paper›PMID 29949919›Full record

ReviewInternational journal of molecular sciences2018

Therapeutic Targeting of mTOR in T-Cell Acute Lymphoblastic Leukemia: An Update.

Camilla Evangelisti, Francesca Chiarini, James A McCubrey, Alberto M Martelli

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. A novel regulatory circuit of ATG4B and SESN3 promotes T cell leukemogenesis.Journal of experimental & clinical cancer research : CR · 2025
    Article
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  19. Review
  20. mTOR in Human Diseases.International journal of molecular sciences · 2019
    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

4 authors at 3 institutions in 2 countries.

Camilla EvangelistiCNR Istituto di Genetica Molecolare, Unità di Bologna, 40136 Bologna, Italy. camilla.evangelisti@cnr.it.
Francesca ChiariniCNR Istituto di Genetica Molecolare, Unità di Bologna, 40136 Bologna, Italy. francesca.chiarini@cnr.it.
James A McCubreyDepartment of Microbiology & Immunology, Brody School of Medicine, East Carolina University, Greenville, NC 27834, USA. mccubreyj@ecu.edu.
Alberto M MartelliDepartment of Biomedical and Neuromotor Sciences, University of Bologna, 40126 Bologna, Italy. alberto.martelli@unibo.it.ORCID 0000-0001-5196-7260
Istituto Ortopedico Rizzoli · ITEast Carolina University · USUniversity of Bologna · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive blood malignancy that arises from the clonal expansion of transformed T-cell precursors. Although T-ALL prognosis has significantly improved due to the development of intensive chemotherapeutic protocols, primary drug-resistant and relapsed patients still display a dismal outcome. In addition, lifelong irreversible late effects from conventional therapy are a growing problem for leukemia survivors. Therefore, novel targeted therapies are required to improve the prognosis of high-risk patients. The mechanistic target of rapamycin (mTOR) is the kinase subunit of two structurally and functionally distinct multiprotein complexes, which are referred to as mTOR complex 1 (mTORC1) and mTORC2. These two complexes regulate a variety of physiological cellular processes including protein, lipid, and nucleotide synthesis, as well as autophagy in response to external cues. However, mTOR activity is frequently deregulated in cancer, where it plays a key oncogenetic role driving tumor cell proliferation, survival, metabolic transformation, and metastatic potential. Promising preclinical studies using mTOR inhibitors have demonstrated efficacy in many human cancer types, including T-ALL. Here, we highlight our current knowledge of mTOR signaling and inhibitors in T-ALL, with an emphasis on emerging evidence of the superior efficacy of combinations consisting of mTOR inhibitors and either traditional or targeted therapeutics.

Indexed as

Molecular Targeted TherapyAnimalsClinical Trials as TopicHumansModels, BiologicalPrecursor T-Cell Lymphoblastic Leukemia-LymphomaSignal TransductionTOR Serine-Threonine KinasesTOR Serine-Threonine Kinasescombination therapymTORtargeted therapyT-cell acute lymphoblastic leukemia

Identifiers

PMID29949919
PMCPMC6073309
OpenAlexW2809689507

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.