Evidence map›Paper›PMID 26805380›Full record

ReviewBritish journal of clinical pharmacology2016

Targeting mTOR for the treatment of B cell malignancies.

Jong-Hoon Scott Lee, Thanh-Trang Vo, David A Fruman

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of clinical pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.0field-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

25 citing papers in PubMed, 40 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Jong-Hoon Scott LeeDepartment of Molecular Biology & Biochemistry, University of California, Irvine, USA.
Thanh-Trang VoDepartment of Molecular Biology & Biochemistry, University of California, Irvine, USA.
David A FrumanDepartment of Molecular Biology & Biochemistry, University of California, Irvine, USA. dfruman@uci.edu.
University of California, Irvine · US

Funding

University of California Health Participation in the National COVID Cohort Collaborative (N3C)UL1TR001414 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI COOPER, DAN M, VILAIN, ERIC J. · 2015 to 2023
$35.1M
CARCINOGENESIST32CA009054 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI EDINGER, AIMEE L, FRUMAN, DAVID ALEXANDER · 1985 to 2025
$8.6M
NRSA Training CoreTL1TR001415 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI CAIOZZO, VINCENT JAMES, HEAD, ELIZABETH · 2015 to 2023
$4.2M
TOR kinase inhibitors for leukemia therapy: mechanisms of action and resistanceR01CA158383 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI FRUMAN, DAVID ALEXANDER · 2012 to 2016
$1.5M
Combination strategies to enhance therapy for Ph-like B-ALLR21HD081319 · NICHD · UNIVERSITY OF CALIFORNIA-IRVINE · PI FRUMAN, DAVID ALEXANDER, KONOPLEVA, MARINA Y · 2015 to 2016
$459k
Unleashing the Efficacy of PI3K/AKT/mTOR Pathway Inhibitors in B-ALLF32CA189629 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI VO, THANH-TRANG · 2014 to 2015
$109k
NCATS NIH HHS TL1 TR001415NCATS NIH HHS UL1 TR001414NCI NIH HHS F32 CA189629NCI NIH HHS R01 CA158383NCI NIH HHS T32 CA009054NICHD NIH HHS R21 HD081319
6 · The paper itself

Abstract

Mechanistic target of rapamycin (mTOR) is a serine/threonine kinase that functions as a key regulator of cell growth, division and survival. Many haematologic malignancies exhibit elevated or aberrant mTOR activation, supporting the launch of numerous clinical trials aimed at evaluating the potential of single agent mTOR-targeted therapies. While promising early clinical data using allosteric mTOR inhibitors (rapamycin and its derivatives, rapalogs) have suggested activity in a subset of haematologic malignancies, these agents have shown limited efficacy in most contexts. Whether the efficacy of these partial mTOR inhibitors might be enhanced by more complete target inhibition is being actively addressed with second generation ATP-competitive mTOR kinase inhibitors (TOR-KIs), which have only recently entered clinical trials. However, emerging preclinical data suggest that despite their biochemical advantage over rapalogs, TOR-KIs may retain a primarily cytostatic response. Rather, combinations of mTOR inhibition with other targeted therapies have demonstrated promising efficacy in several preclinical models. This review investigates the current status of rapalogs and TOR-KIs in B cell malignancies, with an emphasis on emerging preclinical evidence of synergistic combinations involving mTOR inhibition.

Indexed as

AnimalsB-LymphocytesHematologic NeoplasmsHumansModels, BiologicalMolecular Targeted TherapyProtein Kinase InhibitorsTOR Serine-Threonine KinasesMTOR protein, humanProtein Kinase InhibitorsTOR Serine-Threonine KinasesleukemialymphomamTORrapalogsrapamycinTOR-KIs

Identifiers

PMID26805380
PMCPMC5061788
OpenAlexW2262064572

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.