Evidence map›Paper›PMID 26413753›Full record

ArticleLeukemia research2015

Identification of ILK as a novel therapeutic target for acute and chronic myeloid leukemia.

Pilar de la Puente, Ellen Weisberg, Barbara Muz, Atsushi Nonami, Micah Luderer, Richard M Stone, Junia V Melo, James D Griffin, Abdel Kareem Azab

Abstract read
In one paragraph

Article in Leukemia research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

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  13. Enhancing proteasome-inhibitory activity and specificity of bortezomib by CD38 targeted nanoparticles in multiple myeloma.Journal of controlled release : official journal of the Controlled Release Society · 2018
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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

9 authors.

Pilar de la PuenteDepartment of Radiation Oncology, Cancer Biology Division, Washington University in Saint Louis School of Medicine, St. Louis, MO, USA.
Ellen WeisbergDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Barbara MuzDepartment of Radiation Oncology, Cancer Biology Division, Washington University in Saint Louis School of Medicine, St. Louis, MO, USA.
Atsushi NonamiDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Micah LudererDepartment of Radiation Oncology, Cancer Biology Division, Washington University in Saint Louis School of Medicine, St. Louis, MO, USA.
Richard M StoneDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Junia V MeloUniversity of Adelaide, Adelaide, Australia.
James D GriffinDepartment of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Abdel Kareem AzabDepartment of Radiation Oncology, Cancer Biology Division, Washington University in Saint Louis School of Medicine, St. Louis, MO, USA. Electronic address: aazab@radonc.wustl.edu.

Funding

TYROSINE KINASE ONCOGENESIS IN MYELOID LEUKEMIAP01CA066996 · NCI · DANA-FARBER CANCER INSTITUTE · PI SCOTT A ARMSTRONG · 1996 to 2026
$52.5M
NCI NIH HHS P01 CA066996
6 · The paper itself

Abstract

Current treatment options as well as clinical efficacy are limited for chronic myelogenous leukemia (CML), Ph+ acute lymphoblastic leukemia (ALL), and acute myeloid leukemia (AML). In response to the pressing need for more efficacious treatment approaches and strategies to override drug resistance in advanced stage CML, Ph+ ALL, and AML, we investigated the effects of inhibition of ILK as a potentially novel and effective approach to treatment of these challenging malignancies. Using the small molecule ILK inhibitor, Cpd22, and ILK knockdown, we investigated the importance of ILK in the growth and viability of leukemia. Our results suggest that the ILK inhibition may be an effective treatment for CML, Ph+ ALL, and AML as a single therapy, with ILK expression levels positively correlating with the efficacy of ILK inhibition. The identification of ILK as a novel target for leukemia therapy warrants further investigation as a therapeutic approach that could be of potential clinical benefit in both acute and chronic myeloid leukemias.

Indexed as

Acute myeloid leukemiaChronic myelogenous leukemiaCompound 22ILK inhibitorTargeted therapies

Identifiers

PMID26413753
PMCPMC5016250

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.