Evidence map›Paper›PMID 25320008›Full record

ArticleCancer research2014

Syntheses and discovery of a novel class of cinnamic hydroxamates as histone deacetylase inhibitors by multimodality molecular imaging in living subjects.

C T Chan, J Qi, W Smith, R Paranol, R Mazitschek, N West, R Reeves, G Chiosis, S L Schreiber, J E Bradner and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

4 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Engineering cancer microenvironments forMaterials today (Kidlington, England) · 2015
    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

12 authors at 1 institution in 1 country.

C T ChanDepartment of Radiology, Stanford University School of Medicine, Stanford, California. Molecular Imaging Program at Stanford (MIPS), Stanford University School of Medicine, Stanford, California. Bio-X Program, Stanford University School of Medicine, Stanford, California.
J QiMedical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
W SmithMedical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
R ParanolMedical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
R MazitschekHarvard Medical School, Boston, Massachusetts. Massachusetts General Hospital, Boston, Massachusetts. Broad Institute, Cambridge, Massachusetts.
N WestMedical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
R ReevesDepartment of Radiology, Stanford University School of Medicine, Stanford, California. Molecular Imaging Program at Stanford (MIPS), Stanford University School of Medicine, Stanford, California. Bio-X Program, Stanford University School of Medicine, Stanford, California.
G ChiosisDepartment of Medicine and Program in Molecular Pharmacology and Medical Chemistry, Memorial Sloan-Kettering Cancer Center, New York, New York.
S L SchreiberBroad Institute, Cambridge, Massachusetts.
J E BradnerMedical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts. Harvard Medical School, Boston, Massachusetts. Broad Institute, Cambridge, Massachusetts.
R PaulmuruganDepartment of Radiology, Stanford University School of Medicine, Stanford, California. Molecular Imaging Program at Stanford (MIPS), Stanford University School of Medicine, Stanford, California. Bio-X Program, Stanford University School of Medicine, Stanford, California.
S S GambhirDepartment of Radiology, Stanford University School of Medicine, Stanford, California. Molecular Imaging Program at Stanford (MIPS), Stanford University School of Medicine, Stanford, California. Bio-X Program, Stanford University School of Medicine, Stanford, California. Department of Bioengineering, Stanford University School of Medicine, Stanford, California. Division of Nuclear Medicine, Stanford University School of Medicine, Stanford, California. sgambhir@stanford.edu.
Broad Institute · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Elisa de Stanchina · 1985 to 2026
$347.4M
StatisticsP50CA086355 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI HILDERBRAND, SCOTT A · 2000 to 2015
$27.8M
Small Animal ImagingP50CA114747 · NCI · STANFORD UNIVERSITY · PI GAMBHIR, SANJIV S · 2005 to 2014
$18.2M
Project 3: Structural Basis for grp94 Drug Development and Chaperone FunctionP01CA186866 · NCI · OHIO STATE UNIVERSITY · PI LI, ZIHAI · 2015 to 2019
$6.7M
Reporter Imaging of Protein-Protein InteractionsR01CA082214 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GAMBHIR, SANJIV S · 1999 to 2019
$5.9M
Biomarkers for predicting response to Hsp90 therapyR01CA172546 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI CHIOSIS, GABRIELA, DUNPHY, MARK P. · 2013 to 2017
$2.9M
Targeting the heat shock response for the therapy of DLBCLR01CA155226 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHIOSIS, GABRIELA, MELNICK, ARI M. · 2011 to 2015
$2.5M
NCI NIH HHS NCI ICMIC P50CA114747NCI NIH HHS NCI RO1 CA082214NCI NIH HHS NIH P50CA086355NCI NIH HHS P01 CA186866NCI NIH HHS P30 CA008748NCI NIH HHS P50 CA086355NCI NIH HHS P50 CA114747NCI NIH HHS R01 CA082214NCI NIH HHS R01 CA155226NCI NIH HHS R01 CA172546
6 · The paper itself

Abstract

Histone deacetylases (HDAC) that regulate gene expression are being explored as cancer therapeutic targets. In this study, we focused on HDAC6 based on its ability to inhibit cancerous Hsp90 chaperone activities by disrupting Hsp90/p23 interactions. To identify novel HDAC6 inhibitors, we used a dual-luciferase reporter system in cell culture and living mice by bioluminescence imaging (BLI). On the basis of existing knowledge, a library of hydrazone compounds was generated for screening by coupling cinnamic hydroxamates with aldehydes and ketones. Potency and selectivity were determined by in vitro HDAC profiling assays, with further evaluation to inhibit Hsp90(α/β)/p23 interactions by BLI. In this manner, we identified compound 1A12 as a dose-dependent inhibitor of Hsp90(α/β)/p23 interactions, UKE-1 myeloid cell proliferation, p21(waf1) upregulation, and acetylated histone H3 levels. 1A12 was efficacious in tumor xenografts expressing Hsp90(α)/p23 reporters relative to carrier control-treated mice as determined by BLI. Small animal (18)F-FDG PET/CT imaging on the same cohort showed that 1A12 also inhibited glucose metabolism relative to control subjects. Ex vivo analyses of tumor lysates showed that 1A12 administration upregulated acetylated-H3 by approximately 3.5-fold. Taken together, our results describe the discovery and initial preclinical validation of a novel selective HDAC inhibitor.

Indexed as

Molecular ImagingMultimodal ImagingAcetylationAnimalsCell Line, TumorCell ProliferationCinnamatesFluorodeoxyglucose F18Histone Deacetylase 6Histone Deacetylase InhibitorsHistone DeacetylasesHumansHydroxamic AcidsMiceMyeloid CellsCinnamatescinnamic acidFluorodeoxyglucose F18HDAC6 protein, humanHistone Deacetylase 6Histone Deacetylase InhibitorsHistone DeacetylasesHydroxamic Acids

Identifiers

PMID25320008
PMCPMC4315624
OpenAlexW2116918062

What OpenQuestion holds

Textmetadata
LicenceTDM
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.