Evidence map›Paper›PMID 31582534›Full record

ArticleMolecular cancer therapeutics2020

Ibrutinib Potentiates Antihepatocarcinogenic Efficacy of Sorafenib by Targeting EGFR in Tumor Cells and BTK in Immune Cells in the Stroma.

Cho-Hao Lin, Khadija H Elkholy, Nissar A Wani, Ding Li, Peng Hu, Juan M Barajas, Lianbo Yu, Xiaoli Zhang, Samson T Jacob, Wasif N Khan and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed, 29 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

13 authors at 3 institutions in 1 country.

Cho-Hao LinDepartment of Pathology, The Ohio State University, Columbus, Ohio.
Khadija H ElkholyDepartment of Pathology, The Ohio State University, Columbus, Ohio.
Nissar A WaniComprehensive Cancer Center, The Ohio State University, Columbus, Ohio.
Ding LiDepartment of Pathology, The Ohio State University, Columbus, Ohio.
Peng HuDepartment of Pathology, The Ohio State University, Columbus, Ohio.
Juan M BarajasDepartment of Pathology, The Ohio State University, Columbus, Ohio.
Lianbo YuComprehensive Cancer Center, The Ohio State University, Columbus, Ohio.
Xiaoli ZhangComprehensive Cancer Center, The Ohio State University, Columbus, Ohio.
Samson T JacobComprehensive Cancer Center, The Ohio State University, Columbus, Ohio.
Wasif N KhanDepartment of Microbiology & Immunology and Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, Florida.ORCID 0000-0002-7354-8312
Xue-Feng BaiDepartment of Pathology, The Ohio State University, Columbus, Ohio.
Anne M NoonanComprehensive Cancer Center, The Ohio State University, Columbus, Ohio.
Kalpana GhoshalDepartment of Pathology, The Ohio State University, Columbus, Ohio. kalpana.ghoshal@osumc.edu.
The Ohio State University · USCancer Genetics (United States) · USSylvester Comprehensive Cancer Center · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Jennifer A. Woyach · 1985 to 2026
$132.3M
MOLECULAR MECHANISMS OF DIET-INDUCED CARCINOGENESISR01CA086978 · NCI · OHIO STATE UNIVERSITY · PI GHOSHAL, KALPANA, JACOB, SAMSON T · 2002 to 2018
$4.9M
Role of microR-122 in Hepatocarcinogenesis using Conditional Knockout MiceR01CA193244 · NCI · OHIO STATE UNIVERSITY · PI GHOSHAL, KALPANA · 2015 to 2019
$2.3M
NCI NIH HHS P30 CA016058NCI NIH HHS R01 CA086978NCI NIH HHS R01 CA193244
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC), the most prevalent primary liver cancer, is a leading cause of cancer-related death worldwide because of rising incidence and limited therapy. Although treatment with sorafenib or lenvatinib is the standard of care in patients with advanced-stage HCC, the survival benefit from sorafenib is limited due to low response rate and drug resistance. Ibrutinib, an irreversible tyrosine kinase inhibitor (TKI) of the TEC (e.g., BTK) and ErbB (e.g., EGFR) families, is an approved treatment for B-cell malignancies. Here, we demonstrate that ibrutinib inhibits proliferation, spheroid formation, and clonogenic survival of HCC cells, including sorafenib-resistant cells. Mechanistically, ibrutinib inactivated EGFR and its downstream Akt and ERK signaling in HCC cells, and downregulated a set of critical genes involved in cell proliferation, migration, survival, and stemness, and upregulated genes promoting differentiation. Moreover, ibrutinib showed synergy with sorafenib or regorafenib, a sorafenib congener, by inducing apoptosis of HCC cells.

Indexed as

AdenineAnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsCarcinoma, HepatocellularCell Line, TumorDrug SynergismFemaleHumansLiver NeoplasmsMicePiperidinesSorafenibAdenineAntineoplastic AgentsibrutinibPiperidinesSorafenib

Identifiers

PMID31582534
PMCPMC7007841
OpenAlexW2977353899

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.