Evidence map›Paper›PMID 33898309›Full record

ReviewFrontiers in oncology2021

Molecular Chaperone GRP94/GP96 in Cancers: Oncogenesis and Therapeutic Target.

Xiaofeng Duan, Stephen Iwanowycz, Soo Ngoi, Megan Hill, Qiang Zhao, Bei Liu

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 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

6 authors at 4 institutions in 2 countries.

Xiaofeng DuanDepartment of Microbiology & Immunology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, United States.
Stephen IwanowyczDepartment of Microbiology & Immunology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, United States.
Soo NgoiDivision of Hematology, Department of Internal Medicine, The Ohio State University Comprehensive Cancer Center, Columbus, OH, United States.
Megan HillDivision of Hematology, Department of Internal Medicine, The Ohio State University Comprehensive Cancer Center, Columbus, OH, United States.
Qiang ZhaoDepartment of Pediatric Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy of Tianjin, Tianjin Clinical Research Center for Cancer, Tianjin, China.
Bei LiuDepartment of Microbiology & Immunology, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC, United States.
The Ohio State University · USMedical University of South Carolina · USMUSC Hollings Cancer Center · USTianjin Medical University Cancer Institute and Hospital · CN

Funding

Extrinsic and intrinsic factors regulating commensal-specific T helper-17 cellsU01AI125859 · NIAID · OHIO STATE UNIVERSITY · PI LIU, BEI · 2016 to 2020
$2.5M
Mechanism of gp96/grp94 in regulating plasma cells and myelomaR01CA193939 · NCI · OHIO STATE UNIVERSITY · PI LIU, BEI · 2016 to 2020
$1.7M
Program in Immunology Research and Entrepreneurship (PIRE)T32AI132164 · NIAID · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TOMLINSON, STEPHEN · 2017 to 2021
$1.2M
NCI NIH HHS R01 CA193939NIAID NIH HHS T32 AI132164NIAID NIH HHS U01 AI125859
6 · The paper itself

Abstract

During tumor development and progression, intrinsic and extrinsic factors trigger endoplasmic reticulum (ER) stress and the unfolded protein response, resulting in the increased expression of molecular chaperones to cope with the stress and maintain tumor cell survival. Heat shock protein (HSP) GRP94, also known as GP96, is an ER paralog of HSP90 and has been shown to promote survival signaling during tumor-induced stress and modulate the immune response through its multiple clients, including TLRs, integrins, LRP6, GARP, IGF, and HER2. Clinically, elevated expression of GRP94 correlates with an aggressive phenotype and poor clinical outcome in a variety of cancers. Thus, GRP94 is a potential molecular marker and therapeutic target in malignancies. In this review, we will undergo deep molecular profiling of GRP94 in tumor development and summarize the individual roles of GRP94 in common cancers, including breast cancer, colon cancer, lung cancer, liver cancer, multiple myeloma, and others. Finally, we will briefly review the therapeutic potential of selectively targeting GRP94 for the treatment of cancers.

Indexed as

biomarkercancerchaperoneendoplasmic reticulum stressGRP94/GP96therapeutic target

Identifiers

PMID33898309
PMCPMC8062746
OpenAlexW3155051801

What OpenQuestion 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 OpenQuestion graph.