Evidence map›Paper›PMID 36414127›Full record

ReviewBiochimica et biophysica acta. Reviews on cancer2023

Unfolded protein response and angiogenesis in malignancies.

Amin Izadpanah, Kurtis Willingham, Bysani Chandrasekar, Eckhard U Alt, Reza Izadpanah

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Reviews on cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 13 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

5 authors at 2 institutions in 1 country.

Amin IzadpanahApplied Stem Cell Laboratory, Department of Medicine/Heart and Vascular Institute, Tulane University School of Medicine, New Orleans, LA, USA.
Kurtis WillinghamApplied Stem Cell Laboratory, Department of Medicine/Heart and Vascular Institute, Tulane University School of Medicine, New Orleans, LA, USA.
Bysani ChandrasekarDepartment of Medicine, University of Missouri School of Medicine and Harry S. Truman Memorial Veterans Hospital, Columbia, MO, USA.
Eckhard U AltApplied Stem Cell Laboratory, Department of Medicine/Heart and Vascular Institute, Tulane University School of Medicine, New Orleans, LA, USA. Electronic address: ealt@tulane.edu.
Reza IzadpanahApplied Stem Cell Laboratory, Department of Medicine/Heart and Vascular Institute, Tulane University School of Medicine, New Orleans, LA, USA; Department of Surgery, Tulane University School of Medicine, New Orleans, LA, USA. Electronic address: rizadpan@tulane.edu.
Tulane University · USHarry S. Truman Memorial Veterans' Hospital · US

Funding

Pilot Projects ProgramP30GM145498 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI Victoria Perepelitsa Belancio · 2022 to 2026
$8.6M
RECK regulation of NASH and fibrosisR01DK130243 · NIDDK · UNIVERSITY OF MISSOURI-COLUMBIA · PI BYSANI, CHANDRASEKAR, RECTOR, RANDY SCOTT · 2022 to 2025
$2.2M
RECK as a Therapeutic Target for AtherosclerosisR01HL170056 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI Chandrasekar Bysani, Shiyou Chen · 2025 to 2026
$1.3M
RECK in Adverse Cardiac Remodeling and Heart FailureI01BX005845 · VA · HARRY S. TRUMAN MEMORIAL VA HOSPITAL · PI BYSANI, CHANDRASEKAR · 2022 to 2025
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BLRD Research Career Scientist Award ApplicationIK6BX004016 · VA · HARRY S. TRUMAN MEMORIAL VA HOSPITAL · PI Chandrasekar Bysani · 2018 to 2026
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BLRD VA I01 BX005845BLRD VA IK6 BX004016NHLBI NIH HHS R01 HL170056NIDDK NIH HHS R01 DK130243NIGMS NIH HHS P30 GM145498
6 · The paper itself

Abstract

Cellular stress, arising from accumulation of unfolded proteins, occurs frequently in rapidly proliferating cancer cells. This cellular stress, in turn, activates the unfolded protein response (UPR), an interconnected set of signal transduction pathways that alleviate the proteostatic stress. The UPR is implicated in cancer cell survival and proliferation through upregulation of pro-tumorigenic pathways that ultimately promote malignant metabolism and neoangiogenesis. Here, we reviewed mechanisms of signaling crosstalk between the UPR and angiogenesis pathways, as well as transmissible ER stress and the role in tumor growth and development. To characterize differences in UPR and UPR-mediated angiogenesis in malignancy, we employed a data mining approach using patient tumor data from The Cancer Genome Atlas (TCGA). The analysis of TCGA revealed differences in UPR between malignant samples versus their non-malignant counterparts.

Indexed as

NeoplasmsUnfolded Protein ResponseHumansNeovascularization, PathologicSignal TransductionTranscriptional ActivationATF6IRE1αPERKTumor microenvironmentUnfolded protein responseXBP1

Identifiers

PMID36414127
PMCPMC10167724
OpenAlexW4309580402

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.