Evidence map›Paper›PMID 37943821›Full record

ArticlePloS one2023

AUM302, a novel triple kinase PIM/PI3K/mTOR inhibitor, is a potent in vitro pancreatic cancer growth inhibitor.

Komala Ingle, Joseph F LaComb, Lee M Graves, Antonio T Baines, Agnieszka B Bialkowska

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. PIM1 kinase and its diverse substrate in solid tumors.Cell communication and signaling : CCS · 2024
    Review
  4. Review
  5. 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

5 authors at 2 institutions in 1 country.

Komala IngleDepartment of Medicine, Renaissance School of Medicine at Stony Brook University, Stony Brook, New York, United States of America.
Joseph F LaCombDepartment of Medicine, Renaissance School of Medicine at Stony Brook University, Stony Brook, New York, United States of America.
Lee M GravesDepartment of Pharmacology, School of Medicine, the University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
Antonio T BainesDepartment of Pharmacology, School of Medicine, the University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
Agnieszka B BialkowskaDepartment of Medicine, Renaissance School of Medicine at Stony Brook University, Stony Brook, New York, United States of America.ORCID 0000-0003-2127-7714
Stony Brook School · USUniversity of North Carolina at Chapel Hill · US

Funding

Mechanisms of injury-induced pancreatic neoplasiaR01DK124342 · NIDDK · STATE UNIVERSITY NEW YORK STONY BROOK · PI BIALKOWSKA, AGNIESZKA BEATA · 2020 to 2023
$1.4M
NIDDK NIH HHS R01 DK124342
6 · The paper itself

Abstract

Pancreatic cancer is one of the leading causes of cancer deaths, with pancreatic ductal adenocarcinoma (PDAC) being the most common subtype. Advanced stage diagnosis of PDAC is common, causing limited treatment opportunities. Gemcitabine is a frequently used chemotherapeutic agent which can be used as a monotherapy or in combination. However, tumors often develop resistance to gemcitabine. Previous studies show that the proto-oncogene PIM kinases (PIM1 and PIM3) are upregulated in PDAC compared to matched normal tissue and are related to chemoresistance and PDAC cell growth. The PIM kinases are also involved in the PI3K/AKT/mTOR pathway to promote cell survival. In this study, we evaluate the effect of the novel multikinase PIM/PI3K/mTOR inhibitor, AUM302, and commercially available PIM inhibitor, TP-3654. Using five human PDAC cell lines, we found AUM302 to be a potent inhibitor of cell proliferation, cell viability, cell cycle progression, and phosphoprotein expression, while TP-3654 was less effective. Significantly, AUM302 had a strong impact on the viability of gemcitabine-resistant PDAC cells. Taken together, these results demonstrate that AUM302 exhibits antitumor activity in human PDAC cells and thus has the potential to be an effective drug for PDAC therapy.

Indexed as

Antineoplastic AgentsCarcinoma, Pancreatic DuctalPancreatic NeoplasmsCell Line, TumorCell ProliferationGemcitabineGrowth InhibitorsHumansPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsTOR Serine-Threonine KinasesAntineoplastic AgentsGemcitabineGrowth InhibitorsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsTOR Serine-Threonine Kinases

Identifiers

PMID37943821
PMCPMC10635512
OpenAlexW4388522087

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.