Evidence map›Paper›PMID 24563620›Full record

ArticleNeoplasia (New York, N.Y.)2014

Paradoxically augmented anti-tumorigenic action of proton pump inhibitor and GastrininAPCMin/+ intestinal polyposis model.

Young-Min Han, Ki Baik Hahm, Jong-Min Park, Sung Pyo Hong, Eun-Hee Kim

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 3 pooled it
3.2field-weighted citation impact, top 9% 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, 3 syntheses or guidelines pooled it, 27 citations in OpenAlex.

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  15. Acid suppression therapy and allergic reactions.Allergo journal international · 2015
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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 1 institution in 1 country.

Young-Min HanCHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul, South Korea ; College of Pharmacy, CHA University, Pocheon, South Korea.
Ki Baik HahmCHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul, South Korea ; College of Pharmacy, CHA University, Pocheon, South Korea.
Jong-Min ParkCHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul, South Korea.
Sung Pyo HongCollege of Pharmacy, CHA University, Pocheon, South Korea.
Eun-Hee KimCHA Cancer Prevention Research Center, CHA Cancer Institute, CHA University, Seoul, South Korea ; College of Pharmacy, CHA University, Pocheon, South Korea.
CHA University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Though long-term administration of proton pump inhibitor (PPI) imposed the risk of gastrointestinal track tumorigenesis by accompanied hypergastrinemia, no overt increases of colon cancer risk were witnessed after a long-term cohort study. Our recent investigation revealed that PPI prevented colitis-associated carcinogenesis through anti-inflammatory, anti-oxidative, and anti-mutagenic mechanisms in spite of hypergastrinemia. Therefore, we hypothesized that PPI might either antagonize the trophic action of gastrin on gastrointestinal tumorigenesis or synergize to exert augmented anti-tumorigenic actions. We challenged APCMin/+ mice with gastrin, PPI, PPI and gastrin together for 10 weeks and counted intestinal polyposis accompanied with molecular changes. Gastrin significantly increased intestinal polyposis, but combination of PPI and gastrin markedly attenuated intestinal polyposis compared to gastrin-promoted APCMin/+ mice (P<.001), in which significant β-catenin phosphorylation and inhibition of β-catenin nuclear translocation were observed with PPI alone or combination of PPI and gastrin, whereas gastrin treatment significantly increased β-catenin nuclear translocation. Significant footprints of apoptosis, G0/G1 accumulation, inactivation of p38 and extracellular signal-regulated kinase, decreased expressions of CD31, and inhibition of tumor necrosis factor-α and cyclooxygenase-2 were noted in the combination group. In vitro investigations were similar to in vivo findings as shown that PPI treatment inhibited the binding of gastrin to its receptor, inactivated β-catenin-associated signaling including Tcf/Lef and glycogen synthase kinase β, and paradoxically inhibited β-catenin-associated proliferative activities. Our investigations explain why colon cancer risk has not increased despite long-term use of PPIs and provide a rationale for using PPI to achieve anti-tumorigenesis beyond acid suppression.

Indexed as

2-PyridinylmethylsulfinylbenzimidazolesActive Transport, Cell NucleusAnimalsAntineoplastic AgentsApoptosisbeta CateninCell CycleCell Line, TumorCell ProliferationColonic NeoplasmsCyclooxygenase 2GastrinsGene Expression Regulation, NeoplasticInflammationIntestinal PolyposisMale2-PyridinylmethylsulfinylbenzimidazolesAntineoplastic Agentsbeta CateninCTNNB1 protein, mouseCyclooxygenase 2GastrinsPantoprazolePlatelet Endothelial Cell Adhesion Molecule-1Proton Pump InhibitorsPtgs2 protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID24563620
PMCPMC3924549
OpenAlexW77587221

What OpenQuestion holds

Textmetadata
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.