Evidence map›Paper›PMID 25592047›Full record

ReviewInternational journal of colorectal disease2015

Interactions of the renin-angiotensin system in colorectal cancer and metastasis.

W Kurtis Childers

Abstract readReview
PubMed Publisher
In one paragraph

Review in International journal of colorectal disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

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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

1 author.

W Kurtis ChildersDepartment of Surgery, Pinnacle Health System, Harrisburg, PA, 17104, USA, wchilders@pinnaclehealth.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The novel function of the renin-angiotensin system (RAS) is cardiovascular homeostasis. While the major active mediator angiotensin II (ANG II) produces most of the physiologic responses via angiotensin II type I receptor (AT1R), recent insights have looked at the implications of ANG II and its impact on solid tumor formation. Preclinical studies have demonstrated the direct effect of ANG II on the stimulation of angiogenesis via VEGF and other proliferative mediators. RAS components have thus been identified in numerous malignant tissues. Inhibition of the AT1R via angiotensin-converting enzyme inhibitors (ACE-Is) has demonstrated a decrease in solid tumor development and metastasis. Numerous retrospective analyses have demonstrated a reduction in colorectal cancer incidence, polyp formation, and distant metastasis in patients taking inhibitors of the RAS. The use of commonly prescribed anti-hypertensive medications as a chemo-preventative medication may have a remarkable impact in the colorectal cancer community. Further investigation and prospective clinical trials may provide further insight into the potentially beneficial use of ACE-Is and their impact on colorectal cancer.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAnimalsColorectal NeoplasmsDiabetes ComplicationsHumansHyperglycemiaLiver NeoplasmsNeovascularization, PathologicRenin-Angiotensin SystemAngiotensin-Converting Enzyme Inhibitors

Identifiers

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.