Evidence map›Paper›PMID 24442969›Full record

ArticleClinical & experimental metastasis2014

Blockade of the renin-angiotensin system inhibits growth of colorectal cancer liver metastases in the regenerating liver.

Shir Lin Koh, E I Ager, P L N Costa, C Malcontenti-Wilson, V Muralidharan, C Christophi

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Clinical & experimental metastasis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 26% 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, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. 20(Frontiers in pharmacology · 2019
    Article
  14. Review
  15. Review
  16. 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

6 authors at 2 institutions in 1 country.

Shir Lin KohDepartment of Surgery, Austin Health, The University of Melbourne, Burgundy Street, Heidelberg, VIC, 3084, Australia. shir_lin@hotmail.com.
E I AgerDepartment of Surgery, Austin Health, The University of Melbourne, Burgundy Street, Heidelberg, VIC, 3084, Australia.
P L N CostaDepartment of Surgery, Austin Health, The University of Melbourne, Burgundy Street, Heidelberg, VIC, 3084, Australia.
C Malcontenti-WilsonDepartment of Surgery, Austin Health, The University of Melbourne, Burgundy Street, Heidelberg, VIC, 3084, Australia.
V MuralidharanDepartment of Surgery, Austin Health, The University of Melbourne, Burgundy Street, Heidelberg, VIC, 3084, Australia.
C ChristophiDepartment of Surgery, Austin Health, The University of Melbourne, Burgundy Street, Heidelberg, VIC, 3084, Australia.
Austin Health · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Partial hepatectomy (PH), the preferred option for selected patients with colorectal cancer liver metastases (CRCLM), is associated with 40-80% tumor recurrence rates. Renin-angiotensin system (RAS) blockade inhibits tumor growth and has been suggested to improve liver regeneration. We documented the effect of RAS blockade on tumor growth and liver regeneration in a murine model. CRCLM induction followed by 70% PH was performed on 78 CBA mice. Liver regeneration (days 2, 6) and CRCLM tumor load were measured by liver (and tumor) weights, percentage of CRCLM burden and tumor nodule count (days 16, 21). mRNA expression of the RAS components was characterised. Statistical analysis was performed using 2-independent sample T test or Mann-Whitney test (SPSS). Captopril did not impair liver regeneration. By day 21, Captopril decreased tumor burden (percentage of CRCLM in the liver) (48.7 ± 4.7% control, 24.4 ± 6.2 Captopril; p = 0.008), tumor volume (1046.2 ± 200.2 mm(3), 388.3 ± 150.4; p = 0.02), tumor nodule count per image field (181.1 ± 28.5, 68 ± 17.6; p = 0.005) and tumor angiogenesis (71.8 ± 6.4 vessels/mm(2), 43.1 ± 7.6; p = 0.015) compared to controls. Captopril enhanced tumor apoptosis (1 ± 0.2%, 2.5 ± 0.7; p = 0.028). Liver regeneration and tumor development increased liver ACE levels. Blockade of the RAS effectively retarded CRCLM tumor growth at the late stage of tumor development within the regenerating liver without impeding liver regeneration following PH, via anti-angiogenesis and pro-tumor apoptosis. Captopril may be of therapeutic benefit in patients undergoing PH for CRCLM.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAnimalsApoptosisCaptoprilCell ProliferationColorectal NeoplasmsImmunoenzyme TechniquesLiver NeoplasmsLiver RegenerationMaleMiceMice, Inbred CBANeovascularization, PathologicReal-Time Polymerase Chain ReactionRenin-Angiotensin SystemReverse Transcriptase Polymerase Chain ReactionAngiotensin-Converting Enzyme InhibitorsCaptoprilRNA, MessengerColorectal cancer liver metastasesLiver regenerationMouse modelPartial hepatectomyTumor growth and stimulation

Identifiers

PMID24442969
OpenAlexW2006043903

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.