Evidence map›Paper›PMID 26109908›Full record

ArticleBMC clinical pathology2015

Tumor-specific expression of HMG-CoA reductase in a population-based cohort of breast cancer patients.

Emma Gustbée, Helga Tryggvadottir, Andrea Markkula, Maria Simonsson, Björn Nodin, Karin Jirström, Carsten Rose, Christian Ingvar, Signe Borgquist, Helena Jernström

Open access · hybridAbstract read
In one paragraph

Article in BMC clinical pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
1.5field-weighted citation impact, top 19% 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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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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

10 authors at 3 institutions in 1 country.

Emma GustbéeDivision of Oncology and Pathology, Department of Clinical Sciences, Lund, Lund University, Barngatan 2B, SE 22185 Lund, Sweden.
Helga TryggvadottirDivision of Oncology and Pathology, Department of Clinical Sciences, Lund, Lund University, Barngatan 2B, SE 22185 Lund, Sweden ; Department of Oncology, Skåne University Hospital, Lund, Sweden.
Andrea MarkkulaDivision of Oncology and Pathology, Department of Clinical Sciences, Lund, Lund University, Barngatan 2B, SE 22185 Lund, Sweden.
Maria SimonssonDivision of Oncology and Pathology, Department of Clinical Sciences, Lund, Lund University, Barngatan 2B, SE 22185 Lund, Sweden.
Björn NodinDivision of Oncology and Pathology, Department of Clinical Sciences, Lund, Lund University, Barngatan 2B, SE 22185 Lund, Sweden.
Karin JirströmDivision of Oncology and Pathology, Department of Clinical Sciences, Lund, Lund University, Barngatan 2B, SE 22185 Lund, Sweden.
Carsten RoseCREATE Health and Department of Immunotechnology, Lund University, Medicon Village, Building 406, Lund, Sweden.
Christian IngvarDepartment of Clinical Sciences, Division of Surgery, Lund, Lund University, Lund, Sweden and Skåne University Hospital, Lund, Sweden.
Signe BorgquistDivision of Oncology and Pathology, Department of Clinical Sciences, Lund, Lund University, Barngatan 2B, SE 22185 Lund, Sweden ; Department of Oncology, Skåne University Hospital, Lund, Sweden.
Helena JernströmDivision of Oncology and Pathology, Department of Clinical Sciences, Lund, Lund University, Barngatan 2B, SE 22185 Lund, Sweden.
Lund University · SESkåne University Hospital · SEMedicon Village · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe mevalonate pathway synthetizes cholesterol, steroid hormones, and non-steriod isoprenoids necessary for cell survival. 3-Hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) is the rate-limiting enzyme of the mevalonate pathway and the target for statin treatment. HMGCR expression in breast tumors has recently been proposed to hold prognostic and treatment-predictive information. This study aimed to investigate whether HMGCR expression in breast cancer patients was associated with patient and tumor characteristics and disease-free survival (DFS).

methodsA population-based cohort of primary breast cancer patients in Lund, Sweden was assembled between October 2002 and June 2012 enrolling 1,116 patients. Tumor tissue microarrays were constructed and stained with a polyclonal HMGCR antibody (Cat. No HPA008338, Atlas Antibodies AB, Stockholm, Sweden, diluted 1:100) to assess the HMGCR expression in tumor tissue from 885 patients. HMGCR expression was analyzed in relation to patient- and tumor characteristics and disease-free survival (DFS) with last follow-up June 30(th) 2014.

resultsModerate/strong HMGCR expression was associated with less axillary lymph node involvement, lower histological grade, estrogen and progesterone receptor positivity, HER2 negativity, and older patient age at diagnosis compared to weak or no HMGCR expression. Patients were followed for up to 11 years. The median follow-up time was 5.0 years for the 739 patients who were alive and still at risk at the last follow-up. HMGCR expression was not associated with DFS.

conclusionIn this study, HMGCR expression was associated with less aggressive tumor characteristics. However, no association between HMGCR expression and DFS was observed. Longer follow-up may be needed to evaluate HMGCR as prognostic or predictive marker in breast cancer.

Indexed as

Breast cancerEarly breast cancer eventsHMG-CoA reductasePrognosisTreatmentTumor characteristics

Identifiers

PMID26109908
PMCPMC4479235
OpenAlexW1951539597

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.