Evidence map›Paper›PMID 24879564›Full record

ArticleCancer research2014

Loss of LRIG1 locus increases risk of early and late relapse of stage I/II breast cancer.

Patricia A Thompson, Ingrid Ljuslinder, Spyros Tsavachidis, Abenaa Brewster, Aysegul Sahin, Håkan Hedman, Roger Henriksson, Melissa L Bondy, Beatrice S Melin

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

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  14. Prognostic factor analysis for breast cancer using gene expression profiles.BMC medical informatics and decision making · 2016
    Article
  15. Article
  16. Article
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  18. Article
  19. LRIG and cancer prognosis.Acta oncologica (Stockholm, Sweden) · 2014
    Review
  20. Review
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

9 authors at 3 institutions in 2 countries.

Patricia A ThompsonAuthors' Affiliations: Department of Cellular and Molecular Medicine, The University of Arizona Cancer Center, Tucson, Arizona; Department of Pediatrics, Baylor College of Medicine, One Baylor Plaza; Dan L. Duncan Center, Baylor College of Medicine; Departments of Clinical Cancer Prevention and Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas; and Department of Radiation Sciences, Umeå University, Sweden PThompson@azcc.arizona.edu mbondy@bcm.edu.
Ingrid LjuslinderAuthors' Affiliations: Department of Cellular and Molecular Medicine, The University of Arizona Cancer Center, Tucson, Arizona; Department of Pediatrics, Baylor College of Medicine, One Baylor Plaza; Dan L. Duncan Center, Baylor College of Medicine; Departments of Clinical Cancer Prevention and Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas; and Department of Radiation Sciences, Umeå University, Sweden.
Spyros TsavachidisAuthors' Affiliations: Department of Cellular and Molecular Medicine, The University of Arizona Cancer Center, Tucson, Arizona; Department of Pediatrics, Baylor College of Medicine, One Baylor Plaza; Dan L. Duncan Center, Baylor College of Medicine; Departments of Clinical Cancer Prevention and Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas; and Department of Radiation Sciences, Umeå University, Sweden.
Abenaa BrewsterAuthors' Affiliations: Department of Cellular and Molecular Medicine, The University of Arizona Cancer Center, Tucson, Arizona; Department of Pediatrics, Baylor College of Medicine, One Baylor Plaza; Dan L. Duncan Center, Baylor College of Medicine; Departments of Clinical Cancer Prevention and Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas; and Department of Radiation Sciences, Umeå University, Sweden.
Aysegul SahinAuthors' Affiliations: Department of Cellular and Molecular Medicine, The University of Arizona Cancer Center, Tucson, Arizona; Department of Pediatrics, Baylor College of Medicine, One Baylor Plaza; Dan L. Duncan Center, Baylor College of Medicine; Departments of Clinical Cancer Prevention and Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas; and Department of Radiation Sciences, Umeå University, Sweden.
Håkan HedmanAuthors' Affiliations: Department of Cellular and Molecular Medicine, The University of Arizona Cancer Center, Tucson, Arizona; Department of Pediatrics, Baylor College of Medicine, One Baylor Plaza; Dan L. Duncan Center, Baylor College of Medicine; Departments of Clinical Cancer Prevention and Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas; and Department of Radiation Sciences, Umeå University, Sweden.
Roger HenrikssonAuthors' Affiliations: Department of Cellular and Molecular Medicine, The University of Arizona Cancer Center, Tucson, Arizona; Department of Pediatrics, Baylor College of Medicine, One Baylor Plaza; Dan L. Duncan Center, Baylor College of Medicine; Departments of Clinical Cancer Prevention and Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas; and Department of Radiation Sciences, Umeå University, Sweden.
Melissa L BondyAuthors' Affiliations: Department of Cellular and Molecular Medicine, The University of Arizona Cancer Center, Tucson, Arizona; Department of Pediatrics, Baylor College of Medicine, One Baylor Plaza; Dan L. Duncan Center, Baylor College of Medicine; Departments of Clinical Cancer Prevention and Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas; and Department of Radiation Sciences, Umeå University, Sweden PThompson@azcc.arizona.edu mbondy@bcm.edu.
Beatrice S MelinAuthors' Affiliations: Department of Cellular and Molecular Medicine, The University of Arizona Cancer Center, Tucson, Arizona; Department of Pediatrics, Baylor College of Medicine, One Baylor Plaza; Dan L. Duncan Center, Baylor College of Medicine; Departments of Clinical Cancer Prevention and Pathology, The University of Texas MD Anderson Cancer Center, Houston, Texas; and Department of Radiation Sciences, Umeå University, Sweden.
Umeå University · SEUniversity of Arizona · USBaylor College of Medicine · US

Funding

Risk Prediction for ER Negative Breast Cancer RecurrenceR01CA172511 · NCI · BAYLOR COLLEGE OF MEDICINE · PI BONDY, MELISSA L., BREWSTER, ABENAA M · 2013 to 2017
$3.1M
Determinants of Breast Cancer SurvivalR01CA089608 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BONDY, MELISSA L · 2002 to 2006
$3.1M
NCI NIH HHS R01 CA089608NCI NIH HHS R01 CA172511
6 · The paper itself

Abstract

Gains and losses at chromosome 3p12-21 are common in breast tumors and associated with patient outcomes. We hypothesized that the LRIG1 gene at 3p14.1, whose product functions in ErbB-family member degradation, is a critical tumor modifier at this locus. We analyzed 971 stage I/II breast tumors using Affymetrix Oncoscan molecular inversion probe arrays that include 12 probes located within LRIG1. Copy number results were validated against gene expression data available in the public database. By partitioning the LRIG1 probes nearest exon 12/13, we confirm a breakpoint in the gene and show that gains and losses in the subregions differ by tumor and patient characteristics including race/ethnicity. In analyses adjusted for known prognostic factors, loss of LRIG1 was independently associated with risk of any relapse (HR, 1.90; 95% CI, 1.32-2.73), relapse≥5 years (HR, 2.39; 95% CI, 1.31-4.36), and death (HR, 1.55; 95% CI, 1.11-2.16). Analyses of copy number across chromosome 3, as well as expression data from pooled, publicly available datasets, corroborated the hypothesis of an elevated and persistent risk among cases with loss of or low LRIG1. We concluded that loss/low expression of LRIG1 is an independent risk factor for breast cancer metastasis and death in stage I/II patients. Increased hazard in patients with loss/low LRIG1 persists years after diagnosis, suggesting that LRIG1 is acting as a critical suppressor of tumor metastasis and is an early clinical indicator of risk for late recurrences in otherwise low-risk patients.

Indexed as

Breast NeoplasmsCase-Control StudiesChromosomes, Human, Pair 3FemaleGene DosageGene ExpressionGenetic Predisposition to DiseaseHumansMembrane GlycoproteinsMiddle AgedNeoplasm Recurrence, LocalNeoplasm StagingLRIG1 protein, humanMembrane Glycoproteins

Identifiers

PMID24879564
PMCPMC8759715
OpenAlexW1964969316

What OpenQuestion holds

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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.