Evidence mapPaperPMID 31490549Full record

ArticleInternational journal of cancer2020

IGF-1R pathway activation as putative biomarker for linsitinib therapy to revert tamoxifen resistance in ER-positive breast cancer.

Dinja T Kruger, Xanthippi Alexi, Mark Opdam, Karianne Schuurman, Leonie Voorwerk, Joyce Sanders, Vincent van der Noort, Epie Boven, Wilbert Zwart, Sabine C Linn

Open access · hybridAbstract read
In one paragraph

Article in International journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

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  18. Hierarchical clustering of PI3K and MAPK pathway proteins in breast cancer intrinsic subtypes.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2020
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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.

Dinja T KrugerDepartment of Medical Oncology, Amsterdam UMC, Vrije Universiteit Amsterdam/Cancer Center Amsterdam, Amsterdam, The Netherlands.ORCID 0000-0002-8439-8188
Xanthippi AlexiDivision of Oncogenomics, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Mark OpdamDivision of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Karianne SchuurmanDivision of Oncogenomics, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Leonie VoorwerkDivision of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Joyce SandersDepartment of Pathology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Vincent van der NoortDivision of Biometrics, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Epie BovenDepartment of Medical Oncology, Amsterdam UMC, Vrije Universiteit Amsterdam/Cancer Center Amsterdam, Amsterdam, The Netherlands.
Wilbert ZwartDivision of Oncogenomics, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0002-9823-7289
Sabine C LinnDivision of Molecular Pathology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0001-5541-0347
The Netherlands Cancer Institute · NLAmsterdam Neuroscience · NLDutch Cancer Society · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preclinical studies indicate that activated IGF-1R can drive endocrine resistance in ER-positive (ER+) breast cancer, but its clinical relevance is unknown. We studied the effect of IGF-1R signaling on tamoxifen benefit in patients and we searched for approaches to overcome IGF-1R-mediated tamoxifen failure in cell lines. Primary tumor blocks from postmenopausal ER+ breast cancer patients randomized between adjuvant tamoxifen versus nil were recollected. Immunohistochemistry for IGF-1R, p-IGF-1R/InsR, p-ERα(Ser118), p-ERα(Ser167) and PI3K/MAPK pathway proteins was performed. Multivariate Cox models were employed to assess tamoxifen efficacy. The association between p-IGF-1R/InsR and PI3K/MAPK pathway activation in MCF-7 and T47D cells was analyzed with Western blots. Cell proliferation experiments were performed under various growth-stimulating and -inhibiting conditions. Patients with ER+, IGF-1R-positive breast cancer without p-IGF-1R/InsR staining (n = 242) had tamoxifen benefit (HR 0.41, p = 0.0038), while the results for p-IGF-1R/InsR-positive patients (n = 125) were not significant (HR 0.95, p = 0.3). High p-ERα(Ser118) or p-ERα(Ser167) expression was associated with less tamoxifen benefit. In MCF-7 cells, IGF-1R stimulation increased phosphorylation of PI3K/MAPK proteins and ERα(Ser167) regardless of IGF-1R overexpression. This could be abrogated by the dual IGF-1R/InsR inhibitor linsitinib, but not by the IGF-IR-selective antibody 1H7. In MCF-7 and T47D cells, stimulation of the IGF-1R/InsR pathway resulted in cell proliferation regardless of tamoxifen. Abrogation of cell growth was regained by addition of linsitinib. In conclusion, p-IGF-1R/InsR positivity in ER+ breast cancer is associated with reduced benefit from adjuvant tamoxifen in postmenopausal patients. In cell lines, stimulation rather than overexpression of IGF-1R is driving tamoxifen resistance to be abrogated by linsitinib.

Indexed as

AgedAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorBreast NeoplasmsCell Line, TumorDrug Resistance, NeoplasmDrug SynergismFemaleHumansImidazolesImmunohistochemistryMAP Kinase Signaling SystemMCF-7 CellsMiddle AgedNeoplasm StagingPhosphatidylinositol 3-Kinases3-(8-amino-1-(2-phenylquinolin-7-yl)imidazo(1,5-a)pyrazin-3-yl)-1-methylcyclobutanolBiomarkers, TumorIGF1R protein, humanImidazolesPhosphatidylinositol 3-KinasesPyrazinesReceptor, IGF Type 1Receptors, EstrogenTamoxifenadjuvant tamoxifenbreast cancerIGF-1 receptorlinsitinibPI3K/MAPK pathway

Identifiers

PMID31490549
PMCPMC7065127
OpenAlexW2972169320

What Socratic 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 Socratic graph.