Evidence map›Paper›PMID 30343280›Full record

ArticleCancer genomics & proteomics

Evaluation of the Insulin-like Growth Factor Receptor Pathway in Patients with Advanced Breast Cancer Treated with Trastuzumab.

Christos Christodoulou, Georgios Oikonomopoulos, Georgia Angeliki Koliou, Ioannis Kostopoulos, Vassiliki Kotoula, Mattheos Bobos, George Pentheroudakis, George Lazaridis, Maria Skondra, Sofia Chrisafi and 10 more

Open access · diamondAbstract readEvaluation Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.8field-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

6 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
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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

20 authors at 7 institutions in 1 country.

Christos ChristodoulouSecond Department of Medical Oncology, Metropolitan Hospital, Piraeus, Greece c_christodoulou@yahoo.gr.
Georgios OikonomopoulosSecond Department of Medical Oncology, Metropolitan Hospital, Piraeus, Greece.
Georgia Angeliki KoliouSection of Biostatistics, Hellenic Cooperative Oncology Group, Data Office, Athens, Greece.
Ioannis KostopoulosDepartment of Pathology, Aristotle University of Thessaloniki, School of Health Sciences, Faculty of Medicine, Thessaloniki, Greece.
Vassiliki KotoulaDepartment of Pathology, Aristotle University of Thessaloniki, School of Health Sciences, Faculty of Medicine, Thessaloniki, Greece.
Mattheos BobosLaboratory of Molecular Oncology, Hellenic Foundation for Cancer Research/Aristotle University of Thessaloniki, Thessaloniki, Greece.
George PentheroudakisDepartment of Medical Oncology, Ioannina University Hospital, Ioannina, Greece.
George LazaridisDepartment of Medical Oncology, Papageorgiou Hospital, Aristotle University of Thessaloniki, School of Health Sciences, Faculty of Medicine, Thessaloniki, Greece.
Maria SkondraOncology Section, Second Department of Internal Medicine, Hippokration Hospital, Athens, Greece.
Sofia ChrisafiLaboratory of Molecular Oncology, Hellenic Foundation for Cancer Research/Aristotle University of Thessaloniki, Thessaloniki, Greece.
Angelos KoutrasDivision of Oncology, Department of Medicine, University Hospital, University of Patras Medical School, Patras, Greece.
Dimitrios BafaloukosFirst Department of Medical Oncology, Metropolitan Hospital, Piraeus, Greece.
Evangelia RazisThird Department of Medical Oncology, Hygeia Hospital, Athens, Greece.
Kyriaki PapadopoulouLaboratory of Molecular Oncology, Hellenic Foundation for Cancer Research/Aristotle University of Thessaloniki, Thessaloniki, Greece.
Pavlos PapakostasOncology Unit, Hippokration Hospital, Athens, Greece.
Haralambos P KalofonosDivision of Oncology, Department of Medicine, University Hospital, University of Patras Medical School, Patras, Greece.
Dimitrios PectasidesOncology Section, Second Department of Internal Medicine, Hippokration Hospital, Athens, Greece.
Pantelis SkarlosDepartment of Radiotherapy, Metropolitan Hospital, Piraeus, Greece.
Konstantine T KalogerasLaboratory of Molecular Oncology, Hellenic Foundation for Cancer Research/Aristotle University of Thessaloniki, Thessaloniki, Greece.
George FountzilasLaboratory of Molecular Oncology, Hellenic Foundation for Cancer Research/Aristotle University of Thessaloniki, Thessaloniki, Greece.
Aristotle University of Thessaloniki · GRMetropolitan Hospital · GRHippocration General Hospital · GRHellenic Cooperative Oncology Group · GRUniversity of Patras · GRHygeia Hospital · GRUniversity Hospital of Ioannina · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTrastuzumab is a monoclonal antibody against HER2-positive breast cancer. Despite improving the natural history of the disease, there is a number of patients who are resistant to it, whereas all patients will eventually develop resistance and disease will progress. Inconsistent preclinical data show that the IGF-R pathway may contribute to either de novo or acquired resistance to trastuzumab. MATERIALS AND

methodsIn total, 227 trastuzumab-treated metastatic breast cancer patients were evaluated for IGF-1, IGF-1R, GLP-1R, Akt1, Akt2 Akt3 mRNA expression, and IGF-1Rα, IGF-1Rβ, IGF-2R protein expression.

resultsOnly 139 patients were truly HER2-positive by central assessment. Among HER2-positive patients, high Akt2 and GLP-1R mRNA expression showed a trend towards higher and lower risk of progression, respectively (HR=1.83, 95%CI=0.90-3.72, p=0.094 and HR=0.62, 95%CI=0.36-1.06, p=0.079), while high Akt1 and GLP-1R mRNA expression presented a trend towards unfavorable survival (HR=1.67, 95%CI=0.93-2.99, p=0.086 and HR=1.67, 95%CI=0.94-2.96, p=0.080). Among HER2-negative patients, high GLP-1R mRNA expression and negative stromal IGF-1Rβ protein expression showed a trend towards worse survival (HR=2.31, 95%CI=0.87-6.13, p=0.094 and HR=2.03, 95%CI=0.94-4.35, p=0.071, respectively). In the multivariate analyses, HER2-positive patients with high Akt1 and GLP-1R mRNA expression had a worse survival (HR=1.86, 95%CI=1.01-3.43, p=0.045 and HR=1.83, 95%CI=0.99-3.41, p=0.055, respectively).

conclusionThis study revealed a crosstalk between the IGF-R pathway and HER2. There was evidence that high Akt1 and GLP-1R mRNA expression might affect survival among HER2-positive metastatic breast cancer patients treated with trastuzumab.

Indexed as

Breast NeoplasmsAdultAgedAged, 80 and overDisease-Free SurvivalFemaleGene Expression RegulationHumansMiddle AgedNeoplasm MetastasisNeoplasm ProteinsReceptor, IGF Type 1Retrospective StudiesSignal TransductionSurvival RateTrastuzumabNeoplasm ProteinsReceptor, IGF Type 1Trastuzumabadvanced breast cancerHER2-negative breast cancerHER2-positive breast cancerIGF-Rtrastuzumab

Identifiers

PMID30343280
PMCPMC6299784
OpenAlexW2895927699

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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.