ArticleAntioxidants & redox signaling2015
Receptor-Independent Ectopic Activity of Prolactin Predicts Aggressive Lung Tumors and Indicates HDACi-Based Therapeutic Strategies.
Article in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03436069 (Identification de Nouveaux Marqueurs Pronostiques Des Cancers du Sein), which is not on this map. Cited by 11 papers.
What it found
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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.
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.
Identification de Nouveaux Marqueurs Pronostiques Des Cancers du Sein
Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Review
- Endocrine paraneoplastic syndromes in lung cancer: A call for clinical vigilance (Review).Molecular and clinical oncology · 2025Review
- Current Insights in Prolactin Signaling and Ovulatory Function.International journal of molecular sciences · 2024Review
- Ectopic expression of a combination of 5 genes detects high risk forms of T-cell acute lymphoblastic leukemia.BMC genomics · 2022Article
- The combined detection of Amphiregulin, Cyclin A1 and DDX20/Gemin3 expression predicts aggressive forms of oral squamous cell carcinoma.British journal of cancer · 2021Article
- Unique genomic profiles obtained from cerebrospinal fluid cell-free DNA of non-small cell lung cancer patients with leptomeningeal metastases.Cancer biology & therapy · 2019Article
- Neuroendocrine Pulmonary Tumors of Low, Intermediate and High Grade: Anatomopathological Diagnosis-Prognostic and Predictive Factors.Molecular diagnosis & therapy · 2018Review
- The Role of Bromodomain Testis-Specific Factor, BRDT, in Cancer: A Biomarker and A Possible Therapeutic Target.Cell journal · 2017Review
- Atad2 is a generalist facilitator of chromatin dynamics in embryonic stem cells.Journal of molecular cell biology · 2016Article
- Gene-set Analysis with CGI Information for Differential DNA Methylation Profiling.Scientific reports · 2016Article
- A six gene expression signature defines aggressive subtypes and predicts outcome in childhood and adult acute lymphoblastic leukemia.Oncotarget · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsEctopic activation of tissue-specific genes accompanies malignant transformation in many cancers. Prolactin (PRL) aberrant activation in lung cancer was investigated here to highlight its value as a biomarker.
resultsPRL is ectopically activated in a subset of very aggressive lung tumors, associated with a rapid fatal outcome, in our cohort of 293 lung tumor patients and in an external independent series of patients. Surprisingly PRL receptor expression was not detected in the vast majority of PRL-expressing lung tumors. Additionally, the analysis of the PRL transcripts in lung tumors and cell lines revealed systematic truncations of their 5' regions, including the signal peptide-encoding portions. PRL expression was found to sustain cancer-specific gene expression circuits encompassing genes that are normally responsive to hypoxia. Interestingly, this analysis also indicated that histone deacetylase (HDAC) inhibitors could counteract the PRL-associated transcriptional activity. INNOVATION AND
conclusionAltogether, this work not only unravels a yet unknown oncogenic mechanism but also indicates that the specific category of PRL-expressing aggressive lung cancers could be particularly responsive to an HDAC inhibitor-based treatment.
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Registered trials
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.