ArticleOncogene2010
Janus kinase 2 is required for the initiation but not maintenance of prolactin-induced mammary cancer.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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.
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.
Who cites it
36 citing papers in PubMed, 49 citations in OpenAlex.
- An In Silico Approach to Uncover Selective JAK1 Inhibitors for Breast Cancer from Life Chemicals Database.Applied biochemistry and biotechnology · 2025Article
- The influence of two neurohormones on breast cancer: prolactin and melatonin.Revista da Associacao Medica Brasileira (1992) · 2025Article
- Modulation of JAK-STAT Signaling by LNK: A Forgotten Oncogenic Pathway in Hormone Receptor-Positive Breast Cancer.International journal of molecular sciences · 2023Review
- Dual recombinase action in the normal and neoplastic mammary gland epithelium.Scientific reports · 2021Article
- Article
- Inhibition of the Activity of Cyclophilin A Impedes Prolactin Receptor-Mediated Signaling, Mammary Tumorigenesis, and Metastases.iScience · 2020Article
- Article
- Janus Kinase 1 Plays a Critical Role in Mammary Cancer Progression.Cell reports · 2018Article
- Cyclophilin A Function in Mammary Epithelium Impacts Jak2/Stat5 Signaling, Morphogenesis, Differentiation, and Tumorigenesis in the Mammary Gland.Cancer research · 2018Article
- Developmental Contribution of Wnt-signal-responsive Cells to Mouse Reproductive Tract Formation.Acta histochemica et cytochemica · 2017Article
- Crosstalk between STAT5 activation and PI3K/AKT functions in normal and transformed mammary epithelial cells.Molecular and cellular endocrinology · 2017Review
- Elevated collagen-I augments tumor progressive signals, intravasation and metastasis of prolactin-induced estrogen receptor alpha positive mammary tumor cells.Breast cancer research : BCR · 2017Article
- Generation of Janus kinase 1 (JAK1) conditional knockout mice.Genesis (New York, N.Y. : 2000) · 2016Article
- HDAC6 Deacetylates HMGN2 to Regulate Stat5a Activity and Breast Cancer Growth.Molecular cancer research : MCR · 2016Article
- Janus Kinase 1 Is Essential for Inflammatory Cytokine Signaling and Mammary Gland Remodeling.Molecular and cellular biology · 2016Article
- Src tyrosyl phosphorylates cortactin in response to prolactin.Biochemical and biophysical research communications · 2015Article
- Chlorpromazine-Induced Hyperprolactinemia on Rat's Uterus.Iranian biomedical journal · 2015Article
- Modeling prolactin actions in breast cancer in vivo: insights from the NRL-PRL mouse.Advances in experimental medicine and biology · 2015Article
- Mouse models of breast cancer.Methods in molecular biology (Clifton, N.J.) · 2015Article
- STAT3 activation is required for the antiapoptotic effects of prolactin in cervical cancer cells.Cancer cell international · 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
4 authors at 2 institutions in 1 country.
Funding
Abstract
The prolactin receptor (PRLR), its associated Janus kinase 2 (Jak2) and the signal transducer and activator of transcription 5 (Stat5) are essential for normal mammary gland development. Owing to the upregulation of the PRLR and the local synthesis of its ligand in neoplastic cells, it has been proposed that PRL can act as a local growth factor in human breast cancers. This notion is supported by experimental evidence in transgenic mice, which showed that the mammary-specific expression of PRL contributes to carcinogenesis in vivo. To assess the importance of Jak2/Stat5 signaling during mammary cancer initiation and progression, we generated a PRL-induced mammary cancer model that allows the functional ablation of the Jak2 gene in the mammary epithelium before and after neoplastic transformation. Collectively, the results of this study show that the functional ablation of Jak2 protects against the onset of PRL-induced mammary tumorigenesis, suggesting that targeting this kinase is a relevant strategy for mammary cancer prevention. Surprisingly, Jak2 deficiency did not affect the growth and survival of PRL-induced mammary cancer cells in culture and in vivo. Consequently, Jak2 cannot be a sole therapeutic target to treat the established disease. PRL-induced mammary cancers exhibited an upregulation of ErbB2 and other ErbB receptor tyrosine kinases that may supersede the functionality of PRLR signaling through Jak2.
Indexed as
Identifiers
What OpenQuestion holds
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.