ArticleNPJ breast cancer2021
The human intermediate prolactin receptor is a mammary proto-oncogene.
Article in NPJ breast cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 26 citations in OpenAlex.
- Prolactin as a Candidate Biomarker in Non-Small Cell Lung Cancer: Implications for Personalized Medicine and Post-Treatment Risk Stratification.Journal of personalized medicine · 2026Review
- B lymphoproliferative diseases: Effective treatment, inhibited progression, and potential cures through isoform-specific targeting of the prolactin receptor.Vitamins and hormones · 2025Review
- Prolactin and DNA damage trigger an anti-breast cancer cell immune response.Frontiers in endocrinology · 2025Article
- Simple and Scalable Algorithms for Cluster-Aware Precision Medicine.Proceedings of machine learning research · 2024Article
- The Human Intermediate Prolactin Receptor I-tail Contributes Breast Oncogenesis by Targeting Ras/MAPK Pathway.Endocrinology · 2024Article
- Isoform-specific knockdown of long and intermediate prolactin receptors interferes with evolution of B-cell neoplasms.Communications biology · 2023Article
- Prolactin levels and breast cancer risk by tumor expression of prolactin-related markers.Breast cancer research : BCR · 2023Article
- Hyperprolactinaemia is common in Chinese premenopausal women with breast diseases.Frontiers in genetics · 2023Article
- PRLR and CACNA2D1 Impact the Prognosis of Breast Cancer by Regulating Tumor Immunity.Journal of personalized medicine · 2022Article
- Breast Cancer and Prolactin - New Mechanisms and Models.Endocrinology · 2022Review
- Hormones and Sex-Specific Medicine in Human Physiopathology.Biomolecules · 2022Review
- Terminal differentiation and anti-tumorigenic effects of prolactin in breast cancer.Frontiers in endocrinology · 2022Review
- Prolactin: The Third Hormone in Breast Cancer.Frontiers in endocrinology · 2022Review
- Prolactin receptor gene transcriptional control, regulatory modalities relevant to breast cancer resistance and invasiveness.Frontiers in endocrinology · 2022Review
- The Expression of Prolactin Receptors in Benign Breast Tumors Is Not Associated with Serum Prolactin Level.Journal of clinical medicine · 2021Article
- Review
- Serine residues 726 and 780 have nonredundant roles regulating STAT5a activity in luminal breast cancer.Scientific reports · 2021Article
- Article
- The human intermediate prolactin receptor is a mammary proto-oncogene.NPJ breast cancer · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The hormone prolactin (PRL) and its receptor (hPRLr) are significantly involved in breast cancer pathogenesis. The intermediate hPRLr (hPRLrI) is an alternatively-spliced isoform, capable of stimulating cellular viability and proliferation. An analogous truncated mouse PRLr (mPRLr) was recently found to be oncogenic when co-expressed with wild-type mPRLr. The goal of this study was to determine if a similar transforming event occurs with the hPRLr in human breast epithelial cells and to better understand the mechanism behind such transformation. hPRLrL+I co-expression in MCF10AT cells resulted in robust in vivo and in vitro transformation, while hPRLrI knock-down in MCF7 cells significantly decreased in vitro malignant potential. hPRLrL+I heterodimers displayed greater stability than hPRLrL homodimers, and while being capable of activating Jak2, Ras, and MAPK, they were unable to induce Stat5a tyrosine phosphorylation. Both immunohistochemical breast cancer tissue microarray data and RNA sequencing analyses using The Cancer Genome Atlas (TCGA) identified that higher hPRLrI expression associates with triple-negative breast cancer. These studies indicate the hPRLrI, when expressed alongside hPRLrL, participates in mammary transformation, and represents a novel oncogenic mechanism.
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.