ReviewJournal of mammary gland biology and neoplasia2008
Rational design of competitive prolactin/growth hormone receptor antagonists.
Review in Journal of mammary gland biology and neoplasia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Preparation of a Growth Hormone Receptor/Prolactin Receptor Bispecific Antibody Antagonist Which Exhibited Anti-Cancer Activity.Frontiers in pharmacology · 2020Article
- Properties of antibodies to a synthetic peptide representing an epitope shared by receptors of the type I cytokine family.Clinical and experimental medicine · 2013Article
- Growth hormone receptor expression in human primary gastric adenocarcinoma.Journal of biomedical research · 2012Article
- Prolactin regulation of the prostate gland: a female player in a male game.Nature reviews. Urology · 2011Review
- Growth hormone signaling in human T47D breast cancer cells: potential role for a growth hormone receptor-prolactin receptor complex.Molecular endocrinology (Baltimore, Md.) · 2011Article
- Investigation of prolactin receptor activation and blockade using time-resolved fluorescence resonance energy transfer.Frontiers in endocrinology · 2011Article
- Extrapituitary growth hormone.Endocrine · 2010Review
- Sequence and structure continuity of evolutionary importance improves protein functional site discovery and annotation.Protein science : a publication of the Protein Society · 2010Article
- Complex prolactin crosstalk in breast cancer: new therapeutic implications.Molecular and cellular endocrinology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is increasing evidence that prolactin (PRL) and growth hormone (GH) act as growth-promoters of breast tumors. Recent arguments have accumulated to suggest that when they are locally-produced within the mammary tissue, these hormones, acting by an autocrine-paracrine mechanism may have enhanced, or even specific functions compared to endocrine PRL and GH. Classical drugs blocking pituitary hormone production (dopamine and somatostatin analogs) are ineffective on extrapituitary expression of PRL/GH genes, therefore the undesirable effects of these locally-produced hormones remain a target of interest for alternative strategies. This has encouraged the development of competitive PRL and/or GH receptor antagonists, which involve engineered variants of natural receptor ligands (PRL or GH) aimed at blocking receptor activation rather than hormone production in peripheral tissues. This article overviews the rational design of this new class of molecules, their specific molecular features (receptor specificity, biological properties, etc.) and whenever available, the data that have been obtained in cell or animal models of breast cancer.
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.