Subtype‐specific enhancer RNAs define transcriptional regulators and prognosis in breast cancers
This study employed machine learning methodologies to perform the subtype‐specific classification of RNA‐seq data sets, which are mapped on enhancers from TCGA‐derived breast cancer patients. Their integration with gene expression (referred to as ProxCReAM eRNAs) and chromatin accessibility profiles has the potential to identify lineage‐specific and ...
Aamena Y. Patel +6 more
wiley +1 more source
Hedgehog Signalling in Androgen Independent Prostate Cancer [PDF]
Objectives: Androgen-deprivation therapy effectively shrinks hormone-naïve prostate cancer, both in the prostate and at sites of distant metastasis.
Bisson, Isabelle +7 more
core +1 more source
Tumors contain diverse cellular states whose behavior is shaped by context‐dependent gene coordination. By comparing gene–gene relationships across biological contexts, we identify adaptive transcriptional modules that reorganize into distinct vulnerability axes.
Brian Nelson +9 more
wiley +1 more source
Growth Hormone (GH)-Releasing Peptide Stimulation of GH Release from Human Somatotroph Adenoma Cells: Interaction with GH-Releasing Hormone, Thyrotropin- Releasing Hormone, and Octreotide. [PDF]
The synthetic hexapeptide GH-releasing peptide (GHRP; His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) specifically stimulates GH secretion in humans in vivo and in animals in vitro and in vivo via a still unknown receptor and mechanism.
Brockmeier, S. +7 more
core +1 more source
COMP–PMEPA1 axis promotes epithelial‐to‐mesenchymal transition in breast cancer cells
This study reveals that cartilage oligomeric matrix protein (COMP) promotes epithelial‐to‐mesenchymal transition (EMT) in breast cancer. We identify PMEPA1 (protein TMEPAI) as a novel COMP‐binding partner that mediates EMT via binding to the TSP domains of COMP, establishing the COMP–PMEPA1 axis as a key EMT driver in breast cancer.
Konstantinos S. Papadakos +6 more
wiley +1 more source
Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer
Dysregulation of the Hippo pathway drives nuclear accumulation of YAP/TAZ, activating stemness‐related transcriptional programs that sustain breast cancer stemness and fuel therapeutic resistance across subtypes, underscoring Hippo signaling as a targetable vulnerability. Figure created and edited with BioRender.com.
Giulia Schiavoni +11 more
wiley +1 more source
Vitamin D and growth hormone in children: a review of the current scientific knowledge
Background Human growth is a complex mechanism that depends on genetic, environmental, nutritional and hormonal factors. The main hormone involved in growth at each stage of development is growth hormone (GH) and its mediator, insulin-like growth factor ...
Susanna Esposito +5 more
doaj +1 more source
RNAseq analysis of fast skeletal muscle in restriction-fed transgenic coho salmon (Oncorhynchus kisutch) : an experimental model uncoupling the growth hormone and nutritional signals regulating growth [PDF]
Background Coho salmon (Oncorhynchus kisutch) transgenic for growth hormone (Gh) express Gh in multiple tissues which results in increased appetite and continuous high growth with satiation feeding. Restricting Gh-transgenics to the same lower ration (TR)
Devlin, Robert +2 more
core +2 more sources
KDM7A and KDM1A inhibition suppresses tumour promoting pathways in prostate cancer
Treatment resistance is a major challenge for patients with advanced prostate cancer. This study examined an alternative approach to target the major prostate cancer‐promoting pathway by targeting epigenetic factors, whose levels are higher in tumours.
Jennie N Jeyapalan +16 more
wiley +1 more source
Attribution of ghrelin to cancer; Attempts to unravel an apparent controversy [PDF]
Ghrelin is an endogenous peptide hormone mainly produced in the stomach. It has been known to regulate energy homeostasis, stimulate secretion of growth hormone, and mediate many other physiologic effects. Various effects attributed to ghrelin contribute
Khani, Leila +5 more
core +1 more source

