This case demonstrates the importance of history, physical examination and clinical judgement in the diagnosis of this rare disease. It also highlights the vital role played by the liver in the GH/IGF-1 axis.
This FOSB-mediated upregulation of IGFBP5 expression subsequently weakened the susceptibility of IGF1R to IGF-1 stimulation and suppressed the downstream PI3K/Akt and Ras/Raf/ERK oncogenic pathways. Our findings identify the novel FOSB-IGFBP5-IGF-1 axis upstream of PI3K/Akt and Ras/Raf/ERK signalling as a key regulator of PCa progression.
6 days ago
Journal
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IGF1 (Insulin-like growth factor 1) • IGFBP5 (Insulin Like Growth Factor Binding Protein 5)
Growth hormone receptor (GHR) signalling enhances migratory ability of tumour cells and excess IGF-1 production promotes angiogenesis. Gaining a full understanding of the mechanisms behind GH and breast cancer will allow researchers to develop more therapeutics to treat this devastating disease.
Heart failure secondary to acromegalic cardiomyopathy occurs in approximately 3% of affected patients and is recognized as the leading cause of mortality in individuals with this condition. This case report describes a 53-year-old male diagnosed with acromegalic cardiomyopathy caused by a pituitary adenoma.
Specifically, exercise can enhance muscle protein synthesis by activating the mTOR pathway while reducing protein degradation by suppressing the expression of muscle atrophy genes. In this narrative review, we summarize the mechanisms of action of the genes associated with muscle atrophy, MuRF-1 and ATROGIN-1, and their differential expression patterns following experimental and clinical trials involving chronic and acute exercise exposure, along with other potential regulators implicated in muscle remodeling.
Thus, the tumor was definitively classified as a pituitary somatoprolactinoma. This clinical case highlights the diagnostic and therapeutic challenges associated with acromegaly, the necessity of a multidisciplinary approach, the importance of early diagnosis, and the value of long-term dynamic follow-up of patients.
Our results delineate an unfavorable, trans-chronological biological profile that identifies patients with low host reserve, largely driven by inflammaging and catabolism. This integrated signature provides a robust, objective screening tool to identify biologically frail patients, validating the need for Comprehensive Geriatric Assessment (CGA) and biomarker-guided therapeutic de-escalation (e.g., avoiding adjuvant chemotherapy) to improve individualized outcomes in oncology.