Pituitary neuroendocrine tumors (PitNETs) are common intracranial neoplasms with heterogeneous hormonal activity, invasiveness, and treatment response. Conventional MRI is central to diagnosis, but is limited in quantifying tumor heterogeneity and predicting clinically relevant features such as consistency, molecular subtype, proliferation, and clinical outcomes. To review current evidence on MRI-based radiomics and artificial intelligence (AI) in PitNETs, focusing on clinical applications, methodological quality, and future integration into precision medicine. Narrative review of studies published between 2019 and 2025 evaluating radiomics, machine learning, and deep learning applied to PitNETs, highlighting tumor consistency, molecular and histological subtypes, proliferation, invasiveness, treatment response, recurrence, visual outcomes, and differential diagnosis of sellar lesions. Radiomics has been applied across the PitNET clinical trajectory. Texture- and shape-based features from T2-weighted and multiparametric MRI predict intraoperative tumor consistency with AUCs often > 0.80, outperforming conventional radiology. Radiomic signatures allow non-invasive differentiation of functional vs. non-functional adenomas, somatotroph granulation patterns, silent corticotroph adenomas, prolactinomas, and prediction of Ki-67 and PIT-1 expression. Models also predict cavernous sinus invasion, postoperative regrowth, recurrence, visual outcomes, and treatment response, including dopamine-agonist therapy. Differential diagnosis of hypophysitis and Rathke's cleft cyst has also been explored. Methodological quality remains heterogeneous, with frequent single-center, retrospective designs, limited external validation, and suboptimal adherence to reporting guidelines. Radiomics and AI show promise for risk stratification and personalized therapy in PitNETs, particularly for predicting tumor consistency, molecular subtypes, and recurrence. Clinical implementation requires standardized imaging protocols, multicenter datasets, reproducible segmentation, interpretable models, and prospective validation.
Sabina Ruiz, Anna Oliva, Roger Mateu et al.· Reviews in Endocrine & Metab...· 0 citations
Impaired muscle quality in patients with Cushing's syndrome (CS) and Acromegaly (ACRO) is associated with persistent muscle weakness, altered physical function, and reduced quality of life (QoL), even after long-term biochemical control. The mechanisms underlying sustained myopathy remain unclear.
We hypothesized that skeletal muscle retains a lasting molecular memory of prior hormonal excess.
We performed a multi-omic analysis of rectus femoris muscle samples from hormonally controlled patients with CS (n=6) and ACRO (n=7), all in remission for at least 5 years. Mass spectrometry-based proteomics and phosphoproteomics were integrated with DNA methylation profiling.
Both diseases displayed homogeneous and distinct proteomic signatures. ACRO samples showed 328 differentially expressed (DE) proteins and 1,111 phosphopeptides, consistent with metabolic reprogramming toward glycolysis, structural remodeling associated with hypertrophy, and impaired calcium handling. CS samples exhibited 274 DE proteins and 118 phosphopeptides, reflecting a catabolic phenotype characterized by activation of the ubiquitin–proteasome system and oxidative stress pathways. Comparative analysis revealed a convergent reduction in muscle plasticity, with nearly 50% of DE proteins shared between conditions and enriched in pathways related to metabolic stress adaptation and protein quality control. Both diseases also exhibited selective hypophosphorylation of histone H1.4 and coordinated DNA methylation changes at HOX loci on chromosomes 7 and 12.
These findings support the existence of a persistent molecular footprint in skeletal muscle after biochemical remission. A shared epigenetic memory of prior GH or cortisol excess may contribute to long-term muscle dysfunction and represents a potential target for therapeutic intervention.
J. Gil, L. M. Duguech, R. Díaz et al.· European Journal of Endocrin...· 0 citations
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