Growth Hormone (GH) -secreting Pituitary Adenoma
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ABSTRACT:
PROVIDER: EGAS00001001293 | EGA |
REPOSITORIES: EGA
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Project description:We profiled the somatic landscape of 21 growth hormone (GH) -secreting pituitary adenomas using somatic copy-number alteration (SCNA), whole-genome sequencing (WGS), bisulfate sequencing, and transcriptome approaches. See details in Valimaki et al. Genetic and epigenetic characterization of growth hormone (GH) - secreting pituitary tumors. Manuscript in preparation, 2019.
| EGAS00001003488 | EGA
Project description:Objective Circulating plasma miRNAs have been increasingly studied in the field of pituitary neuroendocrine tumor (PitNET) research. Our aim was to discover circulating plasma miRNAs species associated with growth hormone (GH) secreting PitNETs and assess how the plasma levels of discovered miRNA candidates are impacted by SSA therapy and whether there is a difference in their levels between GH secreting PitNETs and other PitNET types. Methods miRNA candidates were discovered using the whole miRNA sequencing approach and differential expression analysis. Selected miRNAs were then analyzed using real-time polymerase chain reaction (qPCR). Results Whole miRNA sequencing discovered a total of 19 differentially expressed miRNAs (DEMs) in GH secreting PitNET patients' plasma 24 hours after surgery and 19 DEMs between GH secreting PitNET patients’ plasma and non-functioning (NF) PitNET patients’ plasma. Seven miRNAs were selected for further testing of which miR-625-5p, miR-503-5p miR-181a-2-3p and miR-130b-3p showed a significant downregulation in plasma after 1 month of SSA treatment. miR-181a-5p and mir-625-5p were also found to be significantly downregulated in plasma of GH secreting PitNET patients vs. NF PitNET patients. Conclusions Our study suggests that expression of plasma miRNAs miR-625-5p, miR-503-5p miR-181a-2-3p and miR-130b-3p in GH secreting PitNETs is affected by SSA treatment. Additionally, miR-625-5p and miR-181a-5p can distinguish GH secreting PitNETs from other PitNET types warranting further research on these miRNAs for treatment efficacy.
2022-02-16 | GSE196647 | GEO
Project description:This study investigated differential gene expression between granulation patterns in growth hormone (GH)-secreting pituitary tumors, aiming to elucidate novel transcriptomes that explain clinical variances in patients with acromegaly. Transcriptome analysis was conducted on 6 normal pituitary tissues and 15 GH-secreting pituitary tumors, including 9 densely granulated somatotroph tumors (DGSTs) and 6 sparsely granulated somatotroph tumors (SGSTs). We identified 3111 differentially expressed genes (DEGs) in tumors compared to normal pituitaries, with 1117 DEGs unique to a specific granulation within tumors. SGST showed enrichment of neuronal development and acute inflammatory response pathways, along with a significant enhancement of JAK–STAT, phosphatidylinositol 3-kinase, and MAPK signaling. The results suggest that granulation-specific gene expression may underpin diverse clinical presentations in acromegaly, highlighting the potential for further investigation into these transcriptomic variations and their roles in disease pathology, particularly the involvement of genes linked to neuronal development, inflammatory response, and JAK–STAT signaling in SGST.
2024-04-28 | GSE264621 | GEO
Project description:Prader-Willi Syndrome (PWS) is a complex genetic disorder resulting from the deficiency of several maternally imprinted genes, including SNORD116, in the 15q11-q13 region. Loss of Snord116 in mice recapitulates some of the most salient clinical features of PWS, including growth hormone (GH) deficiency and hypogonadism. This study explored the impact of Snord116 deficiency on early postnatal pituitary development and growth in Snord116 KO mice. Snord116 was found to be expressed in both anterior and posterior pituitary. Pituitary transcriptomes of Snord116 KO and wild-type (WT) mice at two developmental stages, postnatal day 0 (P0) and 4 weeks of age, were interrogated and related to ex vivo analyses of GH secretion in the pituitaries of 5-week-old mice. Significant differences in pituitary transcriptomes were detected between Snord116 KO and WT mice at 4 weeks of age but not at P0. The differentially expressed genes and affected molecular pathways play important roles in regulating embryonic and postnatal pituitary development. Our results suggested that PWS GH deficiency was mainly due to pituitary hypoplasia and decreased GH production but not to reduced GH secretory function per se, implicating Snord116 in the specific molecular/cellular pathways that account for impaired postnatal pituitary development and GH deficiency in PWS.
2026-07-30 | GSE333730 | GEO
Project description:We performed single-cell transcriptomic profiling of a pituitary adenoma from a patient with a rare subtype of Cushing's disease using the 10x Genomics platform. The analysis revealed the cellular landscape of the tumor, identifying distinct cell populations, their transcriptional signatures, and the degree of intratumoral heterogeneity. These findings provide insights into the cellular architecture of this uncommon ACTH-secreting pituitary adenoma variant.
2026-07-07 | GSE337357 | GEO
Project description:Gene alteration analysis on 121 GH-producing pituitary adenomas and non-target proteomics analysis with RNA sequencing analysis on 45 non-functioning pituitary adenomas (NFPAs) and 60 growth hormone (GH)-producing pituitary adenomas were performed, and integrated these results with the clinical characteristics of acromegaly. We attempted to identify key players involved in shaping the clinical features of acromegaly, especially those related to treatment efficacy. This project revealed the importance of GNAS mutations in terms of clinical and biochemical characteristics and identified novel molecules that may be involved in the responsiveness to medical treatment.
2022-11-24 | PXD036604 | JPOST Repository
Project description:Aging is associated with appearance of senescent cells secreting the senescence-associated secretome facilitating a milieu favoring age-related changes in microenvironment. Previously, we showed accumulation and secretion of local non-pituitary growth hormone (npGH) in senescent colon epithelial cells. Here, we elucidate mechanisms underlying npGH action in the non-tumorous colon tissue microenvironment. We demonstrate autocrine npGH action in normal human colon cells (hNCC) infected with lentivirus expressing hGH (lentiGH), as well as paracrine npGH action in hNCC cocultured with lentiGH hNCC and in intact human 3-dimensional intestinal organoids co-cultured with organoids infected with lentiGH. Enriched gene ontology and pathway analysis of intact organoids exposed to paracrine npGH identified distorted extracellular matrix (ECM) and focal adhesion pathways concurrent with altered expression of ECM and cytoskeletal proteins. Significant phosphoprotein changes associated with cytoskeleton and cell migration pathway occurred in GH-exposed hNCC. Paracrine npGH triggers these changes by activating epithelial-mesenchymal transition, as shown by suppression of E-cadherin and induction of Twist2 in cellular models, as well as in the colon of nude mice harboring GH-secreting xenografts. These changes are consistent with observed increased migration of hNCC overexpressing lentiGH, or in those co-cultured with GH-secreting hNCC or with GH-secreting normal colon fibroblasts. Furthermore, whole exome sequencing detected increased cell copy number alterations in intact organoids co-cultured with lentiGH-infected organoids, likely as a consequence of GH-mediated suppressed DNA damage repair thereby favoring cell transformation. Our results indicate that accumulated npGH in aging tissue enables a microenvironment landscape favoring age-associated pro-proliferative changes.
2025-01-08 | MSV000096807 | MassIVE
Project description:Acromegaly is a severe and life-threatening disease caused by persistent excess of growth hormone (GH) which stimulates the synthesis and secretion of insulin-like growth factor-1 (IGF-1). In the majority (95%) of patients acromegaly is caused by sporadic GH-secreting neuroendocrine pituitary tumor (PitNET). Acromegaly-causing tumors are histologically diverse. The aim was to determine transcriptomic profiles in different histological subtypes and evaluate clinical implication of differential gene expression.
2022-12-01 | E-MTAB-11889 | biostudies-arrayexpress
Project description:Recurrent single-nucleotide and small indel somatic mutations were infrequent among the three adenoma subtypes. However, somatic copy-number alterations (SCNA) were identified in all three pituitary adenoma subtypes. Methylation analysis revealed adenoma subtype-specific DNA methylation profiles, with GHsecreting adenomas being dominated by hypomethylated sites. Likewise, gene-expression patterns revealed adenoma subtype-specific profiles. Integrating DNA methylation and gene-expression data revealed that hypomethylation of promoter regions are related with increased expression of GH1 and SSTR5 genes in GH-secreting adenomas and POMC gene in ACTH secreting adenomas. Finally, multispectral IHC staining of immune-related proteins showed abundant expression of PD-L1 among all three adenoma subtypes.
2020-03-26 | GSE147548 | GEO
Project description:Growth hormone receptor deficiency (GHRD) results in low serum insulin-like growth factor 1 but high, non-functional GH levels. This study investigates the histomorphological and molecular alterations associated with GHRD. Pituitary glands from 6 months old GHR-KO pigs and control animals were compared using a quantitative stereological approach and label-free proteomics.
2023-05-12 | PXD035833 | Pride