Introdução
O que você precisa saber de cara
Um adenoma de hipófise é um tumor que ocorre na glândula hipófise. A maioria dos tumores hipofisários é benigna, aproximadamente 35% são invasivos e apenas 0,1% a 0,2% são carcinomas. Adenomas de hipófise representam de 10% a 25% de todas as neoplasias intracranianas, com uma taxa de prevalência estimada na população geral de aproximadamente 17%.
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Entender a doença
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Sinais e sintomas
O que aparece no corpo e com que frequência cada sintoma acontece
Linha do tempo da pesquisa
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Genética e causas
O que está alterado no DNA e como passa nas famílias
Genes associados
2 genes identificados com associação a esta condição.
May act as a negative regulator of Aurora-A kinase, by down-regulation through proteasome-dependent degradation
Mitochondrion matrixNucleus
Essential component of a MLL/SET1 histone methyltransferase (HMT) complex, a complex that specifically methylates 'Lys-4' of histone H3 (H3K4). Functions as a transcriptional regulator. Binds to the TERT promoter and represses telomerase expression. Plays a role in TGFB1-mediated inhibition of cell-proliferation, possibly regulating SMAD3 transcriptional activity. Represses JUND-mediated transcriptional activation on AP1 sites, as well as that mediated by NFKB subunit RELA. Positively regulates
Nucleus
Familial multiple endocrine neoplasia type I
Autosomal dominant disorder characterized by tumors of the parathyroid glands, gastro-intestinal endocrine tissue, the anterior pituitary and other tissues. Cutaneous lesions and nervous-tissue tumors can exist. Prognosis in MEN1 patients is related to hormonal hypersecretion by tumors, such as hypergastrinemia causing severe peptic ulcer disease (Zollinger-Ellison syndrome, ZES), primary hyperparathyroidism, and acute forms of hyperinsulinemia.
Variantes genéticas (ClinVar)
1,066 variantes patogênicas registradas no ClinVar.
Vias biológicas (Reactome)
11 vias biológicas associadas aos genes desta condição.
Diagnóstico
Os sinais que médicos procuram e os exames que confirmam
Tratamento e manejo
Remédios, cuidados de apoio e o que precisa acompanhar
Onde tratar no SUS
Hospitais de referência no Brasil e o protocolo oficial do SUS (PCDT)
🇧🇷 Atendimento SUS — Adenoma hipofisário nulo
Selecione um estado ou use sua localização para ver resultados.
Dados de DATASUS/CNES, SBGM, ABNeuro e Ministério da Saúde. Sempre confirme a disponibilidade diretamente com o estabelecimento.
Pesquisa ativa
Ensaios clínicos abertos e novidades científicas recentes
Pesquisa e ensaios clínicos
Nenhum ensaio clínico registrado para esta condição.
Publicações mais relevantes
Transcription Factor-Based Classification of Pituitary Neuroendocrine Tumors: Practical Immunohistochemical Algorithms, Molecular Correlates, and Diagnostic Challenges in the 5th WHO Era.
Pituitary neuroendocrine tumors (PitNETs) constitute a significant proportion of primary intracranial neoplasms and were historically differentiated based on clinical hormone excess syndromes and tinctorial properties. The 5th edition of the WHO classification introduces a paradigm shift towards the lineage-based taxonomy based on the cell-specific expression of transcription factors (TFs). This overview focuses on the biological justifications and diagnostic value of the core TFs of Pituitary-Specific Positive Transcription Factor 1 (PIT1), T-Box Pituitary Transcription Factor (TPIT), and Steroidogenic Factor 1 (SF1), which signify the somatotroph, lactotroph, thyrotroph, corticotroph, and gonadotroph lineages, respectively. By focusing on TF expressions instead of hormone immunoreactivity, pathologists can better subtype clinically non-functioning tumors, effectively relegating the previously overutilized null cell category to about 1% of cases. The TF-based classification is also essential in discriminating high-risk histotypes of silent corticotroph tumors, sparsely granulated somatotrophs, and immature PIT1-lineage PitNETs, which are linked to a higher invasiveness and recurrence. We suggest a practical, stepwise immunohistochemical diagnostic algorithm with the integration of ancillary markers (e.g., GATA3 and ERα) to refine lineage assignment. New molecular correlates such as GNAS and USP8 mutations also add to this framework and guide the use of individualized treatment involving somatostatin analogs or dopamine agonists. And lastly, we discuss the ongoing issues of diagnosis of triple-negative and multilineage tumors and the growing importance of DNA methylation profiling and artificial intelligence in standardized reporting and improving precision management.
The Spectrum of Serum Prolactin Levels in Patients with Non-Functioning Sellar Masses: A Retrospective Analysis.
Differentiating prolactinomas from non-functioning sellar masses causing hyperprolactinemia due to stalk effect is a common diagnostic challenge. While both can result in elevated serum prolactin, accurate discrimination is essential for appropriate management. To determine the upper limit of serum prolactin in non-functioning sellar masses attributable to stalk effect. This retrospective study was conducted at a tertiary care center in South India from January 2015 to December 2024. Patients with both non-pituitary sellar masses and pituitary tumors with negative prolactin immunohistochemistry were included. Patients with functioning pituitary adenomas, hyperprolactinemia-inducing drugs, chronic kidney disease, severe hepatic dysfunction, and PCOS were excluded. The primary objective was to determine the upper limit of serum prolactin levels attributable to stalk effect in patients with non-functioning sellar masses. Preoperative serum prolactin levels were measured using a chemiluminescent immunoassay. The 97th percentile value was taken as the upper limit. Of 288 cases of non-functioning sellar masses, 57 met inclusion criteria. Most of them (87.7%, 50/57) were >1 cm, with 68% (39/57) classified as pituitary adenomas-49% (19/39) being gonadotroph adenomas and 41% (16/39) null cell adenomas. Hyperprolactinemia was observed in 32% of patients. The median serum prolactin level was 14.8 ng/mL, and the 97th percentile was 70 ng/ml. No significant correlation was found between tumor size and serum prolactin level (r = 0.13, P = 0.35). Gender did not significantly affect serum prolactin levels. A serum prolactin threshold of 70 ng/mL was identified, above which non-functioning sellar masses are highly unlikely. In patients with non-functioning sellar masses, serum prolactin levels rarely exceed 70 ng/ml. This threshold may serve as a useful diagnostic marker to distinguish stalk effect from prolactinomas. Prospective validation in larger cohorts is warranted.
Contrast Enhanced T2-Weighted STIR Imaging of Pituitary Adenomas.
This technical report presents the application of a post contrast T2-weighted STIR sequence for improved visualization of pituitary adenomas. Although STIR is traditionally employed to null fat signal, it is typically avoided in post-contrast imaging due to the hypointense appearance of both fat and gadolinium enhanced tissues. Our approach exploits this characteristic to render the normal enhancing pituitary gland hypointense, thereby allowing the adenoma to remain hyperintense and thus increasing its conspicuity.
Biomarkers Driving Precision Medicine in Nonfunctioning Pituitary Neuroendocrine Tumors: A Systematic Review of Recent Literature.
Nonfunctioning pituitary neuroendocrine tumors (NF-PitNETs) display considerable biological heterogeneity, posing challenges for accurate prognostication and personalized management. This systematic review, conducted in Scopus and Web of Science in accordance with PRISMA 2020, identified 29 primary studies and categorized all molecular findings into 3 core themes: (1) invasion biology and epithelial-mesenchymal transition (EMT); (2) noncoding RNAs and liquid biopsy markers; and (3) multiomics, epigenetic, and prognostic signatures. Within the invasion/EMT theme, gonadotroph tumors consistently demonstrated the strongest EMT-linked activity, including SNAI-mediated transitions, Vimentin upregulation, and β-catenin alterations. Corticotroph tumors showed intermediate EMT involvement, while null-cell tumors exhibited invasion patterns driven mainly by hypoxia-related protease dysregulation rather than EMT. In the noncoding RNA and circulating biomarker theme, several candidates, including exosomal miR-486-5p, miR-151a-5p, and exosomal MMP1, have shown diagnostic or prognostic value, although subtype specificity remains limited. The multiomics and epigenetic theme revealed subtype-dependent molecular programs: gonadotroph tumors were associated with PI3K-AKT pathway enrichment and SF-1 labeling heterogeneity; recurrent lesions showed elevated nuclear pEGFR T693 and MCM7; while DNA methylation mapping identified subtype-relevant loci such as NUP93, LGALS1, and GABRA1. Phosphoproteomic and acetylomic profiling further highlighted alterations in metabolic, kinase-driven, and cell-adhesion pathways linked to invasion and recurrence. Overall, the lineage-aligned synthesis indicates that NF-PitNETs progress through diverse molecular pathways, with each subtype dominated by distinct regulatory networks. Although many biomarkers show promise, most remain exploratory, highlighting the need for harmonized methods and multicenter validation to support precision diagnostics and prognostic modeling.
The Roles of PD-L1, Ki-67, P53, and Cyclin D1 in PitNETs: Diagnostic and Prognostic Implications in a Series of 74 Patients.
Pituitary neuroendocrine tumors (PitNETs), also known as pituitary adenomas, are rare tumors that are usually benign. At present, the WHO PitNET classification based on transcription factors is in force. A problem is caused by invasive tumors and silent tumors which, despite a lack of obvious clinical symptoms, tend to behave aggressively. Factors influencing the clinical course of these tumors are currently being sought. The aim of our study was to assess the expression of programmed death-ligand 1 (PD-L1) and proliferation biomarkers (Ki-67, cyclin D1, and P53) in PitNETs depending on the transcription factor and adenoma subtype. The analysis was performed in seventy-four patients operated on in a single neurosurgical center for pituitary tumors. Immunohistochemistry was performed for transcription factors and biomarkers-PD-L1, Ki-67, P53, and cyclin D1-in tissue microarray format. Membranous expression of PD-L1 was scored as 0 (no expression) and ≥1%. Nuclear expression of Ki-67 was scored at <3% and ≥3%, and the expression of P53 and cyclin D1 was scored at <10% and ≥10%. The following tumors expressed PD-L1 at ≥1%: gonadotroph, 21 (28.4%); corticotroph, 5 (6.7%); gonadotroph/lactotroph, 2 (2.7%); null cell adenoma, 3 (4.0%); multiple synchronous PitNET, 2 (2.7%); immature PIT-1 tumor, 1 (1.3%); mature PIT-1 tumor, 1 (1.5%). Ki-67 ≥ 3% was found in the following PitNETs: gonadotroph, 3 (4.0%); corticotroph, 2 (2.7%); lactotroph, 1 (1.3%); multiple synchronous PitNET, 1 (1.3%); immature PIT-1 tumor, 1 (1.3%); and mature PIT-1 tumor, 1 (1.3%). Patients with Ki-67 ≥ 3% were statistically significantly younger (p = 0.03). All tumors (100%) with a combination of cyclin D1 ≥ 10% and P53 < 10% were invasive on the Hardy scale. Of the four factors, PD-L1 increased the odds of invasiveness the most (adjusted OR = 2.35; 95% CI: 0.56-9.90). PD-L1 expression was present in some types of PitNETs. PD-L1 expression may help in identifying null cell adenomas. High cyclin D1 with low P53 may indicate greater tumor invasiveness.
Publicações recentes
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📚 EuropePMCmostrando 130
Transcription Factor-Based Classification of Pituitary Neuroendocrine Tumors: Practical Immunohistochemical Algorithms, Molecular Correlates, and Diagnostic Challenges in the 5th WHO Era.
International journal of molecular sciencesThe Spectrum of Serum Prolactin Levels in Patients with Non-Functioning Sellar Masses: A Retrospective Analysis.
Neurology IndiaContrast Enhanced T2-Weighted STIR Imaging of Pituitary Adenomas.
AJNR. American journal of neuroradiologyAssociation Between the Ki-67 Index, Tumor Size and Postoperative Structural Persistence in Non-functioning Pituitary Neuroendocrine Tumors: A Single-Center Experience.
CureusBiomarkers Driving Precision Medicine in Nonfunctioning Pituitary Neuroendocrine Tumors: A Systematic Review of Recent Literature.
The Journal of clinical endocrinology and metabolismThe Roles of PD-L1, Ki-67, P53, and Cyclin D1 in PitNETs: Diagnostic and Prognostic Implications in a Series of 74 Patients.
International journal of molecular sciencesDevelopmental Plasticity and Stromal Co-option Shape a Pituitary Neuroendocrine Tumor Transcriptional Continuum.
bioRxiv : the preprint server for biologyAn Old New Friend: Folliculo-Stellate Cells in Pituitary Neuroendocrine Tumors.
CellsTranscription factor-based classification of pituitary adenomas / PitNETs: a comparative analysis and clinical implications across WHO 2004, 2017 and 2022 in 921 cases.
Acta neuropathologica communicationsSpatial transcriptomics reveal PI3K-AKT and metabolic alterations in aggressive, treatment-resistant lactotroph pituitary neuroendocrine tumors.
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Endocrine pathologyAssociações
Organizações que acompanham esta doença — pra ter apoio e orientação
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Referências e fontes
Bases de dados externas citadas neste artigo
Publicações científicas
Artigos indexados no PubMed ligados a esta doença no grafo RarasNet — título, periódico e PMID direto da fonte, sem intermediação de IA.
- Transcription Factor-Based Classification of Pituitary Neuroendocrine Tumors: Practical Immunohistochemical Algorithms, Molecular Correlates, and Diagnostic Challenges in the 5th WHO Era.
- The Spectrum of Serum Prolactin Levels in Patients with Non-Functioning Sellar Masses: A Retrospective Analysis.
- Contrast Enhanced T2-Weighted STIR Imaging of Pituitary Adenomas.
- Biomarkers Driving Precision Medicine in Nonfunctioning Pituitary Neuroendocrine Tumors: A Systematic Review of Recent Literature.
- The Roles of PD-L1, Ki-67, P53, and Cyclin D1 in PitNETs: Diagnostic and Prognostic Implications in a Series of 74 Patients.
- Genetic and non-genetic factors influencing phenotypic variability in neurofibromatosis type 1.
- Real-time breath metabolomics as catalyst for personalized lung cancer diagnostics: prospective matched case-control trial (LUCAbreath).
- The mutational burden in os odontoideum patients.
- European Reference Networks - a flagship activity of the EU in the field of rare and complex diseases: from 2017 to 2025.
- Clinical characteristics and long-term prognosis of anti-MDA5-positive dermatomyositis: a comparative study across age groups.
Bases de dados e fontes oficiais
Identificadores e referências canônicas usadas para montar este verbete.
- ORPHA:314790(Orphanet)
- MONDO:0017826(MONDO)
- GARD:21393(GARD (NIH))
- Variantes catalogadas(ClinVar)
- Busca completa no PubMed(PubMed)
- Q55787421(Wikidata)
Dados compilados pelo RarasNet a partir de fontes abertas (Orphanet, OMIM, MONDO, PubMed/EuropePMC, ClinicalTrials.gov, DATASUS, PCDT/MS). Este conteúdo é informativo e não substitui avaliação médica.
Conteúdo mantido por Agente Raras · Médicos e pesquisadores podem colaborar
