Evidence map›Paper›PMID 39579326›Full record

ArticleEndocrine pathology2024

Multilineage Pituitary Neuroendocrine Tumors Expressing TPIT and SF1: A Clinicopathological Series of Six Tumors.

Sylvia L Asa, Gregg H Faiman, Amr Mohamed, Ozgur Mete

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Article in Endocrine pathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

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6citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Sylvia L AsaDepartment of Pathology, Institute of Pathology, University Hospitals Cleveland Medical Center, Case Western Reserve University, 11100 Euclid Avenue, Room 204, Cleveland, OH, 44106, USA. Pathlady01@gmail.com.ORCID http://orcid.org/0000-0001-8418-5054
Gregg H FaimanDepartment of Medicine, Division of Endocrinology, University Hospitals Cleveland, Case Western Reserve University, Cleveland, OH, 44106, USA.
Amr MohamedDepartment of Medical Oncology, Seidman Cancer Center, University Hospitals Cleveland, Case Western Reserve University, Cleveland, OH, 44106, USA.ORCID http://orcid.org/0000-0002-6962-3535
Ozgur MeteDerpartment of Pathology, Department of Laboratory Medicine and Pathology, University Health Network, University of Toronto, Toronto, ON, M5G2C4, Canada. ozgur.mete2@uhn.ca.ORCID http://orcid.org/0000-0003-0469-2801

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumors of adenohypophysial hormone-secreting cells, now classified as pituitary neuroendocrine tumors (PitNETs), have been subclassified based on cell differentiation. Normal adenohypophysial cells have three lineages of differentiation driven by the transcription factors PIT1, TPIT, and SF1 which are responsible for the regulation of hormone gene expression; PIT1 drives expression of GH, PRL, and TSH, TPIT is required for POMC expression that gives rise to ACTH, and SF1 is the transcription factor responsible for FSH and LH expression. The vast majority of PitNETs follow these three lineage differentiation pathways but rare PitNETs show either no lineage differentiation or express biomarkers of more than one lineage. The recent WHO classification continued the terminology "plurihormonal" for tumors that have features of more than one lineage but a better term is "multilineage" since some tumors may express more than one lineage-specific transcription factor without the hormones that are driven by those factors. Recent data indicate that tumors with expression of PIT1 and SF1 are the most common multilineage PitNETs. Here we report the existence of rare PitNETs that express TPIT and SF1. The 6 patients (5 female, 1 male; mean age 54.8 years; range 35-84 years) represent less than 1% of patients in our series of PitNETs. Most patients had clinically silent tumors with no evidence of hormone excess and variable degrees of hypopituitarism; two had Cushing disease. All patients had macrotumors with a mean tumor size of 2.46 cm (range 1.1-5.0 cm). Crooke's hyaline change was identified in the nontumorous adenohypophysis of the two patients with Cushing disease. The mean Ki67 labeling index was 2.91% (range 2.03-3.94%). All tumors were negative for PIT1 and PIT1-lineage hormones (GH, PRL, and TSH). TPIT was focal in one tumor, and the remaining tumors had diffuse reactivity in more than 50% of tumor cells. SF1 expression was focal in 5 tumors and diffuse in one. Three tumors had variable expression of at least one gonadotropin (FSH or LH). GATA3 was expressed in two tumors. Variable ER-alpha expression was noted in three tumors. CAM5.2 was positive in all tumors. With the exception of two tumors causing Cushing disease, p27 expression was intact. Our study confirms that multilineage PitNETs expressing TPIT and SF1 occur but are extremely rare; they can be clinically non-functional or can cause Cushing disease. Irrespective of functional status of a PitNET, routine application of pituitary transcription factors is warranted to identify these tumors. Data on the molecular correlates and clinical significance are still needed for these rare multilineage PitNETs.

Indexed as

Neuroendocrine TumorsPituitary NeoplasmsSteroidogenic Factor 1T-Box Domain ProteinsAdultAgedBiomarkers, TumorCell LineageDNA-Binding ProteinsFemaleHumansMaleMiddle AgedTranscription FactorsBiomarkers, TumorDNA-Binding ProteinsNR5A1 protein, humanSteroidogenic Factor 1T-Box Domain ProteinsTranscription FactorsTTF1 protein, humanACTHCushing diseaseER-alphaGATA3Multilineage pituitary neuroendocrine tumorNeuroendocrine tumorsNonfunctionalp27PIT1PituitaryPituitary adenomaPituitary neuroendocrine tumor with no distinct cell lineagePlurihormonalSF1TPIT

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.