Molecular alterations in non-functioning pituitary adenomas.


Journal

Cancer biomarkers : section A of Disease markers
ISSN: 1875-8592
Titre abrégé: Cancer Biomark
Pays: Netherlands
ID NLM: 101256509

Informations de publication

Date de publication:
2020
Historique:
pubmed: 1 4 2020
medline: 20 1 2021
entrez: 1 4 2020
Statut: ppublish

Résumé

Clinically non-functioning Pituitary Adenomas (NFPA) are among the most common neoplasms of the sellar region. They usually present with compressive symptoms such as headache and visual field defects and not infrequently, are found incidentally. NFPA are classified as gonadotropinomas, null cell adenomas, according to their immunohistochemical phenotype. The molecular alterations responsible for the development of these lesions are incompletely understood, and there is scarce information regarding the molecular alterations and markers. We carried out an in-silico analysis aimed at identifying the molecular alterations in NFPA and to discover new molecular markers. Twenty-three microarray libraries were analyzed. Fourteen correspond to NFPA and 9 to control tissue gland. They were analyzed using Partek Genomic Suite to identify differentially expressed genes and WebGestalt and Metascape to understand the meaning behind the gene lists. Pituitary adenomas showed a markedly different transcriptome compared to the non-tumoral gland, regardless of their putative immunophenotype. Genes related to calcium metabolism such as CACNA2D4, immune-related CXCR4, and stem cell-related KLF8 and PITX2 were altered. Differentially expressed calcium metabolism and immune-related genes in NFPA represent attractive molecular markers and potential therapeutic targets.

Sections du résumé

BACKGROUND BACKGROUND
Clinically non-functioning Pituitary Adenomas (NFPA) are among the most common neoplasms of the sellar region. They usually present with compressive symptoms such as headache and visual field defects and not infrequently, are found incidentally. NFPA are classified as gonadotropinomas, null cell adenomas, according to their immunohistochemical phenotype. The molecular alterations responsible for the development of these lesions are incompletely understood, and there is scarce information regarding the molecular alterations and markers.
OBJECTIVE OBJECTIVE
We carried out an in-silico analysis aimed at identifying the molecular alterations in NFPA and to discover new molecular markers.
METHODS METHODS
Twenty-three microarray libraries were analyzed. Fourteen correspond to NFPA and 9 to control tissue gland. They were analyzed using Partek Genomic Suite to identify differentially expressed genes and WebGestalt and Metascape to understand the meaning behind the gene lists.
RESULTS RESULTS
Pituitary adenomas showed a markedly different transcriptome compared to the non-tumoral gland, regardless of their putative immunophenotype. Genes related to calcium metabolism such as CACNA2D4, immune-related CXCR4, and stem cell-related KLF8 and PITX2 were altered.
CONCLUSIONS CONCLUSIONS
Differentially expressed calcium metabolism and immune-related genes in NFPA represent attractive molecular markers and potential therapeutic targets.

Identifiants

pubmed: 32224525
pii: CBM191121
doi: 10.3233/CBM-191121
doi:

Substances chimiques

Biomarkers, Tumor 0
CACNA2D4 protein, human 0
CXCR4 protein, human 0
Calcium Channels, L-Type 0
Homeodomain Proteins 0
KLF8 protein, human 0
Kruppel-Like Transcription Factors 0
Receptors, CXCR4 0
Transcription Factors 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

193-199

Auteurs

Keiko Taniguchi-Ponciano (K)

Laboratorio de Neuroendocrinología Comparada, Departamento de Ecología y Recursos Naturales, Biología, Facultad de Ciencias, Universidad Nacional Autónoma de México, Mexico City, Mexico.
Unidad de Investigación Médica en Enfermedades Endocrinas, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico.

Erick Gomez-Apo (E)

Área de Neuropatología, Servicio de Anatomía Patológica, Hospital General de México Dr. Eduardo Liceaga, Mexico City, Mexico.

Laura Chavez-Macias (L)

Área de Neuropatología, Servicio de Anatomía Patológica, Hospital General de México Dr. Eduardo Liceaga, Mexico City, Mexico.
Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico.

Guadalupe Vargas (G)

Unidad de Investigación Médica en Enfermedades Endocrinas, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico.
Servicio de Endocrinologia, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico.

Etual Espinosa-Cardenas (E)

Unidad de Investigación Médica en Enfermedades Endocrinas, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico.
Servicio de Endocrinologia, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico.

Claudia Ramirez-Renteria (C)

Unidad de Investigación Médica en Enfermedades Endocrinas, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico.

Aldo Ferreira-Hermosillo (A)

Unidad de Investigación Médica en Enfermedades Endocrinas, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico.

Ernesto Sosa (E)

Unidad de Investigación Médica en Enfermedades Endocrinas, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico.
Servicio de Endocrinologia, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico.

Gloria Silva-Román (G)

Unidad de Investigación Médica en Enfermedades Endocrinas, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico.

Eduardo Peña-Martínez (E)

Unidad de Investigación Médica en Enfermedades Endocrinas, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico.

Sergio Andonegui-Elguera (S)

Unidad de Investigación Médica en Enfermedades Endocrinas, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico.
Departamento de Desarrollo Tecnologico, Instituto Nacional de Medicina Genomica, Mexico City, Mexico.

Sonia Vargas-Chavez (S)

Laboratorio de Neuroendocrinología Comparada, Departamento de Ecología y Recursos Naturales, Biología, Facultad de Ciencias, Universidad Nacional Autónoma de México, Mexico City, Mexico.

Yorgui Santiago-Andres (Y)

Laboratorio de Neuroendocrinología Comparada, Departamento de Ecología y Recursos Naturales, Biología, Facultad de Ciencias, Universidad Nacional Autónoma de México, Mexico City, Mexico.

Raul Peralta (R)

Centro de Investigacion en Dinamica Celular, Universidad Autonoma del Estado de Morelos, Cuernavaca, Mexico.

Daniel Marrero-Rodríguez (D)

Unidad de Investigación Médica en Enfermedades Endocrinas, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico.

Moises Mercado (M)

Unidad de Investigación Médica en Enfermedades Endocrinas, Hospital de Especialidades, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Mexico.

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Classifications MeSH