Artículo

Unveiling the Immune effects of AHR in tumors: a decade of insights from bibliometric analysis (2010–2023)

Resumen

Background: The Aryl Hydrocarbon Receptor (AHR) is a transcription factor that regulates several biological processes. Its potential in anti-tumor immunotherapy is becoming clearer, yet no bibliometric studies on this topic exist. This study aims to understand the current research landscape and identify future directions through a bibliometric analysis of AHR’s anti-tumor immunological effects. Methods : We conducted a comprehensive bibliometric analysis of AHR antitumor immunotherapy papers in the Web of Science Core Collection. Various aspects of the publications were analyzed, and research hotspots and future trends were identified using scientific bibliometric tools and statistical methods. Results: We collected 592 English papers published between 2010 and 2023, with an almost annual increase. Most publications were from the USA, followed by China, Germany, and Italy. The journal “Frontiers in Immunology” had the most papers, and the most cited paper was Christiane A. Opitz’s “An endogenous tumour-promoting ligand of the human aryl hydrocarbon receptor.” The research is centered around AHR gene expression, with a growing focus on intestinal disease and the development of Programmed cell death ligand 1 (PD-L1) drugs. Conclusion: This bibliometric study highlights the significance of AHR in immunomodulatory research, outlining the research trends and key contributors. It suggests AHR’s immune effects may mediate the process of colitis cancer transformation, providing valuable insights for future anti-tumor immunotherapy strategies based on AHR.
Autores
Kohler, AF; Digiampietri, LA
Título
Classification of authors, institutions, and countries, using productivity, centrality, and impact metrics: The field of tourism studies in Brazil (journals), 1990-2018
Afiliaciones
Universidade de Sao Paulo
Año
2021
DOI
10.7784/rbtur.v15i3.2035
Tipo de acceso abierto
Green Published, gold
Referencia
WOS:000891850400004
Artículo obtenido de:
WOS
Fuente
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