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1000 Titel
  • B7-H3 at the crossroads between tumor plasticity and colorectal cancer progression: a potential target for therapeutic intervention
1000 Autor/in
  1. Varghese, Elizabeth |
  2. Mathews Samuel, Samson |
  3. Brockmueller, Aranka |
  4. Shakibaei, Prof. Dr. Mehdi |
  5. Kubatka, Peter |
  6. Büsselberg, Dietrich |
1000 Verlag
  • Springer US
1000 Erscheinungsjahr 2023
1000 Publikationstyp
  1. Artikel |
1000 Online veröffentlicht
  • 2023-09-28
1000 Erschienen in
1000 Quellenangabe
  • 43(1):115-133
1000 Copyrightjahr
  • 2023
1000 Lizenz
1000 Verlagsversion
  • https://doi.org/10.1007/s10555-023-10137-8 |
  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11016009/ |
1000 Publikationsstatus
1000 Begutachtungsstatus
1000 Sprache der Publikation
1000 Abstract/Summary
  • <jats:title>Abstract</jats:title><jats:p>B7-H3 (B7 homology 3 protein) is an important transmembrane immunoregulatory protein expressed in immune cells, antigen-presenting cells, and tumor cells. Studies reveal a multifaceted role of B7-H3 in tumor progression by modulating various cancer hallmarks involving angiogenesis, immune evasion, and tumor microenvironment, and it is also a promising candidate for cancer immunotherapy. In colorectal cancer (CRC), B7-H3 has been associated with various aspects of disease progression, such as evasion of tumor immune surveillance, tumor-node metastasis, and poor prognosis. Strategies to block or interfere with B7-H3 in its immunological and non-immunological functions are under investigation. In this study, we explore the role of B7-H3 in tumor plasticity, emphasizing tumor glucose metabolism, angiogenesis, epithelial-mesenchymal transition, cancer stem cells, apoptosis, and changing immune signatures in the tumor immune landscape. We discuss how B7-H3-induced tumor plasticity contributes to immune evasion, metastasis, and therapy resistance. Furthermore, we delve into the most recent advancements in targeting B7-H3-based tumor immunotherapy as a potential approach to CRC treatment.</jats:p>
1000 Sacherschließung
lokal Colorectal Neoplasms/pathology [MeSH]
lokal Humans [MeSH]
lokal Review
lokal Immunotherapy [MeSH]
lokal B7-H3
lokal Colorectal cancer
lokal Drug resistance
lokal Immunomodulation
lokal Tumor plasticity, immune checkpoint
lokal B7 Antigens/metabolism [MeSH]
lokal Tumor Microenvironment [MeSH]
1000 Fächerklassifikation (DDC)
1000 Liste der Beteiligten
  1. https://orcid.org/0000-0002-8012-3435|https://orcid.org/0000-0002-5541-6623|https://orcid.org/0000-0001-8101-2828|https://orcid.org/0000-0002-6304-7506|https://orcid.org/0000-0003-4312-5076|https://orcid.org/0000-0001-5196-3366
1000 Hinweis
  • DeepGreen-ID: 711463c7489a47ddbff3d64892ac8026 ; metadata provieded by: DeepGreen (https://www.oa-deepgreen.de/api/v1/), LIVIVO search scope life sciences (http://z3950.zbmed.de:6210/livivo), Crossref Unified Resource API (https://api.crossref.org/swagger-ui/index.html), to.science.api (https://frl.publisso.de/), ZDB JSON-API (beta) (https://zeitschriftendatenbank.de/api/), lobid - Dateninfrastruktur für Bibliotheken (https://lobid.org/resources/search)
1000 Label
1000 Förderer
  1. Qatar National Research Fund |
  2. Qatar Foundation |
1000 Fördernummer
  1. -
  2. -
1000 Förderprogramm
  1. -
  2. -
1000 Dateien
1000 Förderung
  1. 1000 joinedFunding-child
    1000 Förderer Qatar National Research Fund |
    1000 Förderprogramm -
    1000 Fördernummer -
  2. 1000 joinedFunding-child
    1000 Förderer Qatar Foundation |
    1000 Förderprogramm -
    1000 Fördernummer -
1000 Objektart article
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1000 Erstellt am 2025-02-06T19:33:06.907+0100
1000 Erstellt von 322
1000 beschreibt frl:6509173
1000 Zuletzt bearbeitet 2025-07-30T08:43:27.820+0200
1000 Objekt bearb. Wed Jul 30 08:43:27 CEST 2025
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