Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

B7-H3 is eligible for predicting clinical outcomes in lung adenocarcinoma patients treated with EGFR tyrosine kinase inhibitors.

World journal of surgical oncology - 20 May 2022

Yang Ying, Huang Jun-Feng, Hu Bing-Qi, Zhou Jing, Wang Xian, Feng Zhen-Zhong, Chen Yu-Ting, Pan Fa-Ming, Cheng Huai-Dong, Chen Li-Wen

Abstract excerpt

BACKGROUND: Not all lung adenocarcinoma (LUAD) patients with activating epidermal growth factor receptor (EGFR) mutations respond to tyrosine kinase inhibitors (TKIs) as intended. Thus, biomarkers are needed to identify patients who benefit most from EGFR-targeted therapy. Our previous in vitro data has shown that the co-signal molecule B7-H3 determines EGFR-TKI gefitinib susceptibility of EGFR-mutated LUAD cell...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adenocarcinoma of Lung
Share to Antineoplastic Agents

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Carcinoma, Non-Small-Cell Lung

Share to ErbB Receptors

Share to Lung Neoplasms

Share to Mutation

Share to Protein Kinase Inhibitors

Share to Transcription Factors

Source

Open in PubMed Open full text

Identifiers

PMID: 35590371
DOI: 10.1186/s12957-022-02634-x
PMCID: PMC9121599

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

B7-H3 is eligible for predicting clinical outcomes in lung adenocarcinoma patients treated with EGFR tyrosine kinase inhibitors.PMID 35590371Read ↗

B7-H3-Induced Signaling in Lung Adenocarcinoma Cell Lines with Divergent Epidermal Growth Factor Receptor Mutation Patterns.Semantic proximity Read ↗

B7-H4 and HHLA2, members of B7 family, are aberrantly expressed in EGFR mutated lung adenocarcinoma.Semantic proximity Read ↗

Multi-omic analysis of colorectal adenocarcinoma identifies a new subtype of myofibroblastic cancer-associated fibroblast expressing high level of B7-H3 and with poor prognosis valueSemantic proximity Read ↗

ELK1 Promotes Epithelial‐Mesenchymal Transition and the Progression of Lung Adenocarcinoma by Upregulating B7‐H3Semantic proximity Read ↗

Overexpression of B7-H3 Is Associated With Poor Prognosis in Laryngeal CancerSemantic proximity Read ↗

To kill a cancer: Targeting the immune inhibitory checkpoint molecule, B7-H3Semantic proximity Read ↗

B7-H3 and its relevance in cancer immunological and non-immunological perspectivesSemantic proximity Read ↗

Multidimensional Analysis of B7 Homolog 3 RNA Expression in Small Cell Lung Cancer Molecular Subtypes.Semantic proximity Read ↗

The novel non‐immunological role and underlying mechanisms of B7‐H3 in tumorigenesisSemantic proximity Read ↗

HHLA2, a New Immune Checkpoint Member of the B7 Family, Is Widely Expressed in Human Lung Cancer and Associated with EGFR Mutational Status.Semantic proximity Read ↗

B7-H3 Negatively Modulates CTL-Mediated Cancer Immunity.Semantic proximity Read ↗

Targeting B7-H1 (PD-L1) sensitizes cancer cells to chemotherapySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.