ReviewDiscover oncology2026
Roles of Her3 in carcinogenesis and advances in Her3-targeted cancer therapy.
Review in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Among the epidermal growth factor receptor tyrosine kinases (EGFR) family, HER3 (Human epidermal growth factor receptor3) stands apart due to its minimal inherent intracellular kinase function. Its kinase domain contains specific amino acid variations not found in other family members, resulting in a stably inactive structural state. The inability to undergo homodimerization necessitates that HER3 pairs with a different receptor to become active; this heterodimerization triggers phosphorylation at its C-terminal tail. Elevated levels of HER3 are linked to enhanced tumor advancement and the spread of cancer, making it a prominent subject of study in oncology. Developing treatments focused on HER3 has become a significant strategy in cancer care. The upregulation of HER3 can initiate signaling through alternative routes that do not require EGFR, via association with other receptor types. This activates compensatory pathways and contributes to resistance against EGFR tyrosine kinase inhibitors (TKIs). Consequently, therapeutic strategies directed at HER3 may help address and surmount such resistance in cancer treatment, this review focuses on the progress in HER3-targeted therapeutic research for tumors and the latest breakthroughs in the development of drugs engaging HER3. Understanding the intricate mechanisms underlying HER3 function and its impact on cancer biology is crucial for devising more effective, precisely targeted interventions in the ongoing war against cancer.
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Registered trials
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.