ArticleDiscover oncology2026
KIF5B-driven unfolded protein response reprograms breast cancer immunosuppressive microenvironment for single-cell guided therapeutic targeting.
Article 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
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
backgroundBreast cancer (BRCA) remains a leading cause of cancer-related mortality among women worldwide. The kinesin family member 5B (KIF5B) has been implicated in various cancers, yet its comprehensive role in BRCA prognosis, tumor microenvironment (TME), and therapeutic response remains poorly understood.
methodsWe integrated single-cell RNA sequencing (scRNA-seq) data and bulk RNA-seq data from multiple datasets. Using hdWGCNA, we identified gene modules related to the unfolded protein response (UPR). Consensus clustering defined UPR-related molecular subtypes, and differential expression analysis revealed key prognostic genes. KIF5B was further evaluated for its prognostic significance, mutational landscape, immune infiltration associations, and potential as a therapeutic target.
resultsMalignant cell-specific KIF5B upregulation drives poor overall survival in pan-cancer cohorts, validating its hazardous molecular function. Functional enrichment analysis linked KIF5B to critical pathways, including immune response, JAK-STAT signaling, and epithelial-mesenchymal transition. Immune infiltration analysis revealed that high KIF5B expression was associated with reduced immune and ESTIMATE scores, but higher tumor purity. Drug sensitivity prediction identified several compounds with potential efficacy in high KIF5B-expressing patients, including Sapitinib and LCL161.
conclusionOur multimodal analysis establishes KIF5B as a prognostic biomarker and potential therapeutic target in BRCA, with implications for understanding immune evasion and guiding precision treatment strategies.
Identifiers
What OpenQuestion holds
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.