ArticleNature medicine2026
Targeting of HIF2-driven cachexia in kidney cancer.
Article in Nature medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed.
- SET1B Drives Sustained HIF Activity and Disease Progression in Clear-Cell Renal Cell Carcinoma.Cancer research · 2026Article
- Target identification and assessment in the era of AI.Nature reviews. Drug discovery · 2026Review
- The clinical landscape of HIF2α inhibitors in oncology.Nature reviews. Clinical oncology · 2026Review
- PTHrP-associated hypercalcemia in gynecologic malignancies: a scoping review.Archives of gynecology and obstetrics · 2026Article
- Comprehensive profiling of RPP40 across human cancers reveals its essential role and multidimensional clinical correlates.Discover oncology · 2026Article
- Targeting HIF2-PTHrP axis in kidney cancer: a paradigm shift in therapy?Clinical kidney journal · 2026Article
- Mechanistic insights make cancer cachexia a targetable syndrome.Nature medicine · 2026Article
- Glycolytic Reprogramming Mediated by the OTUD4-FXR1-HIF1A Axis Drives Gastric Cancer Progression.International journal of biological sciences · 2026Article
- CA9-Targeted Liposomal Delivery of siETS1 Inhibits Clear Cell Renal Cell Carcinoma Progression by Disrupting the ETS1/MYC Regulatory Axis.International journal of nanomedicine · 2026Article
Corrections and comments
- Erratum issued
- Update of
Authors and funding
20 authors.
Funding
Abstract
Kidney cancer frequently causes paraneoplastic syndromes, including hypercalcemia and cachexia, but the underlying mechanisms are incompletely understood. The most common form of kidney cancer, clear cell renal cell carcinoma (ccRCC), is frequently caused by loss of the pVHL tumor suppressor protein and the resulting upregulation of the HIF2 transcription factor. We show that PTHLH, which resides on a ccRCC amplicon on chromosome 12p, is a direct HIF2 transcriptional target in ccRCC. Further, we show that the increased PTHLH expression is both necessary and sufficient for the induction of hypercalcemia and cachexia in preclinical orthotopic cell line tumor models. Consistent with these observations, two different allosteric HIF2 inhibitors, belzutifan and NKT2152, rapidly ameliorated hypercalcemia and cachexia in patients with ccRCC, including in some who did not exhibit objective tumor shrinkage. Our findings support prospective clinical studies to determine whether HIF2 inhibitors can be leveraged not only for tumor control, but also for the treatment of cancer-associated cachexia in renal cell carcinoma.
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What Socratic 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 Socratic graph.