ReviewOncogene2026
Unlocking the potential of targeting the angiotensin II type 1 receptor in cancer.
Review in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Renin-angiotensin system inhibitors and immunotherapy outcomes in lung cancer: a systematic review and meta-analysis with complementary transcriptomic analyses.Frontiers in immunology · 2026Pooled it
- Decoding GPCR signaling reprogramming in cancer: molecular mechanisms and therapeutic implications.Molecular medicine (Cambridge, Mass.) · 2026Review
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
No grant is acknowledged in the PubMed record.
Abstract
The renin-angiotensin system is a key regulator of blood pressure homeostasis, with its primary effector, the angiotensin II type 1 receptor (AT1R), mediating vasoconstriction and processes fundamental to cancer progression, including proliferation, angiogenesis, and metastasis. Elevated AT1R expression is consistently linked to poor prognosis and therapeutic resistance across various malignancies. Preclinical studies provide compelling evidence that AT1R activation drives key cancer related processes, while its inhibition by angiotensin receptor blockers (ARBs) suppresses tumour growth, induces apoptosis, reduces angiogenesis, and inhibits metastasis across a wide range of cancer models. Critically, ARBs effectively modulate the tumour microenvironment (TME), alleviating fibrosis, promoting anti-tumour immune cell phenotypes, and enhancing the efficacy of targeted therapies, chemotherapies, and immunotherapies. Despite this strong preclinical evidence and supporting retrospective population studies, clinical translation of ARBs in oncology remains inconsistent, with trials often limited by design, patient heterogeneity, and supra-therapeutic ARB dosages required for acute anti-cancer effects. This review seeks to summarise the current understanding of AT1R's role in cancer, highlight preclinical and clinical investigations of targeting RAS, and suggest further strategies to unlock its therapeutic potential. Realising the full therapeutic promise of AT1R targeting in oncology requires a multifaceted approach, including the development of innovative delivery systems, such as TME-activated ARBs, and the exploration of advanced therapeutic modalities, such as antibody based AT1R inhibitors. Rigorously designed clinical trials that include biomarker-driven patient stratification to identify responsive cohorts are crucial to define the context-dependent role of AT1R and conclusively establish its clinical utility as a combinatorial strategy to enhance patient outcomes.
Indexed as
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.