Evidence map›Paper›PMID 29931399›Full record

ReviewCurrent oncology reports2018

Tyrosine Kinase Inhibitor-Induced Hypertension.

Megha Agarwal, Nidhi Thareja, Melody Benjamin, Andre Akhondi, George D Mitchell

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current oncology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 3% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Review
  6. Review
  7. Review
  8. Tackling the Cardio-Kidney-Metabolic Burden in Cancer.Current atherosclerosis reports · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Immunotherapy in Renal Cell Carcinoma.Cancer treatment and research · 2025
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Megha AgarwalDepartment of Cardiology, UCLA Health Ventura, 6633 Telephone Rd. Suite 212, Ventura, CA, 93003, USA. magarwal@mednet.ucla.edu.
Nidhi TharejaDepartment of Cardiology, UCLA Health Santa Clarita, 25775 McBean Parkway Suite 202, Santa Clarita, CA, 91355, USA.
Melody BenjaminDepartment of Hematology/Oncology, UCLA Health Ventura, 6633 Telephone Rd. Suite 200, Ventura, CA, 93003, USA.
Andre AkhondiDepartment of Cardiology, UCLA Health Ventura, 6633 Telephone Rd. Suite 212, Ventura, CA, 93003, USA.
George D MitchellDepartment of Cardiology, UCLA Health Ventura, 6633 Telephone Rd. Suite 212, Ventura, CA, 93003, USA.
UCLA Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewThe purpose of this paper is to identify commonly used tyrosine kinase inhibitors (TKIs) that are associated with hypertension, primarily, vascular endothelial growth factor (VEGF) signaling pathway (VSP) inhibitors. We review the incidence, mechanism, and strategies for management of TKI-induced HTN. We hope to provide clinicians with guidance on how to manage similar clinical scenarios. RECENT

findingsMany of the newer VSP inhibitors are reviewed here, including cediranib, axitinib, pazopanib, and ponatinib. Trials utilizing prophylactic treatment with angiotensin system inhibitors (ASIs) are discussed as well as recent data showing an improvement in overall survival and progression-free survival in patients on ASIs and TKI-induced hypertension. The incidence of TKI-induced HTN among the VEGF inhibitors ranges from 5 to 80% and is dose dependent. Newer generation small-molecule TKIs has a lower incidence. The mechanism of action involves VSP inhibition, leading to decreased nitric oxide and increased endothelin production, which causes vasoconstriction, capillary rarefaction, and hypertension. ASIs and calcium channel blockers are first-line therapy for treatment and are associated with improved overall survival. Nitrates and beta-blockers are associated with in vitro cancer regression; however, there is a paucity of trials regarding their use as an anti-hypertensive agent in the TKI-induced HTN patient population.

Indexed as

AngiotensinsAntihypertensive AgentsCalcium Channel BlockersHumansHypertensionNeoplasmsProtein Kinase InhibitorsProtein-Tyrosine KinasesSignal TransductionVascular Endothelial Growth FactorsAngiotensinsAntihypertensive AgentsCalcium Channel BlockersProtein Kinase InhibitorsProtein-Tyrosine KinasesVascular Endothelial Growth FactorsAnti-hypertensive therapyHypertensionIncidenceNitric oxideTyrosine kinase inhibitorVEGF inhibitor

Identifiers

PMID29931399
OpenAlexW2809655255

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.