ArticleExperimental hematology & oncology2025
Anti-angiogenic tyrosine kinase inhibitors and the pathophysiology of their toxic effects: revisiting the treatment of anemia in metastatic cancers.
Article in Experimental hematology & oncology, 2025. 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
12 authors.
Funding
Abstract
backgroundAnti-angiogenic tyrosine kinase inhibitors (TKIs) have become major drugs for the treatment of various cancer types, but with an overall high incidence of severe toxicities, particularly haematological toxicities including severe anemia.
methodsWe treated C57BL6 mice continuously by gavage for 14 days with either sunitinib, pazopanib, or axitinib. In this study, we set out to decipher the pathophysiological mechanisms of anti-angiogenic TKI haematological toxicity.
resultsWe demonstrated that anti-angiogenic TKIs induced a broad range of toxic effects on normal tissues through a cytotoxic effect on normal endothelial cells. Haematological toxicities were particulary marked with sunitinib. Sunitinib-induced hypoxia through the destruction of normal vessels in the bone marrow mainly affected erythrocyte and myeloid lineages, and this was associated with a blockage in erythrocyte maturation. Althought sunitinib-induced anemia was associated with an adaptative response to systemic hypoxia, we demonstrated that erythropoietin (EPO) concentrations in the total bone marrow of sunitinib-treated mice were significantly lower than in untreated mice. This is coherent with the destruction of microvessels in the bone marrow under sunitinib treatment, preventing circulating EPO from reaching the bone marrow at relevant concentrations. However, we demonstrated an additional effect specific to sunitinib that induced autophagy flux inhibition in erythroid progenitors, with a blockage of erythrocyte maturation, leading to more severe anemia.
conclusionsWe deciphered the pathophysiology of anti-angiogenic TKI-induced anemia, which we observed to be mainly linked to a direct effect on normal bone-marrow vessels and to autophagy flux inhibition in erythroid progenitors under sunitinib.
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.