ArticleCancer biology & therapy2013
The flip side of doxorubicin: Inflammatory and tumor promoting cytokines.
Article in Cancer biology & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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, 13 citations in OpenAlex.
- ZAK kinase at the crossroads of cellular stress: functional plasticity, human pathobiology, and precision therapeutics.Frontiers in cell and developmental biology · 2026Review
- A Matrix-Assisted Laser Desorption/Ionization Time-of-Flight Assay Identifies Nilotinib as an Inhibitor of Inflammation in Acute Myeloid Leukemia.Journal of medicinal chemistry · 2022Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Cardiac toxicity is a major dose-limiting factor for the anthracycline drug doxorubicin. The reasons why doxorubicin causes heart damage are not fully understood, and the manuscript by Wong et al. postulates that inflammatory cytokines released from macrophages or other cell types may play a significant role in the damage process in response to doxorubicin and possibly other chemotherapeutic agents.(1) Expression of many cytokines requires activation of both the p38 MAPK and JNK pathways and, additionally, doxorubicin toxicity can be blocked by combined inhibition of both pathways.(2,3) The MAP3K responsible for doxorubicin-induced p38 MAPK and JNK activation in keratinocytes was previously shown by these authors to be ZAK.(4) ZAK is of note because it can be targeted by FDA approved agents such as nilotinib and sorafenib.(4-7)
Indexed as
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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.