Mechanisms of action of arsenic trioxide.

By W. Miller, H. Schipper, Janet S. Lee, J. Singer, S. Waxman. Cancer Research, 2002

1,010 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Arsenic: toxicity, oxidative stress and human disease (2011, background): “Arsenic exposure has been linked with various types of cancer (Miller et al., 2002), cardiovascular diesase (Navas‐Acien et al., 2005), diabetes (Díaz‐Villaseñor et al., 2007), neurological disorders (Vahidnia et al., 2007) and dermal effects (Cohen et al., 2006).”
Arsenic degrades PML or PML–RARα through a SUMO-triggered RNF4/ubiquitin-mediated pathway (2008, background): “Yet, the nature of the degradation pathway and the biological importance of oncogene catabolism have remained controversia”
Heavy Metals Toxicity and the Environment (2012, unknown): “A recent review discusses nine different possible modes of action of arsenic carcinogenesis: induced chromosomal abnormalities, oxidative stress, altered DNA repair, altered DNA methylation patterns, altered growth factors, enhanced cell proliferation, promotion/progression, suppression of p53, and ”