Cda, short for cytidine deaminase, is an enzyme-coding gene. The cytidine deaminase it encodes is responsible for detoxifying cytarabine (Ara-C) in the liver. Cda is highly polymorphic, and its activity can impact the toxicity and efficacy of Ara-C treatment in acute myeloid leukemia (AML) [1].

In a study on 58 adult AML patients treated with the standard 7 + 3 (Ara-C + anthracyclines) protocol, those experiencing severe/lethal toxicities had significantly lower Cda activity (1.5 ± 0.7 U/mg vs 3.95 ± 3.1 U/mg, Student t test P <.001). A Cda activity threshold of 2 U/mg was associated with a poor metabolizer syndrome and an increased risk of severe toxicities. Also, patients with low Cda activity showed a trend towards higher response rates and longer progression-free and overall survival [1].

In conclusion, Cda is crucial in determining the toxicities and efficacy of cytarabine-based chemotherapy in AML. Understanding the role of Cda through such in-vivo-like human patient-based studies helps in predicting treatment-related risks in AML patients, potentially guiding more personalized treatment strategies.

References:

1. Fanciullino, Raphaelle, Farnault, Laure, Donnette, Mélanie, Lacarelle, Bruno, Costello, Regis. . CDA as a predictive marker for life-threatening toxicities in patients with AML treated with cytarabine. In Blood advances, 2, 462-469. doi:10.1182/bloodadvances.2017014126. https://pubmed.ncbi.nlm.nih.gov/29490977/