TY - JOUR
T1 - Potent immune-dependent anticancer effects of the non-cardiotoxic anthracycline aclarubicin
AU - Cerrato, Giulia
AU - Sauvat, Allan
AU - Abdellatif, Mahmoud
AU - Kroemer, Guido
N1 - Publisher Copyright:
© 2025 The Author(s). Published with license by Taylor & Francis Group, LLC.
PY - 2025/1/1
Y1 - 2025/1/1
N2 - Aclarubicin (also called aclacinomycin A) is an antineoplastic from the anthracycline class that is used in China and Japan but not in Europe nor in the USA. Aclarubicin induces much less DNA damage than the classical anthracyclines doxorubicin, daunorubicin, epirubicin, idarubicin, and the anthracene mitoxantrone, but is equally effective in inhibiting DNA-to-RNA transcription and in eliciting immunogenic stress in malignant cells. Accordingly, aclarubicin lacks the DNA damage-associated cardiotoxicity that is dose-limiting for classical anthracyclines. Conversely, aclarubicin is at least as potent as other anthracyclines in inducing immunogenic cell death (ICD), which is key for the mode of action of efficient chemotherapeutics. This combination of reduced toxicity and equivalent ICD-stimulatory activity may explain why, as compared to other anthracyclines, aclarubicin is particularly efficient against acute myeloid leukemia. As a result, we advocate for clinical studies seeking to replace the anthracyclines used in Western medicine by aclarubicin-like compounds. Such clinical studies should not only embrace hematological malignancies but should also concern solid cancers, including those in which ICD-inducing chemotherapies are followed by immunotherapies targeting the PD-1/PD-L1 interaction.
AB - Aclarubicin (also called aclacinomycin A) is an antineoplastic from the anthracycline class that is used in China and Japan but not in Europe nor in the USA. Aclarubicin induces much less DNA damage than the classical anthracyclines doxorubicin, daunorubicin, epirubicin, idarubicin, and the anthracene mitoxantrone, but is equally effective in inhibiting DNA-to-RNA transcription and in eliciting immunogenic stress in malignant cells. Accordingly, aclarubicin lacks the DNA damage-associated cardiotoxicity that is dose-limiting for classical anthracyclines. Conversely, aclarubicin is at least as potent as other anthracyclines in inducing immunogenic cell death (ICD), which is key for the mode of action of efficient chemotherapeutics. This combination of reduced toxicity and equivalent ICD-stimulatory activity may explain why, as compared to other anthracyclines, aclarubicin is particularly efficient against acute myeloid leukemia. As a result, we advocate for clinical studies seeking to replace the anthracyclines used in Western medicine by aclarubicin-like compounds. Such clinical studies should not only embrace hematological malignancies but should also concern solid cancers, including those in which ICD-inducing chemotherapies are followed by immunotherapies targeting the PD-1/PD-L1 interaction.
KW - Anticancer agents
KW - immune checkpoint inhibitors
KW - immunosuppression
KW - integrated stress response
KW - myelosuppression
UR - http://www.scopus.com/inward/record.url?scp=105007466859&partnerID=8YFLogxK
U2 - 10.1080/2162402X.2025.2515176
DO - 10.1080/2162402X.2025.2515176
M3 - Review article
AN - SCOPUS:105007466859
SN - 2162-4011
VL - 14
JO - OncoImmunology
JF - OncoImmunology
IS - 1
M1 - 2515176
ER -