Fluoropyrimidines compose the backbone of regimens to treat many common solid tumors, including gastrointestinal (GI), breast and head/neck. As we continue to use these agents routinely, recognition of rare but real toxicities, such as cardiotoxicity, has also improved. The treatment options for patients who have encountered fluoropyrimidine-induced cardiotoxicity are limited as many anti-angiogenic drugs also pose a cardiac risk.

Fluoropyrimidines have been extensively used for almost 6 decades to treat a variety of solid cancers, especially colon, gastric, anal, rectal, head & neck and breast. However, 31–34% of patients encountered grade 3–4 adverse events (AEs) with 0.5% mortality oftennecessitating dose reduction or discontinuation. A significant proportion of these AEs are likely to be the result of inter-individual genetic variation, in particularly such as dihydropyrimidine dehydrogenase (DPYD). DPYD gene encodes DPD, the rate-limiting enzyme responsible for catabolism of 5-FU and is responsible for >85% of 5-FU elimination.

Advances in oncology such as better access to health care system, earlier cancer diagnosis and new chemotherapies have led to longer survival of oncologic patients over the last decades. However, this population is vulnerable to cardiovascular drug-related adverse events like cardiomyopathy, which leads to heart failure and impairs survival and quality of life.

Immune checkpoint inhibitor (ICI)-associated cardiotoxicity is a rare immune-related adverse event with high mortality. In recent years, more and more reports were reported. It is urgent to improve understanding and management. Cardiac toxicity often occurs in the early stage after ICI treatment, and its clinical manifestations are diverse and nonspecific, and its pathogenesis is still unclear. Among them, the incidence of immune myocarditis is more than 1%, which can be manifested as fulminant, acute or chronic.

Recently we published the article ‘Accumulation of protoporphyrin IX in medulloblastoma cell lines and sensitivity to subsequent photodynamic treatment’. In this commentary, we review protoporphyrin IX accumulation after application of 5-aminolaevulinic acid and the resulting sensitivity of medulloblastoma cells to photodynamic therapy. We compare the results to glioblastoma cells, including glioblastoma stem-like cells, and address the contribution of the transporter adenosine triphosphate binding cassette subfamily G member 2 (ABCG2) as well as the enzyme ferrochelatase to the process.