BER is a highly conserved and major DNA repair mechanism [1], [2] which acts like an immune surveillance system for DNA, ensuring genome stability by correcting base lesions caused by oxidation, deamination, alkylation, and abasic single-base damage. BER corrects thousands of oxidized/alkylated bases and an estimated ∼10,000 apurinic/apyrimidinic (AP) sites per cell per day, underscoring its essential role in preventing diseases such as cancer and aging [3], [4], [5]. Genetic mutations are key drivers of tumorigenesis, and defective DNA repair mechanisms are often associated with cancer development [6], [7], [8]. In addition, cancer treatments, including chemotherapy and radiotherapy, function by inducing DNA damage to kill cancer cells [9], [10]. However, DNA repair mechanisms, including BER, can counteract these treatments and contribute to therapeutic resistance [11].

In this regard, this review aims to discuss the different roles of BER in cancer development and treatment, exploring how defective BER contributes to cancer biology mechanistically. Meanwhile, we review novel detection techniques that may be applicable to clinical samples. Here, we prioritize recent studies but acknowledge foundational work through citations to earlier reviews for more comprehensive appreciation of the whole picture. Due to space constraints, we regret any omissions of significant contributions to this field.