The appearance of tumor cells may reflect not just a failure to repair the genome, but a baseline of compromised quality in the genome itself. This nuance is highlighted by a report from Moscow Phystech (MIPT) via its press service.
For decades, the prevailing view was that cancer arises when the body cannot fix mistakes in DNA, allowing cancerous cells to divide unchecked and amass additional mutations. This traditional narrative positioned defective DNA repair as the primary driver of malignant growth.
New findings from Russian researchers challenge that long-standing assumption. In a broad examination of nine common cancers, including breast, lung, kidney, stomach, thyroid, and pancreas cancers, scientists tracked the activity of DNA repair pathways across tumor samples. Their analysis indicates that most tumor types exhibit heightened activity in many DNA repair systems, not diminished activity. In other words, cancer cells often actively correct errors during replication and cellular processes, which runs counter to the classic idea that cancer stems from a repair deficit.
The study also points to a different potential origin for cancer growth: the quality of the genome may deteriorate as DNA repair becomes more efficient in certain contexts. In many cancer cells, the G2/M checkpoint, which normally verifies and seals DNA corrections and helps halt division when fixes are needed, appears suppressed. When this control mechanism falters, tumor cells can continue to divide despite serious genomic errors, accelerating mutation accumulation and tumor progression.
By highlighting a decoupling between high repair activity and the breakdown of essential genome-checks, the researchers open the door to new therapeutic concepts. If the G2/M checkpoint can be reactivated or reinforced, it may slow cancer cell division and reduce mutation rates. The authors suggest that strategies aimed at restoring this checkpoint could form the basis of innovative anti-cancer therapies.
These insights contribute to a more nuanced understanding of cancer biology. They suggest that therapies focused solely on disabling DNA repair may miss crucial dynamics of tumor behavior. Instead, a balanced approach that considers the context and regulation of repair, plus the integrity of cell cycle checkpoints, could prove more effective in managing malignant disease.
Further investigation is expected to clarify how often enhanced DNA repair accompanies suppressed genome surveillance in various cancers and which patient groups might benefit most from treatments designed to reactivate key checkpoints. The evolving picture underscores the importance of personalized strategies that account for the distinctive repair and checkpoint landscapes within individual tumors.
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