Jerusalem, 12 January, 2026 (TPS-IL) — Some women’s breast cells may show signs of future cancer years before any tumor appears, potentially helping doctors detect breast cancer much earlier — or perhaps even prevent it from developing, the Hebrew University of Jerusalem announced.
On average, one in twenty women globally will be diagnosed with breast cancer, according to the World Health Organization.
A team of Israeli and U.S. scientists opened a previously hidden window into how breast cancer begins in women carrying BRCA1 or BRCA2 mutations. The research shows that even before tumors appear, breast cells in BRCA mutation carriers already exhibit a distinct pattern of DNA “damage spots” that closely resemble the DNA break patterns seen in cancer cells.
The study was led by PhD student Sara Oster Flayshman under the guidance of Professor Rami Aqeilan and Dr. Yotam Drier at Hebrew University’s Faculty of Medicine, in collaboration with Dr. Victoria Seewaldt and Dr. Mark LaBarge from the City of Hope research center in California. Using next-generation sequencing, the team mapped DNA double-strand breaks (DSBs) across the genomes of non-malignant mammary epithelial cells from women carrying high-risk genetic mutations.
The team found that the pattern of DNA damage in these cells was very different from what they saw in healthy cells and, surprisingly, looked much like the patterns found in breast cancer cells. The most affected DNA regions were those linked to cancer, especially the ones that are normally very active in the cell, making them more likely to lead to cancer if damaged.
The study was recently published in the peer-reviewed journal Cell Death & Disease.
Professor Aqeilan told The Press Service of Israel that the study’s significance lies in the early, pre-cancerous cellular instability.
“Our main finding is that non-malignant mammary epithelial cells from high-risk women already show a distinct, non-random ‘breakome’ compared with average-risk controls and, importantly, this breakome partly resembles the pattern seen in breast cancer cells,” he said. A breakome refers to the complete pattern or map of DNA breaks across a cell’s genome.
“This suggests that genome instability–related processes are underway very early, before any tumor is present, and that these early weaknesses can reshape where DNA breaks accumulate,” said Aqeilan.
The researchers emphasized that the DNA break patterns are detectable in young, cancer-free donors, including women under 35. “That means the shift is detectable well before clinical cancer, and plausibly years, potentially decades, before diagnosis for carriers who develop disease later,” Aqeilan said. While the study does not provide a precise lead time to cancer onset, it challenges the traditional view that loss-of-heterozygosity (LOH) events are the first step in malignancy.
The study opens potential avenues for early detection.
“This work provides critical insight into the earliest molecular changes that take place in breast cells of high-risk women,” Aqeilan told TPS-IL. “Understanding these initial events allows us to envision new strategies for identifying cancer at its earliest, most treatable stages.”
Drier noted that these patterns “could one day help us develop more precise biomarkers, so that high-risk women are not only monitored more effectively, but also offered interventions based on the actual biology of their cells.”
While the current study focuses on breast tissue, Aqeilan said the next steps will explore whether similar patterns emerge in other cancer-prone tissues.
“Testing ovarian and fallopian tissue is explicitly a logical next step,” he told TPS-IL.
In addition, his team plans to study larger groups of women over time to see whether early DNA damage patterns can predict who will eventually develop cancer, and to explore minimally invasive tests that could detect these patterns before tumors form.
Understanding these early DNA breaks may also shed light on why some high-risk women develop cancer while others do not. “It could guide new prevention strategies that target these vulnerable regions of the genome before cancer starts,” Aqeilan said.
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