Nikhil Prasad Fact checked by:Thailand Medical News Team Jul 27, 2026 1 hour, 12 minutes ago
Medical News: Researchers uncover unique genetic fingerprints that could reshape future treatment
Scientists from the Institute of Pathology, Kantonsspital Baden AG, Baden, Switzerland, and the Breast Center, Kantonsspital Baden AG, Baden, Switzerland, have identified major genetic differences in a particularly aggressive form of breast cancer known as quadruple-negative breast cancer (QNBC). Their findings suggest that this disease is biologically different from other forms of triple-negative breast cancer and may require its own personalized treatment strategies.
Scientists identify unique DNA alterations that may explain why quadruple-negative breast cancer behaves more
aggressively and may require specialized treatments
What makes QNBC different?
Triple-negative breast cancer (TNBC) is already considered one of the most difficult breast cancers to treat because it lacks three common treatment targets. QNBC goes one step further by also lacking the androgen receptor, leaving patients with even fewer treatment options.
The research team analyzed tumors from 54 patients, comparing 38 QNBC cases with 16 triple-negative tumors that strongly expressed the androgen receptor. Women with QNBC were diagnosed at a much younger average age of 53 years compared to 65 years for the other group. Their tumors were also more aggressive, with nearly all QNBC tumors being high-grade and showing extremely rapid cell growth based on high Ki-67 scores.
DNA damage is far greater in QNBC
One of the most important discoveries was that QNBC tumors carried much higher levels of genomic instability, meaning their DNA had accumulated far more damage and structural changes.
The researchers found significantly higher homologous recombination deficiency (HRD) scores in QNBC. HRD reflects how poorly cancer cells repair damaged DNA. When this repair system fails, mutations accumulate rapidly, making tumors more aggressive but also potentially more vulnerable to certain targeted drugs.
QNBC tumors also contained almost twice as many copy number variants, which are gains or losses of large sections of DNA. Remarkably, 97 percent of QNBC tumors carried at least one major copy number alteration compared with only 56 percent of the comparison group. Amplification of chromosome 8q, which contains the cancer-promoting MYC gene and microRNA-1204, was especially common, suggesting these genetic alterations may fuel rapid tumor growth and disease progression.
This
Medical News report highlights how these extensive DNA abnormalities reinforce the idea that QNBC is not simply another subtype of triple-negative breast cancer but a genetically distinct disease.
Critical cancer genes are altered
The genetic analysis also revealed striking differences in several cancer-driving pathways.
Mutations affecting the TP53 tumor suppressor gene were found far more frequently in QNBC. TP53 normally acts as the body'
s natural defense against damaged cells, so defects can allow abnormal cells to multiply unchecked.
The MYC signaling pathway, which regulates cell growth and division, was also much more commonly altered in QNBC, helping explain why these tumors grow so aggressively.
Perhaps even more significant, several important DNA repair genes—including BRCA2, RAD51, RAD51C, BARD1, BRIP1, FANCD2, ATRX, RAD50, ARID1A, WRN, and ABRAXAS1—were found exclusively in QNBC tumors. Alterations involving the PI3K/AKT and RTK/RAS signaling pathways also showed unique patterns that were absent from androgen receptor-positive tumors.
Although overall survival did not significantly differ between the two patient groups during follow-up, the molecular evidence clearly demonstrated that QNBC possesses a far more unstable and complex genetic profile.
New hope for personalized treatments
The researchers believe these distinctive genetic patterns could eventually help doctors select more effective combinations of targeted therapies. Patients with high HRD scores may benefit from drugs that exploit defective DNA repair systems, while alterations in the PI3K/AKT, MYC, TP53, and other pathways may open additional opportunities for precision medicine as new therapies continue to emerge.
Conclusion
The findings provide compelling evidence that quadruple-negative breast cancer is genetically distinct from other triple-negative breast cancers, displaying greater DNA instability, more aggressive biological behavior, and unique mutations affecting several major cancer pathways. These discoveries strengthen the case for treating QNBC as its own disease subtype and could guide the development of more personalized therapies that improve outcomes for patients facing this challenging form of breast cancer.
The study findings were published in the peer reviewed International Journal of Molecular Sciences.
https://www.mdpi.com/1422-0067/27/15/6654
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