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Freezing treatment effective for breast cancer patients with large tumours- study
Cryoablation could dissipate tumours in breast cancer patients who are not eligible for surgery
A technique that uses ice to freeze and destroy cancerous tumours has been proven effective for breast cancer patients with large tumours, providing a new treatment path for those who are not candidates for surgery.
Cryoablation is a minimally invasive treatment that uses imaging guidance such as ultrasound or a computed tomography (CT) scan to locate tumours.
An interventional radiologist will then insert small, needle-like probes into the breast to create an ice ball that surrounds the tumour, killing the cancer cells. When combined with hormonal therapy and radiation, patients can have nearly 100 per cent of their tumours destroyed.
If the tumours do grow, patients can be treated with cryoablation multiple times to control growth. The treatment has been successfully used to treat tumours smaller than 1.5 cm, but its effectiveness on larger tumours was not extensively demonstrated until now.
A new retrospective study assessed outcomes for 60 patients who underwent cryoablation because they were not candidates for surgery or refused surgery after consultation with a breast surgeon due to age, cardiac issues, hypertension, or currently undergoing chemotherapy for another cancer.
Their tumour sizes ranged from 0.3 – 9 cm with an average size of 2.5cm. Patients with tumours larger than 1.4 cm were treated with multiple probes. In a follow-up after 16 months, the recurrence rate was just 10 per cent.
“For patients who have larger tumours but can’t undergo surgery, this approach could be more effective than the current standard of care for patients who are not surgical candidates,” Dr Yolanda Bryce, an interventional radiologist at Memorial Sloan Kettering Cancer Center, explained.
“When treated with only radiation and hormonal therapy, tumours will eventually return. So, the fact that we saw only a 10 per cent recurrence rate in our study is incredibly promising.”
Bryce said surgery is still the best option for tumour removal, but there are women who, for various reasons, can’t have surgery.
“We are optimistic that this can give more women hope on their treatment journeys,” she added.
The researchers will continue to follow the patient cohort to collect data on long-term effectiveness and to better understand the impact that adjuvant therapies combined with cryoablation can have on this patient population.
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Diagnosis
Lung cancer drug shows breast cancer potential
Ovarian cancer cells quickly activate survival responses after PARP inhibitor treatment, and a lung cancer drug could help block this, research suggests.
PARP inhibitors are a common treatment for ovarian cancer, particularly in tumours with faulty DNA repair. They stop cancer cells fixing DNA damage, which leads to cell death, but many tumours later stop responding.
Researchers identified a way cancer cells may survive PARP inhibitor treatment from the outset, pointing to a potential way to block that response. A Mayo Clinic team found ovarian cancer cells rapidly switch on a pro-survival programme after exposure to PARP inhibitors. A key driver is FRA1, a transcription factor (a protein that turns genes on and off) that helps cancer cells adapt and avoid death.
The team then tested whether brigatinib, a drug approved for certain lung cancers, could block this response and boost the effect of PARP inhibitors. Brigatinib was chosen because it inhibits multiple signalling pathways involved in cancer cell survival.
In laboratory studies, combining brigatinib with a PARP inhibitor was more effective than either treatment alone. Notably, the effect was seen in cancer cells but not normal cells, suggesting a more targeted approach.
Brigatinib also appeared to act in an unexpected way. Rather than working through the usual DNA repair routes, it shut down two signalling molecules, FAK and EPHA2, that aggressive ovarian cancer cells rely on. FAK and EPHA2 are proteins that relay survival signals inside cells. Blocking both at once weakened the cells’ ability to adapt and resist treatment, making them more vulnerable to PARP inhibitors.
Tumours with higher levels of FAK and EPHA2 responded better to the drug combination. Other data link high levels of these molecules to more aggressive disease, pointing to potential benefit in harder-to-treat cases.
Arun Kanakkanthara, an oncology investigator at Mayo Clinic and a senior author of the study, said: “This work shows that drug resistance does not always emerge slowly over time; cancer cells can activate survival programmes very early after treatment begins.”
John Weroha, a medical oncologist at Mayo Clinic and a senior author of the study, said: “From a clinical perspective, resistance remains one of the biggest challenges in treating ovarian cancer. By combining mechanistic insights from Dr Kanakkanthara’s laboratory with my clinical experience, this preclinical work supports the strategy of targeting resistance early, before it has a chance to take hold. This strategy could improve patient outcomes.”
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