News
Groundbreaking 3D mammography system opens in the north of England
The breast cancer screening pod has been installed at Queen Elizabeth Hospital in Gateshead
A new 3D system designed to “reshape” the mammography experience has opened in the north of England.
The Pristina pod, developed by GE HealthCare, will provide breast screening to the population of Gateshead, easing patient anxiety and discomfort during the exam.
Designed in a “more inviting” way, the system has been shown to lower patient anxiety by 37 per cent, resulting in a better overall experience.
Gateshead Health NHS Foundation Trust has become the first organisation in Europe to start using the pod.
“The breast screening team and I are thrilled to have the opportunity to change the way we work to help benefit Gateshead patients,” said lead radiographer for breast imaging, Joanne Brand.
“We are looking forward to welcoming more women to our ‘screening pod’ and the positive impact this will have on our patients.
“We are delighted to be the first in Europe to offer this facility and I look forward to seeing what the future holds for breast screening.”
Gateshead Health has been awarded funding from NHS England to enable the screening units to help recover the screening backlog due to the pandemic.
The pod equipment has been installed at Queen Elizabeth Hospital and has been used by its first patients last month.
Breast screening with a mammogram can help to find breast cancers early when they are too small to see or feel.
In the UK, the NHS Breast Screening Programme invites all women from the age of 50 to 71 for screening every three years.
According to Cancer UK, each year more than two million women undergo breast cancer screening.
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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