News
Angela Spang announced as CEO of EveryBaby
UK start-up, EveryBaby has appointed Angela Spang as its new CEO with the aim of getting this point-of-care instrument to professionals as quickly as possible.
EveryBaby is an innovative preterm diagnostic device that uses impedance spectroscopy to identify changes in cervical tissue when a mother is approaching birth. It provides real-time information that is more accurate than traditional methods such as transvaginal ultrasound or fetal fibronectin tests at a fraction of their usual costs.
Angela Spang brings over 20 years of experience in the biomedical sector to the role. She founded the medical device company, June Medical which received a Queen’s Award for Enterprise for Innovation in 2021. This success led to Angela being named UK CEO of the year in 2021 by Corporate Today. Her experience will be crucial for the success of EveryBaby’s new device and will facilitate the development and adoption of this novel diagnostic method.

EveryBaby innovation
Angela said: “I am delighted and humbled to join the dynamic team at EveryBaby. I was shocked to read how many preterm births there are each year and the resulting chronic health concerns for babies.
EveryBaby can really help to change this, improving access to safe, accurate and cost-effective diagnostics for better management of pregnancies and the prevention of avoidable preterm births all around the world.”
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Cancer
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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