News
Pelvic health start-up wins Imperial College London competition
The entrepreneurship programme run by Imperial Enterprise Lab aims to inspire and accelerate the progress of women-led startups
A London-based start-up has been awarded the top prize of £15,000 in Imperial College London’s WE Innovate programme.
Matrix, a start-up developed by Imperial alumni and health tech entrepreneur Stilliyana Minkovska, aims to reimagine gynaecological examinations with an “AI-supported” pelvic assessment and diagnosis device.
Currently, the speculum is one of the most used instruments for cervical cancer screening and pelvic examinations. However, many people find it uncomfortable and invasive.
The self-use product developed by Matrix is designed to allow women to fully control the experience, whilst transmitting visual data for real-time assessment and a digital archive that can inform treatment and further research.
The tool is fully adaptable to women’s diverse builds and lived experiences, featuring an “empathetic” design to engage more culturally diverse communities.
“It is a replacement for the speculum which has barely changed since the Roman era,” explained Minkovska, adding that the device has the capability to screen for STIs, including cervical warts and could be used for reproductive assessments.
Her innovation comes at a time when “no shows” for cervical screening in the UK are at a 10-year high. A survey by the Department of Health and Social Care found embarrassment was the most common reason for not booking a cervical screening.
As 30 per cent of eligible individuals do not attend their cervical smear appointments, the Matrix device is hoped to help lower the costs of missed NHS appointments and reduce preventable disease by improving patient attendance.
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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