News
Femtech company raises €4.22m to improve gynaecological diagnostics
Endometrial cancer begins as a growth of cells in the uterus and is traditionally diagnosed with the help of an endometrial biopsy
A Spanish femtech company has raised €4.22m in funding to advance gynaecological diagnostics.
Barcelona-based start-up Mimark Diagnostics, a spin-off from the Vall d’Hebron Research Institute (VHIR), aims to speed up the discovery, verification and validation of biomarkers to develop new solutions for gynaecological patients.
Its in vitro diagnostic test for endometrial cancer is now in the last stage of prototyping and is hoped to move to the verification and validation stages.
Endometrial cancer, also known as uterine cancer, is a type of cancer that begins as a growth of cells in the uterus. It is traditionally diagnosed with the help of an endometrial biopsy, a procedure in which a tissue sample is obtained from the endometrium.
However, this could leave up to 30 per cent of patients undiagnosed due to technical failure or an inadequate amount of tissue.
Mimark’s innovation, which looks at five protein biomarkers in uterine fluid samples, aims to provide patients with a better diagnosis method and offer them more information on the histological subtype of the tumour to guide surgical treatment.
“This seed funding represents a significant milestone for Mimark and validates our commitment to improve gynecological diagnostics,” said Marina Rigau, co-founder and CEO of Mimark.
“Thanks to this funding we will advance on bringing our first product to the market; an in vitro diagnostic for endometrial cancer. We are excited about the journey ahead and the positive impact our innovations will have on women’s health.”
The investment is hoped to drive the development of the company’s solutions, with EU participation from the EIC Accelerator (European Innovation Council) and private investors, including Clave Capital, Nara Capital, Namarel Ventures, WA4STEAM, CDTI Innvierte, Inveready and Canterbury Scientific.
The funds, Rigau added, will be “instrumental” in advancing Mimark’s mission.
According to the co-founder, the start-up will be starting to accelerate the verification and clinical validation of WomEC, expand research and development efforts and strengthen collaborations with healthcare institutions in the field of gynaecology.
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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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