News
Israeli medical developer raises US$9m to help women with pelvic organ prolapse
More than three million women in the US suffer from the condition with the rate of diagnosis growing due to the ageing population
An Israeli medical developer has raised US$9m series B financing to advance its prolapse repair technology.
FEMSelect has developed EnPlace, a less invasive, meshless approach to prolapse repair, to help women diagnosed with pelvic organ prolapse – a medical condition that occurs when one or more of the organs in the pelvis slip down from their normal position and bulge into the vagina.
The current standard of care includes hysterectomy or complex mesh surgery which some women want to avoid.
The company says its technology enables a minimally invasive approach in under 30 minutes and according to clinical studies, women can return to normal activities within a few days.
EnPlace system’s approach is cleared by the FDA for pelvic floor ligament fixation for the management of symptomatic uterine prolapse, a complication in the lives of nearly 50 per cent of women over the age of 50.
The investment round, led by New Age Ventures and co-led by TriVentures, will support the growth and market penetration of EnPlace, primarily in the US.
The financing comes after the system’s recent launches in the US and Israel and supported by clinical data on EnPlace’s apical repair success rate of 92.3 per cent at four years, as reported in the peer review International Journal of Gynecology and Obstetrics.
In the past year, FEMSelect has partnered with women’s healthcare company LiNA Medical USA, educating physicians on the technology, currently available in more than 25 states across the US
Earlier this year, EnPlace has obtained a procedure code from the Centers for Medicare and Medicaid Services (CMS) enabling healthcare facilities to receive reimbursement for the procedure.
Debbie Garner, co-CEO of FEMSelect, said: “This investment is a testament to our team and the EnPlace system.
“It enables us to expand the medical and patient communities and to serve many more women who are seeking a minimally invasive treatment option. This is a tremendous step forward for the company.”
Weight loss jabs are being studied to see if they could help women with polycystic ovary syndrome (PCOS)
The condition, which affects up to one in ten women, changes how the ovaries work and is linked to infertility and weight gain.
Dr Shagaf Bakour has won a £60,000 NHS research grant through Sandwell and West Birmingham NHS Trust to look at whether drugs such as Mounjaro and Ozempic might help.
“The research could lead to earlier support, better long-term health, and more joined-up care for a condition that affects many women but is still often overlooked,” she said.
Women with PCOS have higher levels of male hormones and can suffer from irregular periods and symptoms such as excess body or facial hair, the NHS said.
Associated weight gain can also lead to an increased risk of diabetes and heart problems.
Bakour, a gynaecologist and director of medical education at Aston Medical School, will work with a team to evaluate the effect of the weight loss medicines on metabolic and reproductive outcomes.
The drugs mimic a hormone called GLP-1, which suppresses appetite.
Bakour, alongside Dr Hoda Harb, a consultant obstetrician and gynaecologist at the NHS trust, will review existing evidence on their use and assess how they help patients with PCOS.
“The aim is to give women with PCOS evidence-informed, clearer treatment options and more consistent care,” she said.
“The project hopes to show whether these medicines can improve both general health and fertility health, while also helping local services develop clearer care pathways.
Prof Elizabeth Hughes, director of research and development at the NHS trust, said the effects of PCOS, including infertility, were “very emotive subjects”.
“We should be doing all we can within research and development to advance healthcare for women and to better help future generations with this condition,” she added.
An AI tool could help spot breast cancer risk by analysing how individual breast cells behave when squeezed under stress, research suggests.
Researchers at City of Hope and the University of California, Berkeley, created a microfluidic platform that assesses women’s breast cancer risk at the cellular level.
The platform squeezes individual breast epithelial cells, which line breast tissue, to measure how they deform, recover and behave under stress.
Because more than 90 per cent of women do not have a known genetic predisposition to breast cancer or a family history of the disease, the researchers said the approach could help fill a key gap in risk assessment.
Mark LaBarge, professor in the department of population sciences at City of Hope, said: “For women with a known genetic risk factor for breast cancer, there are things you can do like follow a higher-risk screening protocol. For everybody else, you’re left wondering, ‘Am I at high risk?’
“By translating physical changes in cells into quantifiable data, this tool gives women something tangible to discuss with their doctors, not just risk estimates, but evidence drawn directly from their own cells.”
The researchers developed a machine learning algorithm that identifies and measures cells showing signs of accelerated ageing, generating an individual breast cancer risk score.
They said the platform uses simple electronics that could be easy and affordable to replicate on a large scale.
Lydia Sohn, chair in mechanical engineering at UC Berkeley, said: “Our team isn’t the first to measure the mechanical properties of cells; however, other approaches require advanced imaging technology that’s expensive, cumbersome and has limited availability.
“In contrast, MechanoAge uses computer chips that are simpler than an Apple Watch and ‘RadioShack parts’ that are cheap and easy to assemble, potentially making the device highly scalable.”
About 6 per cent of women who develop breast cancer carry known genetic mutations.
For women outside this group, risk is usually estimated indirectly using population models or measures such as breast density, which can both overestimate and underestimate individual risk.
The researchers said there is currently no non-genetic test that can identify women at higher risk of breast cancer.
Screening mammograms can detect cancer only once it has started to grow, but the MechanoAge platform aims to assess risk earlier by looking for physical changes in individual cells.
Using the platform, the researchers found that breast cells appear to have a “mechanical age” separate from a person’s chronological age, based on how the cells respond to stress.
They said this is the first time mechanical age has been quantified in biological cells.
Sohn said: “We learned that the older the mechanical age, as determined by how cells respond to being squeezed through our microfluidic device, the higher the risk for breast cancer.”
In this type of mechano-node-pore sensing, an electrical current is measured across a liquid-filled channel.
As cells pass through, they disrupt the current, generating measurements about their size and shape. By narrowing parts of the channel, researchers squeeze the cells and then measure how long each one takes to return to its normal shape.
The team found that cells from older women were stiffer and took longer to bounce back after being squeezed.
They also identified a subset of younger women whose cells behaved more like those from older women. These cells came from women with genetic mutations linked to a higher breast cancer risk.
The researchers then refined the algorithm to assign a risk score based on the cells’ measured mechanical and physical properties. They said it successfully identified women with known genetic risks.
The team then used it to compare cells from healthy women, women with a family history of breast cancer, and cells taken from the healthy breast of women with breast cancer in the other breast.
LaBarge said: “With accuracy, we were able to figure out which women were at high risk of breast cancer and which women didn’t seem to be.”
The work grew out of more than 12 years of collaboration between the two labs, combining engineering with cancer and ageing biology.
Sohn said: “It’s a true collaboration. We’ve learned a lot from each other.
LaBarge added: “In my view, this is what happens when you have a real collaboration that develops over a long time. This result is not what we imagined at the beginning.”
An experimental drug slowed triple-negative breast cancer in mice by flooding tumour cells with toxic fats.
Triple-negative breast cancer lacks three common drug targets, making it one of the hardest-to-treat and most aggressive forms of the disease.
The compound, known as DH20931, appears to push cancer cells past their limits by triggering a surge in ceramides, fat-like molecules that place the cells under intense stress until they self-destruct.
In lab experiments, the drug also made standard chemotherapy more effective. When combined with doxorubicin, researchers were able to reduce the dose needed to kill cancer cells by about fivefold.
The drug targets an enzyme known as CerS2 to sharply increase production of these lipids and stress cancer cells. Healthy cells, by contrast, showed lower sensitivity to the drug in lab tests.
While the early results are promising, further preclinical and clinical trials would still be needed to determine the safety and effectiveness of DH20931 in humans.
Satya Narayan, a professor in the University of Florida’s College of Medicine, led the study with an international group of collaborators.
The researchers published their results on human-derived tumours on 21 April and presented their findings on combination therapy at the annual meeting of the American Association for Cancer Research in San Diego.
Narayan likened the drug’s effects to a home’s electrical system handling a power surge.
While healthy cells act like a properly grounded and installed circuit, cancer cells are more like a jumble of mismatched wires and faulty fuses. DH20931 overwhelms cells not with electricity, but with fats.
He said: “When that surge goes into the cancer cells, they cannot handle the amount of power they are getting. The fuses burn out, the cell can’t handle the surge and it dies.”
The compound was developed at the University of Florida in the lab of Sukwong Hong.
Hong, now a professor at the Gwangju Institute of Science and Technology in South Korea, created DH20931 as one of many drug candidates tested for efficacy in Narayan’s lab.
In the study, researchers implanted human triple-negative breast cancer tumours into mice and treated them with DH20931.
The drug significantly slowed tumour growth without causing noticeable weight loss or signs of toxicity in the animals. In separate lab experiments, it also showed activity against other breast cancer subtypes.
In addition to increasing lipid levels, DH20931 triggers a second stress signal by flooding cells with calcium.
Together, these effects disrupt the mitochondria, the structures that produce a cell’s energy, ultimately leading to cell death.
Narayan said: “It does not just follow one pathway but it goes through multiple pathways. It’s a two-hit hypothesis.
“These pathways are common in all breast cancer types and other solid tumours, so we think this drug can be useful not only in triple-negative breast cancer but potentially other cancers as well.”
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