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News
Start-up launches workstation to help fertility clinics upgrade ‘outdated’ systems
CryoLink aims to facilitate the digital management of fertility clinics’ frozen specimen inventory
The US fertility technology company TMRW Life Sciences (TMRW) has announced the launch of a workstation aimed at facilitating the digital management of fertility clinics’ frozen specimen inventory.
The introduction of the CryoLink workstation aims to enable the use of TMRW’s Digital Specimen Management system with or without TMRW’s automated storage platforms.
Until now, fertility clinics could only access TMRW’s Digital Specimen Management system by adopting its storage platforms.
While TMRW’s CryoRobot Select, the only FDA-cleared fertility storage system on the market, provides safe storage environments for frozen eggs and embryos, many fertility clinics are interested in an intermediate step that will allow them to quickly improve critical steps in their storage processes without having to make the more significant investments in time, resources and facilities that adopting the entire TMRW automated system sometimes requires.
“The launch of CryoLink lowers the barriers for fertility clinics to improve legacy storage systems that are under severe strain from an explosion in storage needs,” said Louis Villalba, CEO at TMRW.
“More than a million frozen eggs and embryos are put into storage every year in the United States, a number that could grow 10-fold in the coming years. Clinics need a digital solution now to safely manage their inventories and scale successfully.”
CryoLink, Villalba said, now enables TMRW’s Digital Specimen Management system to be used with a wide range of storage options thereby enabling easier, faster adoption by clinics. The workstation can be used with the company’s automated storage platforms, its offsite storage facilities and/or traditional storage tanks currently used by fertility clinics.
He said TMRW’s Digital Specimen Management system offers fertility clinics an immediate and easily adoptable way to upgrade their onsite labs from outdated, manual systems that pre-date computers, the internet and the cloud to a modern, digital system.
“It also enables a truly unique offsite storage experience that provides instant inventory and paperless processing,” Villalba added.
Lori Batta, chief operating officer at TMRW, said: “Every fertility clinic in America should be taking a hard look at their storage safety protocols and upgrading to state-of-the-art technology that helps reduce the risk of egg/embryo damage, mix-up and loss.”
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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