News
Incubator launches in the US and the UK to support genomics start-ups
Labs-based companies will receive direct mentorship as well as connections to other companies
A US-based incubator has officially launched in the US and the UK to support genomics start-ups.
Illumina Ventures Labs, part of the independently managed fund Illumina Ventures, has two genomics labs based in Foster City, California and Cambridge, England. The accelerator is now operational and finalising agreements with several start-up companies.
With its sequencing capabilities and life science technologies from Illumina and Illumina Ventures’ portfolio companies, Illumina Ventures Labs aims to enable early-stage companies to accelerate the time needed to reach their next value inflection point.
“Illumina Ventures Labs offers a unique mechanism to invest in and build early-stage companies,” said Ron Mazumder, partner at Illumina Ventures.
“Our facilities, mentorship and investment model, based on both cash and in-kind contributions, are uniquely suited to the needs of start-ups whose value proposition is enhanced through substantial genomics and sequencing capabilities.”
According to Mazumder, Illumina Ventures Labs capitalises on Illumina Ventures’ deep technical and entrepreneurial expertise to support the development and acceleration of early-stage breakthrough genomics start-ups from company formation through Series A financings.
Labs-based companies will receive direct mentorship as well as connections to other companies within the Illumina Ventures portfolio and will gain access to experts in Illumina’s R&D organisation.
In order to access and fully develop scientific excellence, Illumina Ventures Labs says it will allow companies to stay in labs for up to eighteen months and employ virtual and hybrid formats.
It is anticipated that, after leaving the labs, companies will be significantly “de-risked” and will be attractive investment opportunities for the wider venture capital community.
Ashley Van Zeeland, vice president of corporate development at Illumina, said: “We applaud the significant progress made by Illumina Ventures Labs to launch a company creation engine providing early-stage companies access to enabling technologies to reach value creation milestones.
“We look forward to continuing to work closely with companies pioneering breakthrough applications in genomics.”
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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