News
UN event calls for global inclusivity push
Speakers at a recent UN event have called for leaders, policy experts and change-makers to help accelerate private-sector commitments toward women’s economic empowerment by 2030.
United Nations Global Compact is a non-binding United Nations pact to get businesses and firms worldwide to adopt sustainable and socially responsible policies, and to report on their implementation.
The event was delivered in partnership with UN Women and the Champions of Change Coalition.
Melissa Powell is Deputy Executive Director of the UN Global Compact.
Powell said: “Accelerating women’s full participation is not just a moral imperative, it’s an economic one.
“As we celebrate the 30th anniversary of the Beijing Declaration and 25 years of the UN Global Compact, we have never been closer to a true tipping point.”
Despite decades of progress, on average, women are paid about 20 per cent less than men, according to the International Labour Organization leading to significant lifetime income inequality.
At the current rate it will take 134 years to close the global gender gap.
Yet companies with diverse leadership teams are 25 per cent more likely to outperform their peers.
During the dialogue, participants examined how businesses can apply a gender lens across the value chain by creating gender-responsive supply chains and directing capital to women-owned businesses, engage male allies and advocate for policy enablers to bridge persistent gender gaps worldwide.
Powell added: “By investing in women-led enterprises, championing male allyship and building equitable supply chains, businesses can lead the charge on achieving the Sustainable Development Goals by 2030.”
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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