News
Bias in research may mask earlier onset menopause for Black and Hispanic women
Researchers have found Black and Hispanic women reached menopausal age earlier than their white counterparts
Participant selection bias in women’s health studies may mask earlier onset menopause for Black and Hispanic women, a new study has shown.
Researchers from the University of Michigan School of Public Health have said that failure to account for weathering led to exclusion of many Black and Hispanic women from the Study of Women’s Health Across the Nation (SWAN) cohort and misses critical racial differences in menopausal age.
Established in 1994, SWAN examines midlife health and menopausal transition to improve interventions and educational programs for women of this life stage.
Weathering, a framework developed by Michigan Public Health professor Arline Geronimus, posits earlier health deterioration of oppressed and exploited populations due to social influences and chronic stress. The research is published in the International Journal of Epidemiology.
“We were able to quantify the racial differences in the rate of exclusion from SWAN due to earlier menopause, and then statistically account for it in SWAN’s data,” said Alexis Reeves, a postdoctoral scholar at Stanford University’s School of Medicine who conducted the work while a doctoral student at Michigan Public Health.
“We found that Black and Hispanic women had statistically significant earlier natural, and particularly surgical, menopause than white women. The study suggests that this common bias may lead to underestimation of racial disparities in health and aging, and is important to consider in further research.”
The findings have shown that Black and Hispanic women reached menopausal age approximately 1.2 years earlier than their white counterparts when exclusion due to weathering is accounted for, whereas SWAN’s original data found little to no racial differences in menopausal age.
The study is one of the first to consider that weathering biases an understanding of racial disparities, particularly with data to support it.
“Mistrust of the medical system due to historical injustices is an important part of the lack of inclusion of minoritised populations in studies,” said Reeves.
“However, this study suggests that eligibility criteria—and the given age for inclusion into studies—set by researchers themselves also plays an important part in exclusion of minorities from studies.
Siobán Harlow, professor emerita of epidemiology and senior author of the study, said: “The implications of these findings are incredibly important to understanding the true burden of racial disparities in women’s health and indicate that researchers need to be more thoughtful about eligibility criteria and the potential for underestimating racial disparities in longitudinal health studies.”
“Accounting for data biases in future studies will allow us to better understand and address the negative health outcomes of these marginalised populations.”
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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