News
Non-hormonal therapy successful in reducing hot flushes in women with breast cancer
The therapy developed by an Australian company was shown to reduce hot flushes and night sweats
A non-hormonal oral therapy for the treatment of hot flushes in women taking endocrine therapy for breast cancer has shown positive results in a recent trial.
The Australian company QUE Oncology behind the novel therapy has announced the results of its Phase II study following a clinical trial of 131 women with vasomotor symptoms, commonly known as hot flushes and night sweats, who were taking endocrine therapy after breast cancer.
More than 75 per cent of breast cancers are hormone-sensitive, with endocrine therapy being the standard treatment option.
Endocrine therapy is recommended for five to ten years after cancer treatment for those women that had hormone-sensitive breast cancer, to prevent disease recurrence.
However, approximately 70 per cent of women taking endocrine therapy have vasomotor symptoms that contribute to over one third of women prematurely stopping the therapy.
QUE Oncology developed Q-122 in an effort to treat vasomotor symptoms in postmenopausal women and cancer patients receiving hormone therapy.
In the placebo-control trial, Q-122 was shown to significantly reduce the frequency and severity of moderate and severe vasomotor symptoms, with associated improvement in quality of life, compared with placebo.
The oral therapy was well tolerated with no serious adverse effects, raising hopes of using it as a novel treatment for vasomotor symptoms for women with breast cancer as well as post-menopausal women experiencing similar symptoms.
“Our research findings demonstrate efficacy of Q-122 as a non-hormonal oral treatment for vasomotor symptoms in women taking oral adjuvant endocrine therapy after breast cancer, with no evidence of treatment side effects,” said principal investigator and senior author, Prof Susan Davis, director of the Monash University Women’s Health Research Program.
“In addition to a reduction in flushes and sweats, women who received Q-122 in the study reported a significantly lower likelihood of their hot flushes and sweats interfering with their sleep and social and leisure activities, compared with placebo.
“If Q-122 can provide relief from these symptoms, it holds great potential for reducing discontinuation of endocrine therapy, enabling ongoing protection against breast cancer recurrence.
“This is an extremely important potential benefit of Q-122 beyond symptom relief alone,” she added.
Dr Chris Nave, chairman of QUE Oncology and CEO of Brandon BioCatalyst, said: “It’s great to see extremely positive results from QUE Oncology’s Phase II trials published in The Lancet.
“The research highlights the need for a therapy for patients undergoing endocrine therapy for breast cancer who are experiencing vasomotor symptoms, but also the broader potential for Q-122 beyond this patient group, including postmenopausal women, of which 70-80 per cent experience vasomotor symptoms.”
The results of QUE Oncology’s Phase II study support the conduct of larger and longer studies of Q-122, with potential use extending to postmenopausal women who require an alternative to oestrogen therapy for vasomotor symptoms.
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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