News
Scalp cooling reduces persistent chemotherapy-induced alopecia, study finds
As Breast Cancer Awareness Month begins, medtech company Paxman is raising awareness of a critical and often overlooked side effect faced by many cancer patients: the risk of developing persistent chemotherapy-induced alopecia (PCIA) as a result of cancer treatment.
The efficacy of scalp cooling in preventing PCIA has once again come to the forefront through a recent study, Scalp Cooling in Preventing Persistent Chemotherapy-Induced Alopecia: A Randomised Controlled Trial, published in the Journal of Clinical Oncology by D. Kang et al.
The findings have the potential to reshape our understanding of PCIA and how Scalp Cooling has been proven to have a positive impact in reducing the risk for people navigating a cancer diagnosis.
Chemotherapy-induced alopecia (CIA) is a common side effect experienced by patients undergoing chemotherapy.
While typically temporary, some patients do not experience complete hair regrowth even after treatment ends, a condition known as persistent or permanent CIA (PCIA).
In a previous study, up to 42.3 per cent of breast cancer patients had incomplete hair regrowth three years after chemotherapy.
Moreover, although hair density often returns to baseline levels within six months post-chemotherapy, hair thickness frequently remains compromised, signalling long-term follicle damage.
Scalp cooling has already been established as a viable method to reduce hair loss during chemotherapy.
However, evidence supporting its effectiveness in preventing long-term PCIA has been limited.
This recent study aimed to investigate the impact of scalp cooling on PCIA prevention and hair recovery in breast cancer patients, and the results are promising.
The randomised clinical trial demonstrated that scalp cooling significantly reduces the incidence of PCIA by promoting hair regrowth, particularly in terms of hair thickness, compared to the control group.
The study also revealed that patients who used scalp cooling experienced faster recovery of hair density and thickness and showed significant improvements in their quality of life, including reduced psychological distress.
The need for concealment strategies, such as wigs and scarves, was also significantly lower in the scalp cooling group, further highlighting the emotional and social benefits of this intervention.
The positive outcomes were consistent across different chemotherapy regimens and age groups.
Patients who underwent scalp cooling experienced less CIA-related stress six months after chemotherapy, with reduced reliance on head coverings and lower scores on the Chemotherapy-Induced Alopecia Distress Scale (CADS).
Richard Paxman, CEO of Paxman, commented on the importance of the findings:
“This study underscores the importance of providing patients with the option of scalp cooling as a way to mitigate the risk of persistent hair loss, which can have a lasting emotional impact.
“By reducing the likelihood of PCIA, we can not only improve patients’ physical recovery but also help them regain a sense of normality and confidence post-treatment.”
The study’s results suggest that scalp cooling should be considered a standard care option for patients at risk of PCIA, especially those receiving anthracycline and/or taxane-based chemotherapy.
By offering scalp cooling as part of routine cancer care, healthcare providers can help mitigate the long-term impact of chemotherapy-induced hair loss, improving both the physical recovery and the emotional well-being of patients.
Although the trial demonstrated significant benefits in reducing PCIA within six months of chemotherapy, the authors acknowledged that additional research is needed to establish the long-term advantages of scalp cooling beyond this period.
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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