Dystrophic pathways in human hair follicles after chemotherapy with or without scalp cooling

Chemotherapy acts on rapidly growing cells, including hair follicles. Chemotherapy-induced shedding of hairs usually occurs 7–14 days after infusion. For patients, chemotherapy-induced alopecia (CIA) is one of the most distressing side-effects of treatment. Scalp cooling can prevent or minimise CIA. The rationale for the use of scalp hypothermia has not been completely elucidated and may depend on p53, Caspase-3 and Bax/bcl2. Suppression of these enzymes is possibly one of the underlying mechanisms influencing the effect of scalp cooling.

The objective of this study is to determine the dystrophic pathway factors involved in chemotherapy induced-apoptosis (programmed cell death) in the hair follicle after chemotherapy.
The study will be conducted in the out-patient chemotherapy clinic of the department of Internal Medicine of the Northwest Clinics.

Study population: The study will enroll ten patients with breast cancer (with/ without scalp cooling) evaluable for one cycle of intravenous administered taxane containing chemotherapy.

Damage response pathways can possibly explain the working mechanism of scalp cooling

Hairs will be collected at six different time points T=0 acts as a control time point as no chemotherapy is administered.

Hair sample collection time points:

t=0 (before treatment with chemotherapy)

t=1 (one day after chemotherapy)

t=2 (two days after chemotherapy)

t=3 (three days after chemotheray)

t=5 (five days after chemotherapy)

t=7 (seven days after chemotherapy)

Why scalp cooling is effective in one patient but not in another remains unclear. As the rationale for the use of scalp hypothermia has not been completely elucidated, the cooling protocol may not be optimal. To understand the underlying pathobiology of CIA, we investigate molecular damage-response pathways in hair follicles after chemotherapy and the influence of scalp cooling on these molecular pathways.