Molecular Mechanisms of Antitumor Effect in Targeted Alpha-radionuclide Therapy
Abstract
Targeted α-radionuclide therapy (TAT) is a systemic therapy for cancer with cancer-targeting compounds conjugated with α-emitters. Since the linear energy transfer (LET) of α-particles are high, relative biological effectiveness is higher than low LET radiation, such as X-rays and β-particles, and the damage to the normal tissues surrounding the tumor is minimal because path length of α-particle is short (a few cells). TAT has demonstrated remarkable therapeutic effects in patients and has attracted considerable attention from physicians and researchers worldwide. In particular, a study published in 2016 showed that disseminated tumors in patients with castration-resistant prostate cancer disappeared following treatment with an actinium-225 (225Ac)-labeled prostate-specific membrane antigen ligand. What is the powerful antitumor effect of TAT? The molecular mechanisms underlying the antitumor effects of radiation have been well studied in external beam radiation therapy (EBRT). However, as EBRT and TAT are fundamentally different in terms of dose rate, irradiation uniformity, and exposure time, extrapolating the knowledge of EBRT to TAT is difficult. Compared to the research on the development of new TAT agents, studies focusing on the radiobiology of TAT are limited, and the detailed mechanisms of its antitumor effects remain poorly understood. We have developed α-emitting meta-[astatine-211 (211At)]astato-benzylguanidine ([211At]MABG) as a novel TAT agent, and investigated…
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