Heber Elisa M, Aromando Romina F, Trivillin Verónica A, Itoiz Maria E, Nigg David W, Kreimann Erica L, Schwint Amanda E
Department of Radiobiology, National Atomic Energy Commission, Avenida General Paz 1499, B1650KNA San Martín, Prov Buenos Aires, Argentina.
Arch Oral Biol. 2007 Mar;52(3):273-9. doi: 10.1016/j.archoralbio.2006.10.007. Epub 2006 Nov 29.
We previously reported the therapeutic success of different BNCT protocols in the treatment of oral cancer, employing the hamster cheek pouch model. The aim of the present study was to evaluate the effect of these BNCT protocols on DNA synthesis in precancerous and normal tissue in this model and assess the potential lag in the development of second primary tumors in precancerous tissue. The data are relevant to potential control of field cancerized tissue and tolerance of normal tissue.
We evaluated DNA synthesis in precancerous and normal pouch tissue 1-30 days post-BNCT mediated by boronophenylalanine (BPA), GB-10 (Na(2)(10)B(10)H(10)) or (BPA+GB-10) employing incorporation of 5-bromo-2'-deoxyuridine as an end-point. The BNCT-induced potential lag in the development of second primary tumors from precancerous tissue was monitored.
A drastic, statistically significant reduction in DNA synthesis occurred in precancerous tissue as early as 1 day post-BNCT and was sustained at virtually all time-points until 30 days post-BNCT for all the protocols. The histological categories evaluated individually within precancerous tissue (dysplasia, hyperplasia and NUMF [no unusual microscopic features]) responded similarly. DNA synthesis in normal tissue treated with BNCT oscillated around the very low pre-treatment values. A BNCT-induced lag in the development of second primary tumors was observed.
BNCT induced a drastic fall in DNA synthesis in precancerous tissue that would be associated to the observed lag in the development of second primary tumors. The minimum variations in DNA synthesis in BNCT-treated normal tissue would correlate with the absence of normal tissue radiotoxicity. The present data would support the control of field-cancerized areas by BNCT.
我们之前报道了采用仓鼠颊囊模型，不同的硼中子俘获疗法（BNCT）方案在治疗口腔癌方面取得的治疗成功。本研究的目的是评估这些BNCT方案对该模型中癌前组织和正常组织DNA合成的影响，并评估癌前组织中第二原发性肿瘤发生发展的潜在延迟。这些数据与场癌化组织的潜在控制和正常组织的耐受性相关。
我们在硼苯丙氨酸（BPA）、GB-10（Na₂¹⁰B₁₀H₁₀）或（BPA + GB-10）介导的BNCT后1 - 30天，通过掺入5-溴-2'-脱氧尿苷作为终点来评估癌前组织和正常颊囊组织中的DNA合成。监测BNCT诱导的癌前组织中第二原发性肿瘤发生发展的潜在延迟。
早在BNCT后1天，癌前组织中的DNA合成就出现了急剧的、具有统计学意义的减少，并且在所有方案中，几乎在所有时间点直至BNCT后30天均持续存在。在癌前组织内单独评估的组织学类别（发育异常、增生和NUMF [无异常微观特征]）反应相似。接受BNCT治疗的正常组织中的DNA合成在非常低的治疗前值附近波动。观察到BNCT诱导的第二原发性肿瘤发生发展的延迟。
BNCT导致癌前组织中DNA合成急剧下降，这与观察到的第二原发性肿瘤发生发展的延迟相关。BNCT治疗的正常组织中DNA合成的最小变化与正常组织无放射性毒性相关。目前的数据将支持通过BNCT控制场癌化区域。
