Exposure to ionizing radiation is associated with an increased risk of hematologic malignancies in myeloid and lymphoid lineages in humans and experimental mice. Given that substantial evidence links radiation exposure with the risk of hematologic malignancies, it is imperative to deeply understand the mechanisms underlying cellular and molecular changes during the latency period between radiation exposure and the emergence of fully transformed malignant cells. One experimental model widely used in the field of radiation and cancer biology to study hematologic malignancies induced by radiation exposure is mouse models of radiation-induced thymic lymphoma. Murine radiation-induced thymic lymphoma is primarily driven by aberrant activation of Notch signaling, which occurs frequently in human precursor T-cell lymphoblastic lymphoma (T-LBL) and T-cell lymphoblastic leukemia (T-ALL). Here, we summarize the literature elucidating cell-autonomous and non-cell-autonomous mechanisms underlying cancer initiation, progression, and malignant transformation in the thymus following total-body irradiation (TBI) in mice.
暴露于电离辐射与人类及实验小鼠骨髓系和淋巴系血液系统恶性肿瘤风险增加相关。鉴于大量证据表明辐射暴露与血液系统恶性肿瘤风险存在关联，深入理解从辐射暴露到完全转化的恶性细胞出现之间的潜伏期内细胞与分子变化的机制至关重要。在辐射与癌症生物学领域，广泛用于研究辐射诱发血液系统恶性肿瘤的实验模型之一是辐射诱导胸腺淋巴瘤小鼠模型。小鼠辐射诱导胸腺淋巴瘤主要由Notch信号通路的异常激活驱动，该现象在人类前体T细胞淋巴母细胞淋巴瘤（T-LBL）和T细胞淋巴母细胞白血病（T-ALL）中亦频繁发生。本文综述了阐明小鼠全身照射后胸腺内癌症起始、进展及恶性转化的细胞自主与非细胞自主机制的文献。
肿瘤(癌症)患者之家