A hypothesis: radiation carcinogenesis may result from tissue injuries and subsequent recovery processes which can act as tumor promoters and lead to an earlier onset of cancer.
A hypothesis: radiation carcinogenesis may result from tissue injuries and subsequent recovery processes which can act as tumor promoters and lead to an earlier onset of cancer.
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DOI：
10.1259/bjr.20190843
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发表时间：
2020-11-01
期刊：
影响因子：
--
通讯作者：
Nakamura N
中科院分区：
文献类型：
--
作者：
Nakamura N
与对照组相比，辐射引起的癌症风险可以观察到死亡率的增加。然而，目前尚不清楚这种增加的风险是由于诱发癌症还是由于癌症的早期发病。在小鼠研究中，研究反复表明，辐照后，存活曲线向较低年龄偏移，但仍与对照曲线平行，且向较低年龄偏移的程度与剂量有关。这种转变不能用诱导模型令人满意地解释，该模型假定暴露组中的癌症由自发和诱导事件组成。因此，这种转变似乎可以解释为，暴露组中所有动物的寿命都缩短了。然而，在这种情况下，事实证明，辐射效应不能再被解释为致癌突变的结果，因为这些影响必须涉及所有肿瘤，辐射的有效性随着剂量的变化而变化。这导致推测，辐射暴露诱导大范围的组织损伤，这些损伤随后受到长期的系统性恢复过程，作为肿瘤细胞的促进剂。换句话说，位于辐照场中的潜在癌症干细胞可以逃避致癌损伤，但在生命后期受到辐射诱导的激活微环境的刺激，朝着恶性肿瘤的发展。这是辐射的非目标效应或旁观者效应的一种不同寻常的形式。值得注意的是，该模型表明，可能有一条或多条途径可以用来干预暴露后致癌过程，低剂量的癌症风险可以用几天或几周的生命损失来描述。
Cancer risks from radiation can be observed as an increase in mortality when compared to a control group. However, it is unknown if this increased risk results from the induction of cancer or from an earlier onset of cancer. In mouse studies, it has been repeatedly shown that after an irradiation, the survival curve is shifted toward lower ages, but remains parallel to the control curve, and the extent of the shift in time to lower ages is dose-dependent. This shift is not satisfactorily explained by the induction model which assumes that cancers in the exposed group consist of spontaneous and induced events. Consequently, it seems that this shift could be interpreted to mean that all animals in the exposed group had suffered from life shortening. Under this scenario, however, it turns out that the radiation effects can no longer be interpreted as the result of oncogenic mutations, because these effects would have to involve all tumors, and the effectiveness of radiation changes with the dose. This leads to the speculation that radiation exposures induce a broad range of tissue injuries, and that these injuries are subsequently subjected to longlasting systemic recovery processes which act as promoters for tumor cells. In other words, potential cancer stem cells which were located in the irradiated field can escape oncogenic damage but undergo stimulation later in life toward the development of malignancy from radiation-induced activated microenvironment. This is an unusual form of the non-targeted or bystander effects of radiation. It is worth noting that this model suggests that there could be a path or paths which could be used to intervene in the process of post-exposure carcinogenesis, and that cancer risks at low doses could be described as days or weeks of life lost.
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TGFβ和PDGF信号传导的结合抑制减弱了辐射诱导的肺纤维化。
影响因子：
7.2
作者：
Dadrich M;Nicolay NH;Flechsig P;Bickelhaupt S;Hoeltgen L;Roeder F;Hauser K;Tietz A;Jenne J;Lopez R;Roehrich M;Wirkner U;Lahn M;Huber PE
通讯作者：
Huber PE
影响因子：
50.3
作者：
Nguyen DH;Oketch-Rabah HA;Illa-Bochaca I;Geyer FC;Reis-Filho JS;Mao JH;Ravani SA;Zavadil J;Borowsky AD;Jerry DJ;Dunphy KA;Seo JH;Haslam S;Medina D;Barcellos-Hoff MH
通讯作者：
Barcellos-Hoff MH
影响因子：
3.4
作者：
Ellender, M;Harrison, JD;Cox, R
通讯作者：
Cox, R
DOI：
10.1073/pnas.77.12.7262
发表时间：
1980-01-01
期刊：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES
影响因子：
--
作者：
KENNEDY, AR;FOX, M;LITTLE, JB
通讯作者：
LITTLE, JB
影响因子：
64.8
作者：
Dou Z;Ghosh K;Vizioli MG;Zhu J;Sen P;Wangensteen KJ;Simithy J;Lan Y;Lin Y;Zhou Z;Capell BC;Xu C;Xu M;Kieckhaefer JE;Jiang T;Shoshkes-Carmel M;Tanim KMAA;Barber GN;Seykora JT;Millar SE;Kaestner KH;Garcia BA;Adams PD;Berger SL
通讯作者：
Berger SL