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Journal articles on the topic 'Radiation induced liver disease'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 February 2022

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1

Khozouz, Radwan F., Syed Z. Huq, and Michael C. Perry. "Radiation-Induced Liver Disease." Journal of Clinical Oncology 26, no. 29 (October 10, 2008): 4844–45. http://dx.doi.org/10.1200/jco.2008.18.2931.

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2

Laurie, R. M., M. W. T. Chao, and C. A. Dow. "Radiation induced liver disease: is hereditary haemochromatosis a risk factor?" Journal of Radiotherapy in Practice 3, no. 2 (March 2003): 101–4. http://dx.doi.org/10.1017/s1460396903000086.

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A 71-year-old man with Stage II gastric cancer developed rapid onset radiation induced liver disease after ceasing adjuvant chemotherapy and radiotherapy. Autopsy revealed moderate hepatocellular iron overload. Posthumously, he was found to be a compound heterozygote for hereditary haemochromatosis. Since both radiation and iron overload may induce liver damage through the activation of hepatic stellate cells, it is possible that hepatocellular iron overload may potentiate the effects of irradiation and predispose the patient to radiation induced liver disease.

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3

Koay, Eugene J., Dawn Owen, and Prajnan Das. "Radiation-Induced Liver Disease and Modern Radiotherapy." Seminars in Radiation Oncology 28, no. 4 (October 2018): 321–31. http://dx.doi.org/10.1016/j.semradonc.2018.06.007.

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4

SILVEIRA, E. "Radiation-induced liver disease: a laparoscopic approach." American Journal of Gastroenterology 96, no. 9 (September 2001): S119. http://dx.doi.org/10.1016/s0002-9270(01)03113-6.

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5

Benson, R., R. Madan, R. Kilambi, and S. Chander. "Radiation induced liver disease: A clinical update." Journal of the Egyptian National Cancer Institute 28, no. 1 (March 2016): 7–11. http://dx.doi.org/10.1016/j.jnci.2015.08.001.

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6

da Silveira, Eduardo B. V., Lennox Jeffers, and Eugene R. Schiff. "Diagnostic laparoscopy in radiation-induced liver disease." Gastrointestinal Endoscopy 55, no. 3 (March 2002): 432–34. http://dx.doi.org/10.1067/mge.2002.120879.

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7

Bergamo, A., K. Kaweloa, A. J. Patel, P. Mavroidis, N. Papanikolaou, S. Stathakis, and A. N. Gutierrez. "Hypofractionated Liver Stereotactic Body Radiation Therapy: Biological Effective Dose Correlated Radiation-Induced Liver Disease." International Journal of Radiation Oncology*Biology*Physics 90, no. 1 (September 2014): S849. http://dx.doi.org/10.1016/j.ijrobp.2014.05.2433.

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8

Nakajima, Tetsuo, Yasuharu Ninomiya, and Mitsuru Nenoi. "Radiation-Induced Reactions in The Liver — Modulation of Radiation Effects by Lifestyle-Related Factors —." International Journal of Molecular Sciences 19, no. 12 (December 3, 2018): 3855. http://dx.doi.org/10.3390/ijms19123855.

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Radiation has a wide variety of effects on the liver. Fibrosis is a concern in medical fields as one of the acute effects of high-dose irradiation, such as with cancer radiotherapies. Cancer is also an important concern following exposure to radiation. The liver has an active metabolism and reacts to radiations. In addition, effects are modulated by many environmental factors, such as high-calorie foods or alcohol beverages. Adaptations to other environmental conditions could also influence the effects of radiation. Reactions to radiation may not be optimally regulated under conditions modulated by the environment, possibly leading to dysregulation, disease or cancer. Here, we introduce some reactions to ionizing radiation in the liver, as demonstrated primarily in animal experiments. In addition, modulation of radiation-induced effects in the liver due to factors such as obesity, alcohol drinking, or supplements derived from foods are reviewed. Perspectives on medical applications by modulations of radiation effects are also discussed.

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Iwasa, Satoru, Hiroshi Mayahara, Takashi Tanaka, and Yoshinori Ito. "Ring-Enhancing Lesion Associated With Radiation-Induced Liver Disease." Journal of Clinical Oncology 31, no. 14 (May 10, 2013): e243-e244. http://dx.doi.org/10.1200/jco.2012.46.7217.

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10

Kim, Jieun, and Youngmi Jung. "Radiation-induced liver disease: current understanding and future perspectives." Experimental & Molecular Medicine 49, no. 7 (July 2017): e359-e359. http://dx.doi.org/10.1038/emm.2017.85.

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11

Zhu, Ji, Xiao-Dong Zhu, Shi-Xiong Liang, Zi-Yong Xu, Jian-Dong Zhao, Qi-Fang Huang, An-Yu Wang, Long Chen, Xiao-Long Fu, and Guo-Liang Jiang. "Prediction of Radiation Induced Liver Disease Using Artificial Neural Networks." Japanese Journal of Clinical Oncology 36, no. 12 (October 26, 2006): 783–88. http://dx.doi.org/10.1093/jjco/hyl117.

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12

JIANG, G., S. LIANG, X. ZHU, X. FU, and H. LU. "Radiation-induced liver disease in three-dimensional conformal radiotherapy for primary liver carcinoma." International Journal of Radiation OncologyBiologyPhysics 60 (September 2004): S413. http://dx.doi.org/10.1016/s0360-3016(04)01601-3.

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13

Jiang, G., S. Liang, X. Zhu, X. Fu, and H. Lu. "Radiation-induced liver disease in three-dimensional conformal radiotherapy for primary liver carcinoma." International Journal of Radiation Oncology*Biology*Physics 60, no. 1 (September 2004): S413. http://dx.doi.org/10.1016/j.ijrobp.2004.07.297.

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14

Huang, P., D. Li, D. S. Kapp, H. Li, J. Chen, C. Ma, G. Yu, et al. "Adjusted Dose and the Relation to Radiation-Induced Liver Disease During Liver 3-Dimensional Conformal Radiation Therapy." International Journal of Radiation Oncology*Biology*Physics 96, no. 2 (October 2016): E628—E629. http://dx.doi.org/10.1016/j.ijrobp.2016.06.2202.

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15

Seidensticker, Max, Matthias Philipp Fabritius, Jannik Beller, Ricarda Seidensticker, Andrei Todica, Harun Ilhan, Maciej Pech, et al. "Impact of Pharmaceutical Prophylaxis on Radiation-Induced Liver Disease Following Radioembolization." Cancers 13, no. 9 (April 21, 2021): 1992. http://dx.doi.org/10.3390/cancers13091992.

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Background: Radioembolization (RE) with yttrium-90 (90Y) resin microspheres yields heterogeneous response rates in with primary or secondary liver cancer. Radiation-induced liver disease (RILD) is a potentially life-threatening complication with higher prevalence in cirrhotics or patients exposed to previous chemotherapies. Advances in RILD prevention may help increasing tolerable radiation doses to improve patient outcomes. This study aimed to evaluate the impact of post-therapeutic RILD-prophylaxis in a cohort of intensely pretreated liver metastatic breast cancer patients; Methods: Ninety-three patients with liver metastases of breast cancer received RE between 2007 and 2016. All Patients received RILD prophylaxis for 8 weeks post-RE. From January 2014, RILD prophylaxis was changed from ursodeoxycholic acid (UDCA) and prednisolone (standard prophylaxis [SP]; n = 59) to pentoxifylline (PTX), UDCA and low-dose low molecular weight heparin (LMWH) (modified prophylaxis (MP); n = 34). The primary endpoint was toxicity including symptoms of RILD; Results: Dose exposure of normal liver parenchyma was higher in the modified vs. standard prophylaxis group (47.2 Gy (17.8–86.8) vs. 40.2 Gy (12.5–83.5), p = 0.017). All grade RILD events (mild: bilirubin ≥ 21 µmol/L (but <30 μmol/L); severe: (bilirubin ≥ 30 µmol/L and ascites)) were observed more frequently in the SP group than in the MP group, albeit without significance (7/59 vs. 1/34; p = 0.140). Severe RILD occurred in the SP group only (n = 2; p > 0.1). ALBI grade increased in 16.7% patients in the MP and in 27.1% patients in the SP group, respectively (group difference not significant); Conclusions: At established dose levels, mild or severe RILD events proved rare in our cohort. RILD prophylaxis with PTX, UDCA and LMWH appears to have an independent positive impact on OS in patients with metastatic breast cancer and may reduce the frequency and severity of RILD. Results of this study as well as pathophysiological considerations warrant further investigations of RILD prophylaxis presumably targeting combinations of anticoagulation (MP) and antiinflammation (SP) to increase dose prescriptions in radioembolization.

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16

Janoray, G., S. Chapet, A. Ruffier-Loubière, G. Bernadou, Y. Pointreau, and G. Calais. "Robotic stereotactic body radiation therapy for tumours of the liver: Radiation-induced liver disease, incidence and predictive factors." Cancer/Radiothérapie 18, no. 3 (June 2014): 191–97. http://dx.doi.org/10.1016/j.canrad.2014.03.009.

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17

Castiglioni, S., A. Tozzi, S. Arcangeli, P. Mancosu, G. Reggiori, P. Navarria, E. Clerici, A. Fogliata, L. Cozzi, and M. Scorsetti. "Stereotactic Body Radiation Therapy With Ablative Dose on Liver Metastases: Radiation-induced Liver Disease (RILD) and Toxicity Assessment." International Journal of Radiation Oncology*Biology*Physics 84, no. 3 (November 2012): S12. http://dx.doi.org/10.1016/j.ijrobp.2012.07.036.

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18

Schoenfeld, J. D., H. J. Mamon, L. S. Blaszkowsky, P. C. Enzinger, J. Y. Wo, J. N. Allen, R. C. Wadlow, D. P. Ryan, and T. S. Hong. "Gastric adenocarcinoma treated with radiation with or without epirubicin-based chemotherapy: Evaluation of radiation-induced liver disease." Journal of Clinical Oncology 29, no. 4_suppl (February 1, 2011): 110. http://dx.doi.org/10.1200/jco.2011.29.4_suppl.110.

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110 Background: Anthracycline chemotherapy has been associated with radiation-induced liver disease (RILD). We sought to compare the incidence of liver toxicity among patients with gastric adenocarcinoma treated with radiotherapy (RT) with or without epirubicin-based chemotherapy. Methods: We performed a retrospective analysis of 94 patients with gastric adenocarcinoma treated at Massachusetts General Hospital since November 2005 and the Dana-Farber Cancer Institute since August 1998. All patients underwent definitive surgery and RT (median dose 45 Gray) with a minimum follow up of 6 months. Primary endpoints were development of ascites, radiographic liver change and elevations in liver function tests (LFTs), including alkaline phosphatase (ALP), aspartate transaminase (AST) and alanine transaminase (ALT). Results: In total, 34 patients received epirubicin-based chemotherapy including 9 perioperatively (6 with oxaliplatin and capecitabine [EOX]; 2 with cisplatin and 5-flourouracil [ECF]; 1 with oxaliplatin and 5-flourouracil [EOF]) and 25 postoperatively (2 EOX; 22 ECF; 1 combination). Seven patients were treated with neoadjuvant RT; 87 received adjuvant RT a median of 88 days after surgery (interquartile range 73-108 days). Twenty-one patients developed ascites within 6 months of completing RT, all but one of whom developed peritoneal carcinomatosis or metastatic disease. Among 57 patients that did not develop metastases, maximum elevations in LFTs were similar in patients that received epirubicin-based chemotherapy compared to those who did not (ALP/AST/ALT 150/44/50 vs. 142/41/44, p=0.25/0.36/0.14, respectively), as were rates of radiographic liver change (22% vs. 13%, p=0.44). Conclusions: Epirubicin-based chemotherapy does not significantly increase the risk of RILD in a recent cohort of patients treated with modern RT techniques and dose-constraints. In this setting, treatment of gastric adenocarcinoma with RT and either pre- or postoperative chemotherapy is well tolerated with low rates of liver toxicities. Development of liver toxicity, particularly ascites, within six months of RT may be a harbinger of metastatic disease. No significant financial relationships to disclose.

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19

Dawson, Laura A., Daniel Normolle, James M. Balter, Cornelius J. McGinn, Theodore S. Lawrence, and Randall K. Ten Haken. "Analysis of radiation-induced liver disease using the Lyman NTCP model." International Journal of Radiation Oncology*Biology*Physics 53, no. 4 (July 2002): 810–21. http://dx.doi.org/10.1016/s0360-3016(02)02846-8.

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20

De La Pinta Alonso, Carolina. "Radiation-induced liver disease in the era of SBRT: a review." Expert Review of Gastroenterology & Hepatology 14, no. 12 (September 14, 2020): 1195–201. http://dx.doi.org/10.1080/17474124.2020.1814744.

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21

Liang, Shi-Xiong, Xiao-Dong Zhu, Zhi-Yong Xu, Ji Zhu, Jian-Dong Zhao, Hai-Jie Lu, Yun-Li Yang, et al. "Radiation-induced liver disease in three-dimensional conformal radiation therapy for primary liver carcinoma: The risk factors and hepatic radiation tolerance." International Journal of Radiation Oncology*Biology*Physics 65, no. 2 (June 2006): 426–34. http://dx.doi.org/10.1016/j.ijrobp.2005.12.031.

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22

Naz, Naila, Shakil Ahmad, Silke Cameron, Federico Moriconi, Margret Rave-Fränk, Hans Christiansen, Clemens Friedrich Hess, Giuliano Ramadori, and Ihtzaz A. Malik. "Differential Regulation of Ferritin Subunits and Iron Transport Proteins: An Effect of Targeted Hepatic X-Irradiation." BioMed Research International 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/353106.

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The current study aimed to investigate radiation-induced regulation of iron proteins including ferritin subunits in rats. Rat livers were selectively irradiatedin vivoat 25 Gy. This dose can be used to model radiation effects to the liver without inducing overt radiation-induced liver disease. Sham-irradiated rats served as controls. Isolated hepatocytes were irradiated at 8 Gy. Ferritin light polypeptide (FTL) was detectable in the serum of sham-irradiated rats with an increase after irradiation. Liver irradiation increased hepatic protein expression of both ferritin subunits. A rather early increase (3 h) was observed for hepatic TfR1 and Fpn-1 followed by a decrease at 12 h. The increase in TfR2 persisted over the observed time. Parallel to the elevation of AST levels, a significant increase (24 h) in hepatic iron content was measured. Complete blood count analysis showed a significant decrease in leukocyte number with an early increase in neutrophil granulocytes and a decrease in lymphocytes.In vitro, a significant increase in ferritin subunits at mRNA level was detected after irradiation which was further induced with a combination treatment of irradiation and acute phase cytokine. Irradiation can directly alter the expression of ferritin subunits and this response can be strongly influenced by radiation-induced proinflammatory cytokines. FTL can be used as a serum marker for early phase radiation-induced liver damage.

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23

Ichikawa, Shintaro, Utaroh Motosugi, Mitsuhiko Oguri, and Hiroshi Onishi. "Magnetic resonance elastography for prediction of radiation-induced liver disease after stereotactic body radiation therapy." Hepatology 66, no. 2 (June 22, 2017): 664–65. http://dx.doi.org/10.1002/hep.29128.

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24

Jun, Baek Gyu, Young Don Kim, Gab Jin Cheon, Eun Seog Kim, Eunjin Jwa, Sang Gyune Kim, Young Seok Kim, et al. "Clinical significance of radiation-induced liver disease after stereotactic body radiation therapy for hepatocellular carcinoma." Korean Journal of Internal Medicine 33, no. 6 (November 1, 2018): 1093–102. http://dx.doi.org/10.3904/kjim.2016.412.

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25

Castiglioni, S., A. Tozzi, S. Arcangeli, P. Mancosu, G. Reggiori, P. Navarria, E. Clerici, A. Fogliata, L. Cozzi, and M. Scorsetti. "PO-0769 STEREOTACTIC BODY RADIOTHERAPY ON LIVER METASTASES: RADIATION INDUCED LIVER DISEASE AND TOXICITY ASSESSMENT." Radiotherapy and Oncology 103 (May 2012): S297—S298. http://dx.doi.org/10.1016/s0167-8140(12)71102-7.

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26

CHENG, J., H. LIU, J. WU, H. CHUNG, and G. JAN. "Biological integration of parallel architecture NTCP model for radiation-induced liver disease." International Journal of Radiation OncologyBiologyPhysics 60 (September 2004): S155. http://dx.doi.org/10.1016/s0360-3016(04)01126-5.

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Cheng, J. C., H. Liu, J. Wu, H. Chung, and G. Jan. "Biological integration of parallel architecture NTCP model for radiation-induced liver disease." International Journal of Radiation Oncology*Biology*Physics 60, no. 1 (September 2004): S155. http://dx.doi.org/10.1016/j.ijrobp.2004.06.069.

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28

Peixoto, Armando, Pedro Pereira, Renato Bessa de Melo, and Guilherme Macedo. "Radiation-induced liver disease secondary to adjuvant therapy for extra-hepatic cholangiocarcinoma." Digestive and Liver Disease 49, no. 2 (February 2017): 227. http://dx.doi.org/10.1016/j.dld.2016.12.018.

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29

Zeng, Z., M. Qiang, and S. Du. "The Role of Activating Hepatic Stellate Cell in Radiation Induced Liver Disease." International Journal of Radiation Oncology*Biology*Physics 81, no. 2 (October 2011): S711. http://dx.doi.org/10.1016/j.ijrobp.2011.06.1361.

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Blesl, Andreas, Iva Brcic, Werner Jaschke, Dietmar Öfner, Peter Fickert, and Johannes Plank. "Chronic gastric ulcer disease complicating selective internal radiation therapy (SIRT) in a patient with cholangiocellular carcinoma." Zeitschrift für Gastroenterologie 57, no. 11 (November 2019): 1304–8. http://dx.doi.org/10.1055/a-1016-3698.

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AbstractSelective internal radiation therapy (SIRT) is a therapeutic option for primary and metastatic liver tumors. Microspheres containing Yttrium 90, a beta-emitting radionuclide, are administered into the hepatic artery allowing selective internal radiation of a liver tumor. SIRT-related complications may appear due to migration of the radiation microspheres to organs distant from the tumor site. In order to prevent these complications, unintended non target embolization of Yttrium microspheres has to be avoided. However, data from external-beam radiation therapy (EBRT) suggests that the stomach/small bowel may actually be less radiosensitive than the liver. Gastric ulcers, a well-known SIRT-related complication, may therefore not only be caused by local radiation but also by unusual accumulation of microspheres in the submucosa and small vessel damage. We herein report a more than two- year-long persisting, highly symptomatic, non-neoplastic ulceration of the gastric antrum leading to pyloric stenosis caused by SIRT therapy with Yttrium 90 microspheres for the treatment of intrahepatic cholangiocellular carcinoma. The chronic courses of the ulcer disease together with the specific histological features highlight the pivotal role of radiation-induced small vessel damage in SIRT-induced adverse events.

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31

Shirai, Shintaro, Yoshitaka Kumayama, Morio Sato, Yasutaka Noda, Takahiro Chiba, and Miwa Kawaguchi. "Cutoff Values for Dose-liver Function Parameters to Prevent Radiation-induced Liver Disease in Advanced Hepatoma." Journal of Gastroenterology and Hepatology Research 4, no. 1 (2015): 1425–33. http://dx.doi.org/10.17554/j.issn.2224-3992.2015.04.502.

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Mavroidis, Panayiotis, AngeloM Bergamo, Kevin Kauweloa, Gregory Gan, Zheng Shi, Janeen Daniels, Richard Crownover, et al. "Correlation between biological effective dose and radiation-induced liver disease from hypofractionated radiotherapy." Journal of Medical Physics 44, no. 3 (2019): 185. http://dx.doi.org/10.4103/jmp.jmp_54_18.

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33

Rabe, Tiffany M., Takeshi Yokoo, Jeffrey Meyer, Kemp H. Kernstine, David Wang, and Gaurav Khatri. "Radiation-Induced Liver Injury Mimicking Metastatic Disease in a Patient With Esophageal Cancer." Journal of Computer Assisted Tomography 40, no. 4 (2016): 560–63. http://dx.doi.org/10.1097/rct.0000000000000406.

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34

Janoray, G. J., S. C. Chapet, A. R. L. Ruffier-Loubiere, G. B. Bernadou, Y. P. Pointreau, and G. C. Calais. "PO-0776: Robotic SBRT for tumors of the liver. Radiation induced liver disease, incidence and predictive factors." Radiotherapy and Oncology 111 (2014): S50. http://dx.doi.org/10.1016/s0167-8140(15)30894-x.

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Zhi-Feng, Wu, Zhou Le-Yuan, Zhou Xiao-Hui, Gao Ya-Bo, Zhang Jian-Ying, Hu Yong, and Zeng Zhao-Chong. "TLR4-Dependent Immune Response Promotes Radiation-Induced Liver Disease by Changing the Liver Tissue Interstitial Microenvironment during Liver Cancer Radiotherapy." Radiation Research 182, no. 6 (December 2014): 674–82. http://dx.doi.org/10.1667/rr13630.1.

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Wu, Zhi-Feng, Jian-Ying Zhang, Xiao-Yun Shen, Le-Yuan Zhou, Ya-Bo Gao, Yong Hu, and Zhao-Chong Zeng. "A mouse radiation-induced liver disease model for stereotactic body radiation therapy validated in patients with hepatocellular carcinoma." Medical Physics 43, no. 7 (June 21, 2016): 4349–61. http://dx.doi.org/10.1118/1.4953831.

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Huang, Pu, Gang Yu, Daniel S. Kapp, Xue-Feng Bian, Chang-Sheng Ma, Hong-Sheng Li, Jin-Hu Chen, et al. "Cumulative dose of radiation therapy of hepatocellular carcinoma patients and its deterministic relation to radiation-induced liver disease." Medical Dosimetry 43, no. 3 (2018): 258–66. http://dx.doi.org/10.1016/j.meddos.2017.10.002.

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Wu, Z. F., J. Y. Zhang, X. Y. Shen, L. Y. Zhou, Y. B. Gao, Y. Hu, and Z. C. Zeng. "A Mice Radiation-Induced Liver Disease Model for Stereotactic Body Radiation Therapy Validated in Patients With Hepatocellular Carcinoma." International Journal of Radiation Oncology*Biology*Physics 96, no. 2 (October 2016): E577. http://dx.doi.org/10.1016/j.ijrobp.2016.06.2073.

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Cheng, Jason Chia-Hsien, Jian-Kuen Wu, Chao-Ming Huang, David Y. Huang, Skye H. Cheng, Yu-Mong Lin, James J. Jian, Po-Sheng Yang, Vincent P. Chuang, and Andrew T. Huang. "Radiation-induced liver disease after radiotherapy for hepatocellular carcinoma: clinical manifestation and dosimetric description." Radiotherapy and Oncology 63, no. 1 (April 2002): 41–45. http://dx.doi.org/10.1016/s0167-8140(02)00061-0.

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Cheng, Jason Chia-Hsien, Jian-Kuen Wu, Patricia Chiao-Tzu Lee, Hua-Shan Liu, James Jer-Min Jian, Yu-Mong Lin, Juei-Low Sung, and Gwo-Jen Jan. "Biologic susceptibility of hepatocellular carcinoma patients treated with radiotherapy to radiation-induced liver disease." International Journal of Radiation Oncology*Biology*Physics 60, no. 5 (December 2004): 1502–9. http://dx.doi.org/10.1016/j.ijrobp.2004.05.048.

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Yannam, Govardhana Rao, Bing Han, Kentaro Setoyama, Toshiyuki Yamamoto, Ryotaro Ito, Jenna M. Brooks, Jorge Guzman-Lepe, et al. "A Nonhuman Primate Model of Human Radiation-Induced Venocclusive Liver Disease and Hepatocyte Injury." International Journal of Radiation Oncology*Biology*Physics 88, no. 2 (February 2014): 404–11. http://dx.doi.org/10.1016/j.ijrobp.2013.10.037.

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42

Kabarriti, Rafi, N. Patrik Brodin, Hillary Yaffe, Mark Barahman, Wade R. Koba, Laibin Liu, Patrik Asp, Wolfgang A. Tomé, and Chandan Guha. "Non-Invasive Targeted Hepatic Irradiation and SPECT/CT Functional Imaging to Study Radiation-Induced Liver Damage in Small Animal Models." Cancers 11, no. 11 (November 15, 2019): 1796. http://dx.doi.org/10.3390/cancers11111796.

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Radiation therapy (RT) has traditionally not been widely used in the management of hepatic malignancies for fear of toxicity in the form of radiation-induced liver disease (RILD). Pre-clinical hepatic irradiation models can provide clinicians with better understanding of the radiation tolerance of the liver, which in turn may lead to the development of more effective cancer treatments. Previous models of hepatic irradiation are limited by either invasive laparotomy procedures, or the need to irradiate the whole or large parts of the liver using external skin markers. In the setting of modern-day radiation oncology, a truly translational animal model would require the ability to deliver RT to specific parts of the liver, through non-invasive image guidance methods. To this end, we developed a targeted hepatic irradiation model on the Small Animal Radiation Research Platform (SARRP) using contrast-enhanced cone-beam computed tomography image guidance. Using this model, we showed evidence of the early development of region-specific RILD through functional single photon emission computed tomography (SPECT) imaging.

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43

Kennedy, A. S., W. A. Dezarn, P. McNeillie, M. England, C. Overton, and S. Sailer. "Repeat 90Y-microsphere radioembolization for hepatic malignancies: Safety and patient selection issues." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 15177. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.15177.

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15177 Background: Liver tolerance to reirradiation with multiple doses of 90Y-microspheres is not known. Many patients (pts) have also received external beam radiotherapy to the liver or through the liver and are surviving long enough to be considered for a second and third liver treatments with internal radiation. Methods: The experience of a single center treating liver tumors with resin 90Y-microspheres was used. Pts that received liver radiation prior to or after resin microsphere therapy were studied. Endpoints were toxicity, tumor response, disease type, latency period between radiation treatments, shunting to lung, and effects on liver volume and function. The delivery activity of microspheres selected was not reduced below that which was typically chosen for patients without prior liver radiation which was 25% reduced from the manufacturer’s BSA dose calculation method. All patients received bilobar microsphere delivery during a single session. Results: A total of 40 pts were identified; 14 women, 26 men, treated 6/2003 to 12/2006, with 35 pts receiving 2 courses and 5 pts with 3 courses of liver radiation. Retreatment with resin microspheres 26 pts, prior external beam radiation in 7 pts, prior glass microspheres in 2pts, prior systemic radiotherapy in 2 pts, and prior stereotactic liver radiation in 1 pt. Liver function was stable and adequate in all patients after additional liver radiation, and no pts developed radiation-induced liver dysfunction (RILD) or veno-occlusive disease (VOD). The percentage of shunting to the lung decreased with retreatment. Tumors treated: 14 carcinoid, 11 colorectal, 6 hepatocellular and cholangiocarcinoma, 2 sarcoma, 3 unknown primary, 1 each of breast, esophagus, and head and neck primaries. Conclusions: Repeated radiation to the liver with 90Y-microspheres appears safe in patients that have sufficient normal liver function and reserve based on known laboratory parameters already used for selection of microsphere therapy. No acute life-threatening, fatal, or late liver damage was observed, i.e. RILD or VOD. No specific dose reduction is recommended for retreatment of the liver. No significant financial relationships to disclose.

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Xu, Zhi-Yong, Shi-Xiong Liang, Ji Zhu, Xiao-Dong Zhu, Jian-Dong Zhao, Hai-Jie Lu, Yun-Li Yang, et al. "Prediction of radiation-induced liver disease by Lyman normal-tissue complication probability model in three-dimensional conformal radiation therapy for primary liver carcinoma." International Journal of Radiation Oncology*Biology*Physics 65, no. 1 (May 2006): 189–95. http://dx.doi.org/10.1016/j.ijrobp.2005.11.034.

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Camborde, M., E. Vollans, C. Crumley, R. Ma, R. Kosztyla, V. Moiseenko, C. Duzenli, D. Schellenberg, M. Khan, and S. Loewen. "Mean Liver Dose Evaluation by Lyman NTCP Modeling With Stereotactic Body Radiation therapy to Minimize Radiation-Induced Liver Disease for Inoperable Hepatocellular Carcinoma." International Journal of Radiation Oncology*Biology*Physics 87, no. 2 (October 2013): S318. http://dx.doi.org/10.1016/j.ijrobp.2013.06.835.

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Lee, Sungmin, Beomseok Son, Jaewan Jeon, Gaeul Park, Hyunwoo Kim, Hyunkoo Kang, HyeSook Youn, Sunmi Jo, Jie-Young Song, and BuHyun Youn. "Decreased Hepatic Lactotransferrin Induces Hepatic Steatosis in Chronic Non-Alcoholic Fatty Liver Disease Model." Cellular Physiology and Biochemistry 47, no. 6 (2018): 2233–49. http://dx.doi.org/10.1159/000491535.

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Background/Aims: Non-alcoholic fatty liver disease (NAFLD) is an emerging metabolic disease. Although it leads to severe hepatic diseases including steatohepatitis, cirrhosis, and hepatic cancer, little is known about therapy to prevent and cure hepatic steatosis, the first step of NAFLD. We conducted this investigation to unveil the mechanism of hepatic steatosis. Methods: We established a novel chronic NAFLD mouse model through whole body irradiation and verified the model through histological and biochemical analysis. To find molecular mechanism for hepatic steatosis, we analyzed hepatic transcriptomic profiles in this model and selected target molecule. To induce the expression of lactotransferrin (Ltf) and regulate the NAFLD, growth hormone (GH) and coumestrol was introduced to hepatocyte and mice. The universal effect of coumestrol was confirmed by administration of coumestrol to NAFLD mouse model induced by high-fructose, high-fat, and MCD diet. Results: It was observed that decreased hepatic Ltf expression led to excessive hepatic lipid accumulation in NAFLD mouse. Furthermore, we found that GH was decreased in irradiated mice and functioned as an upstream regulator of Ltf expression. It was observed that GH could stimulate Ltf expression and prevent uptake of dietary lipids in hepatocytes, leading to rescue of NAFLD. Finally, we suggested that coumestrol, a kind of isoflavonoid, could be used as an inducer of hepatic Ltf expression through cooperation with the GH signaling pathway both in vitro and in vivo. Conclusions: Hepatic Ltf prevents hepatic steatosis through inhibition of dietary lipid uptake in radiation-induced NAFLD mouse model. We also suggest coumestrol as a drug candidate for prevention of NAFLD.

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Hsieh, C. E., S. Krishnan, C. H. Lee, S. P. Hung, B. S. Huang, B. P. Venkatesulu, J. T. C. Chang, and J. H. Hong. "Predictors of Radiation-Induced Liver Disease in Patients with Hepatocellular Carcinoma Undergoing Proton Beam Therapy." International Journal of Radiation Oncology*Biology*Physics 102, no. 3 (November 2018): S133—S134. http://dx.doi.org/10.1016/j.ijrobp.2018.06.329.

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Chen, Genwen, Qianqian Zhao, Baoying Yuan, Biao Wang, Yang Zhang, Zongjuan Li, Shisuo Du, and Zhaochong Zeng. "ALKBH5-Modified HMGB1-STING Activation Contributes to Radiation Induced Liver Disease via Innate Immune Response." International Journal of Radiation Oncology*Biology*Physics 111, no. 2 (October 2021): 491–501. http://dx.doi.org/10.1016/j.ijrobp.2021.05.115.

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Songthong, A., Y. M. Ito, N. Katoh, M. Tamura, Y. Dekura, C. Toramatsu, N. Srimaneekarn, et al. "PD-0426: NTCP model for radiation-induced liver disease: Integration of clinical and dosimetric factors." Radiotherapy and Oncology 152 (November 2020): S232—S233. http://dx.doi.org/10.1016/s0167-8140(21)00448-5.

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Zheng, Yijun, and Duming Zhu. "Molecular Hydrogen Therapy Ameliorates Organ Damage Induced by Sepsis." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–6. http://dx.doi.org/10.1155/2016/5806057.

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Since it was proposed in 2007, molecular hydrogen therapy has been widely concerned and researched. Many animal experiments were carried out in a variety of disease fields, such as cerebral infarction, ischemia reperfusion injury, Parkinson syndrome, type 2 diabetes mellitus, metabolic syndrome, chronic kidney disease, radiation injury, chronic hepatitis, rheumatoid arthritis, stress ulcer, acute sports injuries, mitochondrial and inflammatory disease, and acute erythema skin disease and other pathological processes or diseases. Molecular hydrogen therapy is pointed out as there is protective effect for sepsis patients, too. The impact of molecular hydrogen therapy against sepsis is shown from the aspects of basic vital signs, organ functions (brain, lung, liver, kidney, small intestine, etc.), survival rate, and so forth. Molecular hydrogen therapy is able to significantly reduce the release of inflammatory factors and oxidative stress injury. Thereby it can reduce damage of various organ functions from sepsis and improve survival rate. Molecular hydrogen therapy is a prospective method against sepsis.

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