Structure-activity relationships for tumour radiosensitization by analogues of nicotinamide and benzamide.

Nicotinamide has been shown in our laboratory and those of other investigators to be an effective radiosensitizer of a variety of mouse tumours, while producing little or no radiosensitization of normal tissues. Its mechanism of action is different from classical electron-affinic compounds and appears to be the result of improved tumour oxygenation. In this study we have synthesized 29 analogues of nicotinamide and benzamide and characterized them for their tumour radiosensitization and acute toxicity in mice. The data show that a wide range of additions to the nicotinamide and benzamide ring produce tumour radiosensitization similar to that produced by equimolar doses of misonidazole, but that substitutions of the amide tend to reduce radiosensitization. Other structure-activity relationships are evident. Although some compounds produce similar tumour radiosensitization to nicotinamide at equimolar doses, and are comparably low in acute toxicity, none appears sufficiently superior to supplant nicotinamide itself as a candidate for clinical trials. Thus these data provide evidence that nicotinamide, because of the extensive experience with its use in man, is likely to be the best drug in the benzamide-nicotinamide series for development as a radiosensitizer of human tumours.     

The role of fast neutrons in radiooncology--a critical appraisal.

The contribution of fast neutrons to local tumour control has been investigated worldwide since the mid-60's in more than 20 institutions. The high expectations anticipated from the promising results of experimental studies could not be adequately realized in the clinic. The late normal tissue damage was unacceptable due to poor depth dose characteristics and further technical limitations of the first generation low-energy machines. Even with sophisticated therapy planning systems and high-energy cyclotrons as well as comparable late normal tissue damage as witnessed after photons, only a few tumour entities have responded superiorly to fast neutrons. These particularly include macroscopic tumours of the salivary glands, prostate and, potentially, soft and osseous tissues. The role of fast neutrons for head and neck cancer has not yet been definitely proved. For bladder-, cervical- and rectal carcinomas, non-small cell lung-, pancreatic- and breast cancers as well as malignant gliomas, no therapeutic benefit as compared with photons was observed in the case of macroscopic residual or inoperable recurrent tumours.     

Structure–activity Relationships for Tumour Radiosensitization by Analogues of Nicotinamide and Benzamide

Summary

Nicotinamide has been shown in our laboratory and those of other investigators to be an effective radiosensitizer of a variety of mouse tumours, while producing little or no radiosensitization of normal tissues. Its mechanism of action is different from classical electron-affinic compounds and appears to be the result of improved tumour oxygenation. In this study we have synthesized 29 analogues of nicotinamide and benzamide and characterized them for their tumour radiosensitization and acute toxicity in mice. The data show that a wide range of additions to the nicotinamide and benzamide ring produce tumour radiosensitization similar to that produced by equimolar doses of misonidazole, but that substitutions of the amide tend to reduce radiosensitization. Other structure–activity relationships are evident. Although some compounds produce similar tumour radiosensitization to nicotinamide at equimolar doses, and are comparably low in acute toxicity, none appears sufficiently superior to supplant nicotinamide itself as a candidate for clinical trials. Thus these data provide evidence that nicotinamide, because of the extensive experience with its use in man, is likely to be the best drug in the benzamide–nicotinamide series for development as a radiosensitizer of human tumours.     

Radiobiology and Clinical Application of Halogenated Pyrimidine Radiosensitizers

Summary

Halogenated pyrimidines (HP) represent a unique class of non-hypoxic cell radiosensitizers currently under clinical re-investigation. In order for halogenated pyrimidines to sensitize cells to radiation, they must be incorporated into cellular DNA. In the case of human tumors, which have in general rather long cell cycle times, this may require many days of continuous drug infusion to achieve adequate replacement of the DNA base thymidine with HP. In vitro studies support the relationship between the extent of radiosensitization and the percentage of thymidine replacement. Recent clinical studies evaluating the role of iododeoxyuridine (IdUrd) as a radiation sensitizer in large unresectable sarcomas have been extremely encouraging. To support and expand upon these positive clinical findings more information and research is needed regarding: (1) the mechanism of HP-induced radiosensitization; (2) the percentage of HP thymidine replacement in human tumors achievable and how it relates to treatment outcome; (3) the means of increasing HP incorporation in tumor and minimizing incorporation in normal tissues; (4) a better understanding of optimal timing between HP administration and radiation treatment; and (5) methods to evaluate which tumors are appropriate candidates for HP therapy. While presently limited to use in conventional high dose-rate X-ray therapy, laboratory studies suggest that HP might also be effective in low dose-rate brachytherapy and for selected high LET clinical beams. HPs probably will not be ‘general’ non-hypoxic cell radiosensitizers for all tumor types, but with appropriate tumor-type/anatomical site selection and refinement in their administration, HPs may prove beneficial in cancer treatment.     

Radiobiology and clinical application of halogenated pyrimidine radiosensitizers

Halogenated pyrimidines (HP) represent a unique class of non-hypoxic cell radiosensitizers currently under clinical re-investigation. In order for halogenated pyrimidines to sensitize cells to radiation, they must be incorporated into cellular DNA. In the case of human tumors, which have in general rather long cell cycle times, this may require many days of continuous drug infusion to achieve adequate replacement of the DNA base thymidine with HP. In vitro studies support the relationship between the extent of radiosensitization and the percentage of thymidine replacement. Recent clinical studies evaluating the role of iododeoxyuridine (IdUrd) as a radiation sensitizer in large unresectable sarcomas have been extremely encouraging. To support and expand upon these positive clinical findings more information and research is needed regarding: (1) the mechanism of HP-induced radiosensitization; (2) the percentage of HP thymidine replacement in human tumors achievable and how it relates to treatment outcome; (3) the means of increasing HP incorporation in tumor and minimizing incorporation in normal tissues; (4) a better understanding of optimal timing between HP administration and radiation treatment; and (5) methods to evaluate which tumors are appropriate candidates for HP therapy. While presently limited to use in conventional high dose-rate X-ray therapy, laboratory studies suggest that HP might also be effective in low dose-rate brachytherapy and for selected high LET clinical beams. HPs probably will not be 'general' non-hypoxic cell radiosensitizers for all tumor types, but with appropriate tumor-type/anatomical site selection and refinement in their administration, HPs may prove beneficial in cancer treatment.     

Gold microspheres: a selective technique for producing biologically effective dose enhancement

Purpose : To investigate dose enhancement and radiosensitization associated with electrons produced and scattered from gold particles suspended in cells in vitro and with tumour cells growing in vivo irradiated with low-energy photons. Materials and methods : CHO-K1, EMT-6 and DU-145 cells were irradiated with kilovoltage X-ray and Cs-137 beams in slowly stirred suspensions in the presence of various concentrations of gold particles (1.5-3.0 μ m); cell survival was measured by clonogenic assay. Gold particles were injected directly into EMT-6 tumours growing in scid mice prior to their irradiation. Tumour cell killing was assayed by an in vivo-in vitro technique. Results : Dose enhancement was confirmed by both Fricke dosimetry and cell killing for 100, 140, 200 and 240kVp X-rays, but not for Cs-137 γ-rays. For the chemical dosimeter, a dose enhancement (DMF) of 1.42 was measured for 1% gold particle solutions irradiated with 200 kVp X-rays. When rodent and human cells were irradiated in the presence of 1% gold particles, DMF values at the 10% survival level ranged from 1.36 to 1.54, with an overall average value of 1.43. Preliminary attempts to deliver these gold particles to tumour cells in vivo by intra-tumour injection resulted in modest radiosensitization but extremely heterogeneous distribution. Conclusions : An increased biologically effective dose can be produced by gold microspheres suspended in cell culture or distributed in tumour tissue exposed to kilovoltage photon beams. With the increasing use of interstitial brachytherapy with isotopes that produce low-energy photons, high-Z particles might find a role for significantly improving the therapeutic ratio.     

Gold microspheres: a selective technique for producing biologically effective dose enhancement

PURPOSE: To investigate dose enhancement and radiosensitization associated with electrons produced and scattered from gold particles suspended in cells in vitro and with tumour cells growing in vivo irradiated with low-energy photons. MATERIALS AND METHODS: CHO-K1, EMT-6 and DU-145 cells were irradiated with kilovoltage X-ray and Cs-137 beams in slowly stirred suspensions in the presence of various concentrations of gold particles ( 1.5-3.0 microm); cell survival was measured by clonogenic assay. Gold particles were injected directly into EMT-6 tumours growing in scid mice prior to their irradiation. Tumour cell killing was assayed by an in vivo-in vitro technique. RESULTS: Dose enhancement was confirmed by both Fricke dosimetry and cell killing for 100, 140, 200 and 240 kVp X-rays, but not for Cs-137 gamma-rays. For the chemical dosimeter, a dose enhancement (DMF) of 1.42 was measured for 1% gold particle solutions irradiated with 200 kVp X-rays. When rodent and human cells were irradiated in the presence of 1% gold particles, DMF values at the 10% survival level ranged from 1.36 to 1.54, with an overall average value of 1.43. Preliminary attempts to deliver these gold particles to tumour cells in vivo by intra-tumour injection resulted in modest radiosensitization but extremely heterogeneous distribution. CONCLUSIONS: An increased biologically effective dose can be produced by gold microspheres suspended in cell culture or distributed in tumour tissue exposed to kilovoltage photon beams. With the increasing use of interstitial brachytherapy with isotopes that produce low-energy photons, high-Z particles might find a role for significantly improving the therapeutic ratio.     

Review and evolution of clinical results in the EORTC Heavy-Particle Therapy Group

Part of the clinical results from the "EORTC Heavy-Particle Therapy Group" are reviewed (September 1984). Fast neutrons can bring a significant benefit, compared to conventional photon (or electron) techniques, in well defined patient series. A benefit for neutrons is observed, in Hammersmith and in Amsterdam, for locally extended salivary gland tumours. Soft tissue sarcomas can also be considered as a good indication for neutron therapy, especially when they are slowly growing and well differentiated, as shown in Essen, Hammersmith and Louvain-la-Neuve. Neutrons can bring an advantage in the treatment of some melanoma patients as shown in Hammersmith. For locally advanced prostatic carcinoma, better results for neutrons are shown in Hamburg and Louvain-la-Neuve. These data are similar to those observed in the United States from the RTOG studies. Due to a reduced differential effect between tissues after neutron treatment, irradiation of large volumes of normal tissues, at high neutron dose, should be avoided. Different possible combinations between neutrons and photons (boost, mixed schedule) are discussed.     

Measurement of skin dose in primary irradiation of maxillary sinus carcinoma

Subcutaneous involvement frequently occurs in maxillary sinus carcinoma. Radical resection does not include removal of the skin at risk. In standard postoperative wedge-pair treatment plans, the surface dose is dependent upon beam weighting, beam energy, and patient contour. Thermoluminescent dosimetry (TLD) measurements were performed to evaluate the surface dose of patients undergoing postoperative irradiation of maxillary sinus carcinoma following primary resection. When 60 Gy was delivered to isocenter with a 45 degrees wedge pair and 6 MV photons with 1 cm bolus, the subcutaneous tissues at risk received approximately 30 Gy. Based upon presented TLD measurements, supplemental electron beam therapy to the subcutaneous tissues if primarily involved should be considered.     

肿瘤放射增敏药物的研究进展

放射治疗是临床肿瘤治疗的重要手段之一.肿瘤细胞的放射敏感性是影响肿瘤放疗疗效的关键因素.放射增敏药物能够增强机体的放射敏感性,通过提高肿瘤细胞的放射敏感性达到降低照射剂量、提高放疗疗效、降低正常组织损伤的目的.现有的放射增敏药物主要分为细胞毒类药物、靶向药物以及中药制剂3大类.该文将对肿瘤放射增敏药物的作用机制、现状及相关研究进展进行综述.     

Electron density of normal and pathological breast tissues using a compton scattering technique

Compton (incoherently) scattered photons which are directly proportional to the electron density of the scatterer, have been employed in characterising human breast tissues. Gamma ray photons scattered incoherently from normal and pathological breast tissue samples of nine breast cancer patients were measured using a high purity germanium detector and an americium (Am-241) source. The breast tissue samples were obtained from female patients undergoing mastectomy. The samples were examined in freeze dried form and the results were corrected for the reduction in the water content of each tissue type by use of the Mixture Rule. This study is aimed at providing electron density information in support of the introduction of new tissue substitute materials for mammography phantoms.     

高分子纳米材料用于肿瘤放疗增敏的研究进展

放疗是治疗恶性肿瘤的三大常规手段之一,但由于其存在高辐射剂量损伤正常组织和肿瘤细胞辐射抵抗性强等问题,导致治疗后往往达不到预期效果。为提高放疗疗效,并且减少对正常组织的不良作用,探索新型放疗增敏剂及放化疗联合的新策略已成为研究热点。高分子纳米材料凭借其良好的生物相容性和生理稳定性等优点,为提高肿瘤放疗效果开拓了广阔的应用前景。笔者就高分子纳米材料用于放疗增敏的研究进展进行综述。     

The effect of 6 and 15 MV on intensity-modulated radiation therapy prostate cancer treatment: plan evaluation, tumour control probability and normal tissue complication probability analysis, and the theoretical risk of secondary induced malignancies

Objective

The aim of this study was to investigate the effect of 6 and 15-MV photon energies on intensity-modulated radiation therapy (IMRT) prostate cancer treatment plan outcome and to compare the theoretical risks of secondary induced malignancies.

Methods

Separate prostate cancer IMRT plans were prepared for 6 and 15-MV beams. Organ-equivalent doses were obtained through thermoluminescent dosemeter measurements in an anthropomorphic Aldersen radiation therapy human phantom. The neutron dose contribution at 15 MV was measured using polyallyl-diglycol-carbonate neutron track etch detectors. Risk coefficients from the International Commission on Radiological Protection Report 103 were used to compare the risk of fatal secondary induced malignancies in out-of-field organs and tissues for 6 and 15 MV. For the bladder and the rectum, a comparative evaluation of the risk using three separate models was carried out. Dose–volume parameters for the rectum, bladder and prostate planning target volume were evaluated, as well as normal tissue complication probability (NTCP) and tumour control probability calculations.

Results

There is a small increased theoretical risk of developing a fatal cancer from 6 MV compared with 15 MV, taking into account all the organs. Dose–volume parameters for the rectum and bladder show that 15 MV results in better volume sparing in the regions below 70 Gy, but the volume exposed increases slightly beyond this in comparison with 6 MV, resulting in a higher NTCP for the rectum of 3.6% vs 3.0% (p=0.166).

Conclusion

The choice to treat using IMRT at 15 MV should not be excluded, but should be based on risk vs benefit while considering the age and life expectancy of the patient together with the relative risk of radiation-induced cancer and NTCPs.Three-dimensional conformal radiation therapy (3D-CRT) is most commonly delivered with high-energy photons, typically in the range of 6–18 MV. Intensity-modulated radiation therapy (IMRT) is known to improve target coverage and provide better organ-at-risk (OAR) sparing in comparison with 3D-CRT [1]. However, IMRT is associated with an increase in the number of monitor units (MUs) relative to 3D-CRT, which has led to concerns about a potential increased risk of radiation-induced malignancies [2]. This risk becomes more relevant at higher photon energies (>10 MV), where there is a possibility of greater leakage radiation, treatment head scatter, patient scatter and photoneutron contribution [3]. Subsequently, the majority of IMRT treatments being delivered in the UK today use 6-MV photons. The use of higher energies for deep-seated tumours, such as those in the prostate, have been favoured by some as providing better dose coverage to the tumour target, while also improving normal tissue sparing [4].It has been reported in the literature that IMRT may double the risk of fatal second cancers compared with 3D-CRT [5-9]. The risk of fatal cancer has been reported for 6-MV 3D-CRT and IMRT prostate treatments to vary by 0.6–1.5% and 1–3.0%, respectively [7,8,10]. For 15-MV photons, the risk has been reported to be 3.4% [10]. These values have been computed using data from the National Council on Radiation Protection and Measurements (NCRP) Report 116, assuming a linear lifetime risk value of 0.05 per Sievert for all fatal radiation-induced cancers for the general population [11].There are as yet no epidemiological data for radiation-induced malignancy in patients with prostate cancer who received treatment with IMRT. A modest increase in second malignancies of 1 in 70 patients undergoing radiation and surviving for more than 10 years was reported for 3D-CRT, with the most common sites for secondary cancers being the bladder and rectum [12].Currently, at our centre (St Luke''s Cancer Centre, SLCC), 3D-CRT to the prostate is delivered mostly with 15-MV photons, whereas IMRT is delivered with 6-MV photons. During the initial set-up of prostate IMRT at SLCC, all energy beams (6, 10 and 15 MV) were in clinical use. After 10 patients had been treated, it was decided by the clinical team to use only 6-MV photons until the use of higher energy beams was further evaluated, given that the potential advantages related to their use could be offset by a potential increase in the risk of second malignancy.This study has investigated whether high-energy IMRT offers better target coverage and normal tissue sparing for prostate cancer. This work has investigated the organ equivalent doses through thermoluminescent dosemeter (TLD) measurements in an anthropomorphic Alderson radiation therapy (ART) human phantom (RANDO; The Phantom Laboratory, Salem, NY) in order to assess the theoretical risk of secondary malignancies in organs and tissues distant from the tumour target. For the bladder and rectum, a comparative evaluation of calculating the risk using the linear non-threshold model [13-15], linear-plateau model [16] and initiation–inactivation model [17] was performed. The neutron dose contribution at 15 MV was estimated using polyallyl-diglycol-carbonate (PADC) neutron track etch detectors. Dosimetric plan evaluations were carried out for the planning target volume (PTV) and OARs, as well as an assessment of the total number of MUs for plans generated with different energies.     

Volumetric modulated arc therapy: a review of current literature and clinical use in practice

Volumetric modulated arc therapy (VMAT) is a novel radiation technique, which can achieve highly conformal dose distributions with improved target volume coverage and sparing of normal tissues compared with conventional radiotherapy techniques. VMAT also has the potential to offer additional advantages, such as reduced treatment delivery time compared with conventional static field intensity modulated radiotherapy (IMRT). The clinical worldwide use of VMAT is increasing significantly. Currently the majority of published data on VMAT are limited to planning and feasibility studies, although there is emerging clinical outcome data in several tumour sites. This article aims to discuss the current use of VMAT techniques in practice and review the available data from planning and clinical outcome studies in various tumour sites including prostate, pelvis (lower gastrointestinal, gynaecological), head and neck, thoracic, central nervous system, breast and other tumour sites.     

Gold nanoparticles in combination with megavoltage radiation energy increased radiosensitization and apoptosis in colon cancer HT-29 cells

Purpose: Gold nanoparticles (GNP) act as a radiosensitizer in radiation therapy. However, recent studies have shown contradictory evidence in terms of radiosensitization in the presence of GNP combined with X-ray megavoltage energy (MV) on different cell types. In this study, the effect of GNP on radiosensitization enhancement of HT-29 human colorectal cancer cells at MV X-ray energy was evaluated.

Materials and methods: The cytotoxicity and radiosensitization of GNP were evaluated in HT-29 human colorectal cancer cells by MTS-assay and multiple MTS-assay, respectively. Cellular uptake was assayed using graphite furnace atomic absorption spectrometry (GFAAS). Apoptosis and cell cycle progression were determined by an Annexin V-FITC/propidium iodide (PI) kit and PI/RNase solution with flow cytometry, respectively.

Results: Results showed that the cell viability of the HT-29 cells was not influenced by exposure to different concentrations of GNP (10–100 μM). GNP alone did not affect the cell cycle progression and apoptosis. In contrast, GNP, in combination with radiation (9?MV), induced more apoptosis. The interaction of GNP with MV energy resulted in a significant radiosensitization enhancement compared with irradiation alone.

Conclusion: It was concluded that GNP may work as bio-inert material on HT-29 cancer cells and their enhancement of radiosensitization may be due to increase in the absorbed irradiation dose.     

Pharmacological inhibition of EGFR tyrosine kinase affects ILK-mediated cellular radiosensitization in vitro

PURPOSE: Integrin-linked kinase (ILK) mediates signals from beta integrins and links integrins to epidermal growth factor receptor (EGFR). Previous studies have identified an antisurvival effect of ILK in irradiated cells. The aim of this study was to evaluate the role of EGFR tyrosine kinase (tk) activity for ILK-mediated radiosensitization. MATERIALS AND METHODS: Human FaDu squamous cell carcinoma (SCC) cells stably transfected with hyperactive ILK (ILK-hk) and ILK(fl/fl) and ILK(-/-) mouse fibroblasts were treated with the pharmacological EGFR-tk inhibitor BIBX1382BS without or in combination with single doses of X-rays. Clonogenic radiation survival, protein expression and phosphorylation (EGFR, v-akt murine thymoma viral oncogene homolog 1 (Akt), p42/44 mitogen-activated protein kinase), DNA-double strand break (DSB) repair measured by gammaH2AX foci, cell morphology and cell cycle distribution were examined. RESULTS: Expression of ILK-hk or ILK(fl/fl) status resulted in significant radiosensitization relative to vector controls or ILK(-/-). Following BIBX1382BS, clonogenic survival of normal fibroblasts and vector controls remained unaffected while ILK-hk-related radiosensitization was significantly diminished. In contrast to BIBX1382BS, which did not affect DNA-DSB repair, ILK-hk-mediated radiosensitization was associated with reduced DNA-DSB repair. At 10 days after BIBX1382BS treatment, FaDu transfectants, in contrast to fibroblasts, showed reduced cell size, accumulation of G1 phase cells and reduced Akt-serine(S)473 phosphorylation. CONCLUSIONS: Our findings confirm ILK as a cell type-independent antisurvival factor in irradiated cells, which actions in terms of radiosensitization critically depend on proper EGFR-tk activity.     

辐射防护基因治疗现状与展望

放射治疗是恶性肿瘤的主要治疗手段之一,超过50%的肿瘤患者在病程的不同阶段都需要接受放疗。尽管影像引导靶向治疗技术不断发展,使患者受到的辐射剂量大大降低,但仍然存在严重的不良反应——正常组织细胞的辐射损伤。为了减少正常组织损伤,研究人员一直在寻找辐射防护的新方法。目前的辐射防护方法多是采用化学合成小分子物质及天然植物提取物作为辐射防护剂使用,但疗效并不十分理想,研究人员迫切想找到一种高效可行的辐射防护新方法。基因治疗以其靶向明确、细胞毒性小、不良反应少等优点在增强细胞和组织相关性能上具有很大优势,使其成为极好的辐射防护新方法。笔者对辐射防护的基因治疗研究及其未来的改进方向做一综述。     

HSV-TK/GCV自杀基因系统联合γ射线放射治疗宫颈癌的实验研究

目的 探讨HSV-TK／GCV自杀基因系统协同^60Coγ射线放射治疗对人宫颈癌细胞系的体内外联合杀伤作用，以及HSV-TK／GCV对放射治疗的增敏作用。方法 分别以HSV-TK／GCV、^60Coγ射线放射治疗及两者联合治疗人宫颈癌HeLa细胞系和裸鼠宫颈癌移植瘤模型，比较治疗效果；利用增敏效应比值（E／O）、克隆形成实验评价体内外HSV-TK／GCV对放射敏感性的影响。结果 在体外实验中，自杀基因对宫颈癌HeLa细胞生长的抑制率为45．8％，单纯放疗的抑制率为42．4％，而基因治疗与放疗联用的抑制率为87．5％，与前两者比较，差异有统计学意义（P〈0．01）；且联合治疗组对射线敏感性较单独治疗组明显增加，克隆形成率明显下降（P〈0．05）；在体内实验中，单纯基因治疗与放疗对HeLa细胞裸鼠皮下移植瘤生长的抑瘤率分别为39．5％和35．8％，而基因治疗放疗联用的抑瘤率达到87．9％，与前两者比较，差异均有统计学意义（P〈0．01）；增敏效应比值（E／O）为3．2（〉1．4），提示HSV-TK／GCV对放疗具有增敏作用。结论 HSV-TK／GCV自杀基因系统具有放射增敏作用，二者联合治疗可作为宫颈癌综合治疗的有效补充方法。     

核受体在肿瘤放疗增敏中作用机制的研究进展

放疗是肿瘤治疗的主要方法之一,但肿瘤存在辐射抗性,且正常组织存在辐射耐受剂量问题,两者严重影响肿瘤的放疗效果。因此,研究辐射增敏新策略以提高肿瘤细胞的辐射敏感性尤其重要。核受体是细胞内含量丰富的一类转录因子超家族,参与机体多种病理生理过程。近年来的研究结果表明,核受体及其相关配体可能参与肿瘤的放疗抵抗,因而核受体可能是肿瘤放疗增敏的新靶点。笔者总结了核受体及相关配体在肿瘤放疗增敏方面的研究进展。     

Spectrum of imaging findings in the abdomen after radiotherapy

OBJECTIVE: The objective of this article is to describe the imaging appearances of radiation injury to normal tissues in the abdomen that may be seen during imaging surveillance of oncology patients. CONCLUSION: Therapeutic radiation is used to treat various malignant conditions in the abdomen. Radiation damages normal surrounding tissues as well as the intended tumor. Radiation changes vary based on the target organ and the time from completion of therapy. Familiarity with the spectrum of changes that may be seen on follow-up imaging studies should help in the differentiation of radiation injury from other causes such as recurrent malignancy.