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Radiation-induced Arteritis: Thickened Wall with Prominent Enhancement on Cranial MR Images—Report of Five Cases and Comparison with 18 Cases of Moyamoya Disease¹

¹ From the Department of Radiology, University of Tokyo Hospital, 7-3-1 Hongo, Bunkyoku, Tokyo 113-8655, Japan (S.A., N.H., O.A., I.S., K.N., K.O.); and Department of Radiology, Yamanashi Medical University, Yamanashi, Japan (K.I., T.O., T.A.). From the 2000 RSNA scientific assembly. Received April 24, 2001; revision requested May 25; revision received September 19; accepted November 12. Address correspondence to S.A. (e-mail: saoki-dis@h.u-tokyo.ac.jp).

	ABSTRACT

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PURPOSE: To evaluate magnetic resonance (MR) imaging findings of radiation-induced cranial arteritis regarding arterial wall thickening and degree of enhancement, as well as to compare the findings with those of idiopathic moyamoya disease.

MATERIALS AND METHODS: We reviewed cerebral MR images in five patients with radiation-induced large cerebral arteritis. All patients had undergone irradiation 2–25 years prior to this study. Conventional nonenhanced MR, MR angiographic, and contrast material–enhanced MR images were evaluated. Special attention was paid to wall enhancement of the affected arteries (distal internal carotid artery). Wall enhancement was staged in three levels by two neuroradiologists. We also reviewed MR images in 18 patients with primary moyamoya disease for comparison and analyzed them statistically (Fisher exact test).

RESULTS: Wall thickening and prominent ring enhancement of the wall of the affected large cerebral arteries were observed in all (five of five) patients with radiation-induced arteritis. In contrast, wall thickening and prominent ring enhancement of the wall of the occluded arteries either were not seen (13 of 18 patients) or were faint (five of 18 patients) in patients with moyamoya disease. Contrast enhancement of the arterial walls in patients with radiation-induced arteritis was significantly more prominent than in patients with moyamoya disease (P = .003).

CONCLUSION: MR images of wall thickening and prominent ring enhancement of the wall of affected large cerebral arteries may be a diagnostic clue in differentiating radiation-induced arteritis from moyamoya disease.

© RSNA, 2002

Index terms: Carotid arteries, MR, 17.12142 • Cerebral blood vessels, stenosis or obstruction, 17.7213 • Moyamoya disease, 17.7694 • Radiations, injurious effects, 17.47, 17.729, 17.7694

	INTRODUCTION

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Radiation-induced vascular injury is a well-known phenomenon (1–8) in which small arteries and capillaries are commonly and severely affected. Injury from radiation to large arteries that results in occlusive vasculopathy has been considered relatively rare, although it has been suggested in some reports (7,8) that clinically important damage to large arteries is more common than previously thought.

On contrast material–enhanced magnetic resonance (MR) images, arterial wall thickening and enhancement can be observed in aortitis syndrome (9) and atherosclerosis (10). Histologically, arteritis is an inflammatory process in the arterial wall that results in arterial wall thickening and morphologically resembles spontaneous atherosclerosis (1–3).

We postulate that similar findings on MR images can be observed in radiation-induced large-vessel injuries, and the findings may contribute to differential diagnosis between other large-vessel occlusive diseases, that is, idiopathic (primary) moyamoya disease. In idiopathic moyamoya disease, the outer diameter of occluded and/or stenotic arteries is decreased, and the internal carotid artery (ICA) may show a 1–2-mm outer diameter (including the wall) at the terminal portion at pathologic examination (11,12).

The purpose of this study was to evaluate the MR imaging findings of radiation-induced cranial arteritis with regard to arterial wall thickening and degree of enhancement, as well as to compare the findings with those of idiopathic moyamoya disease.

	MATERIALS AND METHODS

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Retrospective evaluation of the computerized imaging records of two university hospitals from 1992 to 2000 revealed five patients with radiation-induced large-vessel arteritis of the cerebral arteries. All of these were female and 15–40 years of age (mean age, 26.8 years ± 11.8 [SD]). Indications for irradiation were as follows: two basal ganglial large arteriovenous malformations, a suprasellar germinoma, an optic glioma, and a craniopharyngioma. Radiation-induced occlusive large-vessel arteritis was diagnosed by using clinical information (history of irradiation, radiation field, lack of risk factors of atherosclerosis), as well as by using conventional angiography (four patients) or MR angiography (one patient). There was no evidence of vasculitis, collagen disease, atherosclerosis, neurofibromatosis, or other causes of occlusive vasculopathy according to patient history and findings of clinical and laboratory studies. The interval between the first exposure to irradiation and the first imaging-based evidence of stenosis and/or occlusion was 2–19 years (mean, 7.4 years ± 6.8). Irradiation was performed by using either the conventional method (four patients) or a gamma knife (one patient), with a dose of 45–120 Gy (120 Gy = 60 + 60 Gy in a 15-year interval). For this kind of limited retrospective review, our institutional review board did not require its approval or informed consent.

Eighteen patients (six male and 12 female patients) 2–60 years of age (mean age, 24.8 years ± 18.0) who had idiopathic moyamoya disease were evaluated. In these patients, moyamoya disease was considered to be idiopathic (primary), and there was no evidence of vasculitis, collagen disease, atherosclerosis, neurofibromatosis, or other causes of occlusive vasculopathy according to patient history or findings of clinical and laboratory studies.

Transverse nonenhanced T1-weighted spin-echo (repetition time msec/echo time msec, 400–600/8–15), intermediate-weighted spin-echo (2,000–4,000/14–30), and T2-weighted spin-echo or fast spin-echo (3,000–4,000/80–100) MR images and transverse contrast-enhanced T1-weighted spin-echo (400–600/8–15) MR images were obtained with 1.5-T imagers (Signa; GE Medical Systems, Milwaukee, Wis; and Magnetom Vision; Siemens, Erlangen, Germany) after intravenous administration of 0.1 mmol per kilogram of body weight of gadoteridol (ProHance; Bracco, Milan, Italy). A presaturation band below the imaging slab was used. High-spatial-resolution contrast-enhanced coronal and/or sagittal T1-weighted images were obtained in most patients. Additional coronal nonenhanced and enhanced T1-weighted images also were reviewed if obtained, but wall enhancement was evaluated in the transverse plane.

Enhancement of the wall of the distal ICAs (cavernous to communicating segments) was evaluated according to the previously reported grading system (10) as follows: Stage 1 = no substantial enhancement of the arterial wall (arteries identified by using flow void), stage 2 = thin faint enhancement, and stage 3 = definite enhancement of the arterial wall (thick and prominent ring enhancement). The stage of each lesion was determined by means of consensus by two experienced neuroradiologists (S.A., K.I.). The staging of the carotid arteries was analyzed by using the Fisher exact test to compare patients who had radiation arteritis with patients who had moyamoya disease. Enhancement of the wall of the proximal anterior and middle cerebral arteries (MCAs) also was evaluated.

MR imaging, computed tomographic (CT), angiographic, and other radiologic images and clinical records also were reviewed to estimate the interval between irradiation and onset of vascular occlusion and between vascular occlusion and onset of contrast enhancement. This was done to rule out coexistent occlusive disorders before irradiation and to specify the duration of contrast enhancement after occlusion. Loss of flow void on intermediate-weighted images (2,000–4,000/14–30) was used as the imaging sign of occlusion.

	RESULTS

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Thick and prominent ring enhancement of the arterial wall was observed at the occluded and/or stenotic distal ICAs in all patients with radiation-induced arteritis (stage 3, five of five patients) (Figs 1, 2). Such thick and prominent ring enhancement (stage 3) of the ICAs was not observed in patients with idiopathic moyamoya disease (Fig 3). Of the 18 patients with idiopathic moyamoya disease, 13 had stage 1 enhancement and five had stage 2 enhancement. According to the Fisher exact test, contrast enhancement of the arterial walls in the patients with radiation-induced arteritis was significantly more prominent than that in the patients with moyamoya disease (P = .003).

View larger version (92K): [in this window] [in a new window] [Download PPT slide]   Figure 1a. Radiation-induced arteritis in a 15-year-old girl (patient 2) who had undergone irradiation with a conventional method at 10 years of age because of suprasellar germinoma. (a) Superior-inferior time-of-flight MR angiographic image (33/6.9; 20° flip angle) shows bilateral distal ICA occlusion (arrows). (b) Coronal precontrast T1-weighted spin-echo MR image (500/11) shows the isointense thickened wall (arrows) of each distal ICA. (c) Coronal postcontrast T1-weighted spin-echo MR image (500/11) shows ring enhancement (arrows) of the wall of each distal ICA.

View larger version (147K): [in this window] [in a new window] [Download PPT slide]   Figure 1b. Radiation-induced arteritis in a 15-year-old girl (patient 2) who had undergone irradiation with a conventional method at 10 years of age because of suprasellar germinoma. (a) Superior-inferior time-of-flight MR angiographic image (33/6.9; 20° flip angle) shows bilateral distal ICA occlusion (arrows). (b) Coronal precontrast T1-weighted spin-echo MR image (500/11) shows the isointense thickened wall (arrows) of each distal ICA. (c) Coronal postcontrast T1-weighted spin-echo MR image (500/11) shows ring enhancement (arrows) of the wall of each distal ICA.

View larger version (162K): [in this window] [in a new window] [Download PPT slide]   Figure 1c. Radiation-induced arteritis in a 15-year-old girl (patient 2) who had undergone irradiation with a conventional method at 10 years of age because of suprasellar germinoma. (a) Superior-inferior time-of-flight MR angiographic image (33/6.9; 20° flip angle) shows bilateral distal ICA occlusion (arrows). (b) Coronal precontrast T1-weighted spin-echo MR image (500/11) shows the isointense thickened wall (arrows) of each distal ICA. (c) Coronal postcontrast T1-weighted spin-echo MR image (500/11) shows ring enhancement (arrows) of the wall of each distal ICA.

View larger version (147K): [in this window] [in a new window] [Download PPT slide]   Figure 2a. Radiation-induced arteritis in a 27-year-old woman (patient 3) who had undergone gamma-knife irradiation at 25 years of age because of a large right basal ganglial arteriovenous malformation. (a) Conventional angiogram of the right common carotid artery (Towne view) shows right distal ICA occlusion (arrow). (b) Transverse precontrast T1-weighted spin-echo MR image (600/14) shows the isointense thickened wall (arrow) of the right distal ICA. (c) Transverse contrast-enhanced T1-weighted spin-echo MR image (600/14) shows intense ring enhancement (arrow) of the distal ICA wall.

View larger version (185K): [in this window] [in a new window] [Download PPT slide]   Figure 2b. Radiation-induced arteritis in a 27-year-old woman (patient 3) who had undergone gamma-knife irradiation at 25 years of age because of a large right basal ganglial arteriovenous malformation. (a) Conventional angiogram of the right common carotid artery (Towne view) shows right distal ICA occlusion (arrow). (b) Transverse precontrast T1-weighted spin-echo MR image (600/14) shows the isointense thickened wall (arrow) of the right distal ICA. (c) Transverse contrast-enhanced T1-weighted spin-echo MR image (600/14) shows intense ring enhancement (arrow) of the distal ICA wall.

View larger version (161K): [in this window] [in a new window] [Download PPT slide]   Figure 2c. Radiation-induced arteritis in a 27-year-old woman (patient 3) who had undergone gamma-knife irradiation at 25 years of age because of a large right basal ganglial arteriovenous malformation. (a) Conventional angiogram of the right common carotid artery (Towne view) shows right distal ICA occlusion (arrow). (b) Transverse precontrast T1-weighted spin-echo MR image (600/14) shows the isointense thickened wall (arrow) of the right distal ICA. (c) Transverse contrast-enhanced T1-weighted spin-echo MR image (600/14) shows intense ring enhancement (arrow) of the distal ICA wall.

View larger version (167K): [in this window] [in a new window] [Download PPT slide]   Figure 3a. MR images show idiopathic moyamoya disease in a 15-year-old boy. (a) Transverse precontrast intermediate-weighted spin-echo MR images (fast spin echo, 3,200/14) show narrowing of both distal ICAs (arrows) and MCAs (arrowheads). Moyamoya vessels also were seen. (b) Transverse contrast-enhanced T1-weighted spin-echo MR images (500/9) show no definite enhancement of the narrowed arteries (arrows).

View larger version (130K): [in this window] [in a new window] [Download PPT slide]   Figure 3b. MR images show idiopathic moyamoya disease in a 15-year-old boy. (a) Transverse precontrast intermediate-weighted spin-echo MR images (fast spin echo, 3,200/14) show narrowing of both distal ICAs (arrows) and MCAs (arrowheads). Moyamoya vessels also were seen. (b) Transverse contrast-enhanced T1-weighted spin-echo MR images (500/9) show no definite enhancement of the narrowed arteries (arrows).

However, in the anterior cerebral arteries and MCAs, it was difficult to differentiate between luminal enhancement resulting from slow flow and wall enhancement resulting from the smaller caliber of these vessels. Twenty-two of the 23 patients showed luminal and/or wall enhancement in the anterior cerebral arteries and/or MCAs.

Findings on the conventional MR and MR angiographic images obtained in the five patients with radiation-induced arteritis are summarized in the Table. The time between irradiation and the onset of stenosis and/or occlusion was 2–19 years (mean, 7.4 years ± 6.8). The duration of contrast enhancement was 1–3 years (mean, 1.9 years ± 0.4) in four patients who underwent follow-up contrast-enhanced MR imaging, and none of the contrast enhancement had diminished at the time this article was written. The time between the first observed stenosis and/or occlusion and the onset of the first observed contrast enhancement, with sufficient image quality for vascular wall evaluation, was 0–9 years (mean, 3.2 years ± 4.4); in three of five patients, stenosis and/or occlusion and contrast enhancement were depicted in the same period, and two of five were followed up mainly with nonenhanced imaging. All of the diseased vessels were patent at the time of irradiation. The initial patency of the arteries was confirmed with conventional angiography (four of five patients) and with flow void on intermediate-weighted spin-echo MR images (2,000/30), as well as with contrast enhancement on CT scans (one of five patients).

Patient 2 underwent irradiation at 10 years of age because of suprasellar germinoma, with a total dose of 50 Gy in 2-Gy fractions, with opposed lateral fields. Bilateral para- and suprasellar regions were included in the field, and the dose for both distal ICAs and both proximal MCAs and anterior cerebral arteries was estimated at about 50 Gy. Both ICAs were patent at the time of irradiation and through several years of follow-up. At 15 years of age, bilateral carotid occlusion with development of moyamoya-like collaterals was first recognized on MR and MR angiographic images. Marked ring enhancement of both carotid walls also was detected (Fig 1). Three months after the study, the patient had a stroke.

Patient 3 underwent gamma-knife irradiation at 25 years of age, with a dose of 18 (margin) to 45 Gy (center) to treat a relatively large arteriovenous malformation in the inferior aspect of the right basal ganglia. The target volume was 36.68 cm³. The dose for the right MCA and right distal ICA was estimated at about 18 Gy. At the time of irradiation, the right carotid artery and MCAs were patent. Two years later, at 27 years of age, contrast-enhanced MR images showed marked ring enhancement of the right distal carotid artery (Fig 2) and bandlike enhancement along the M1 portion of the MCAs. Selective catheter angiography performed on that occasion showed occlusion of the right distal carotid and the M1 portion of the MCAs. No special symptom related to this occlusion was observed.

Patient 4 underwent irradiation at 31 years of age with conventional irradiation equipment (linear accelerator), with a dose of 60 Gy in 2-Gy fractions, to treat a large arteriovenous malformation in the right basal ganglia. The dose for the right MCA and right distal ICA was estimated at just less than 60 Gy. No special symptom related to occlusion of the primary lesion was observed. Six years later, at 37 years of age, the patient had stenosis of the distal ICA and of the M1 segment of the MCAs. Marked ring enhancement with wall thickening was observed on contrast-enhanced MR images obtained at that time.

Patient 5 underwent irradiation twice, at 12 and 27 years of age, with a dose of 60 Gy each time to treat suprasellar craniopharyngioma. The former was performed locally with opposed lateral fields, and the latter was performed on the whole brain. The dose for both distal ICAs and proximal MCAs and anterior cerebral arteries was about 60 Gy each. Stenosis of the carotid arteries was first recognized at 31 years of age as a decreased flow void on MR images. At 40 years of age, contrast-enhanced MR imaging was performed, with sufficient image quality for evaluation of the vascular wall. Ring enhancement of both distal carotid arteries was observed. Selective catheter angiography showed severe stenosis almost to the point of occlusion of both carotid arteries. Cerebral infarction occurred 1 year later.

	DISCUSSION

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Radiation-induced injuries to large arteries that result in stenotic and/or occlusive vasculopathy have been considered relatively rare, although some investigators (7,8,13) have suggested that such clinically important damage to large arteries is more common than previously thought. A few case studies and experimental radiation damage studies (1–6,14) have typically shown subintimal collections of foam cells with myointimal proliferation, which has been broadly characterized as premature or accelerated arteriosclerosis. Prominent thickened wall with an increased outer diameter was demonstrated in some studies (3,5). On the other hand, in idiopathic (primary) moyamoya disease, the outer diameter of occluded and/or stenotic arteries is decreased; the ICA has shown marked 1–2-mm thinning of the outer diameter at the terminal portion (11). Usually, thinning occurred distal to the origin of the ophthalmic artery, but occasionally, a slight to moderate decrease in diameter was also noted on the cervical portion of the carotid artery (11,12).

With contrast-enhanced MR imaging, arterial wall thickening and enhancement were frequently observed in aortitis syndrome (9) and atherosclerosis (10). We had similar findings in patients with radiation-induced large-vessel vasculopathy. In contrast with the patients who had radiation-induced vasculopathy, the arteries of the patients who had idiopathic moyamoya disease showed no prominent enhancement of the arterial wall. These MR imaging findings correlated well with the abnormal findings mentioned previously (11,12). Accordingly, this suggests that contrast enhancement of the occluded arterial wall may contribute to differentiation between radiation-induced vasculopathy and idiopathic moyamoya disease. Differential diagnosis of these two diseases has been difficult with use of other imaging modalities, even selective intraarterial angiography, because the intraluminal morphologies of the two diseases may appear to be the same. The authors of one report (2) have discussed a common cause of a radiation-induced moyamoya-like state and of idiopathic moyamoya disease by examining angiographic similarity, without any pathologic evidence. Our results suggest a different pathophysiology of these two conditions. Attention should be paid to the arterial wall when discussing these conditions. Findings of wall enhancement might also contribute to determining whether the moyamoya-like state of patients who have previously undergone irradiation is really radiation-induced or if it is idiopathic. It is rare, but coexisting parasellar tumor and idiopathic moyamoya disease have been reported (15). Although radiation-induced arteritis and idiopathic moyamoya disease produced differences in contrast enhancement of the carotid wall in the small group of patients in the current study, the results need to be validated in a larger study.

The incidence of radiation-induced occlusive vasculopathy of the large intracranial arteries is not well recognized. In a review of 105 patients with irradiated germ cell tumors (16), three patients showed occlusive vasculopathy of the large intracranial arteries. Radiation-induced occlusive vasculopathy of the large cerebral arteries is an important delayed complication of radiation therapy, usually evolving slowly to produce ischemic effects years or even decades after irradiation. Patients show relatively acute changes in neurologic status after many years of irradiation (2,3). Early detection of vasculopathy in follow-up MR imaging studies of primary disorders may be important to reduce the occurrence and extent of such ischemic changes.

To our knowledge, the natural history and progress of radiation-induced vasculopathy, as seen with contrast-enhanced studies, have not yet been established. It is not clear whether the contrast enhancement decreases correlation with the reduction of the inflammatory process of the arterial wall or if enhancement is prolonged after inflammation because of irreversible development of the vasa vasorum. We observed prominent enhancement after several years of occlusion (patient 1, 7 years; patient 5, 9 years). Our results suggest that contrast enhancement on MR images may be prolonged at least several years after occlusion and/or stenosis occurs. However, it is clear that these results need to be validated in a larger study.

In conclusion, wall thickening and prominent ring enhancement of the ICAs were seen on MR images obtained in patients with radiation-induced arteritis, whereas the same degree of wall thickening and ring enhancement of the carotid arteries was not seen in patients with idiopathic moyamoya disease. We suggest that enhancement of the large cerebral arteries may be a diagnostic clue in differentiating radiation-induced arteritis from idiopathic moyamoya disease.

	FOOTNOTES

 
Abbreviations: ICA = internal carotid artery, MCA = middle cerebral artery

Author contributions: Guarantor of integrity of entire study, S.A.; study concepts, S.A., T.A.; study design, S.A., I.S.; literature research, S.A., I.S.; clinical studies, S.A., K.N.; data acquisition, S.A., N.H., O.A., I.S., K.I., T.O., K.N.; data analysis/interpretation, S.A., K.I.; statistical analysis, S.A.; manuscript preparation, S.A.; manuscript definition of intellectual content, K.O.; manuscript editing, K.O., T.A.; manuscript revision/review, S.A., T.A.; manuscript final version approval, S.A., K.O.

	REFERENCES

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 

1. Chuang VP. Radiation-induced arteritis. Semin Roentgenol 1994; 24:64-69.[CrossRef]
2. Bitzer M, Topka H. Progressive cerebral occlusive disease after radiation therapy. Stroke 1995; 26:131-136.[Abstract/Free Full Text]
3. Brant-Zawadzki M, Anderson M, DeArmond SJ, Conley FK, Jahnke RW. Radiation-induced large intracranial vessel occlusive vasculopathy. AJR Am J Roentgenol 1980; 134:51-55.[Abstract]
4. Foreman NK, Laitt RD, Chambers J, et al. Intracranial large vessel vasculopathy and anaplastic meningioma 19 years after cranial irradiation for acute lymphoblastic leukaemia. Med Pediatr Oncol 1995; 24:265-268.[Medline]
5. Kamiryo T, Lopes MBS, Berr SS, Lee KS, Kassell NF, Steiner L. Occlusion of the anterior cerebral artery after gamma knife irradiation in a rat. Acta Neurochir 1996; 138:983-991.[CrossRef][Medline]
6. Kallfass E, Kraemling HJ, Schultz-Hector S. Early inflammatory reaction of the rabbit coeliac artery wall after combined intraoperative (IORT) and external (ERT) irradiation. Radiother Oncol 1996; 39:167-178.[CrossRef][Medline]
7. Zidar N, Ferluga D, Hvala A, Popovic M, Sova E. Contribution to the pathogenesis of radiation-induced injury to large arteries. J Laryngol Otol 1997; 111:988-990.[Medline]
8. Fajardo LF. Basic mechanisms and general morphology of radiation injury. Semin Roentgenol 1993; 28:297-302.[CrossRef][Medline]
9. Choe YH, Han BK, Koh EM, et al. Takayasu’s arteritis: assessment of disease activity with contrast-enhanced MR imaging. AJR Am J Roentgenol 2000; 175:505-511.[Abstract/Free Full Text]
10. Aoki S, Shirouzu I, Sasaki Y, et al. Enhancement of the intracranial arterial wall at MR imaging. Radiology 1995; 194:477-481.[Abstract/Free Full Text]
11. Hosoda Y. Pathology of so-called "spontaneous occlusion of the circle of Willis.". Pathol Ann 1984; 19:221-244(pt 2).
12. Haltia M, Iivanainen M, Majuri H, Puranen M. Spontaneous occlusion of the circle of Willis (moyamoya syndrome). Clin Neuropathol 1982; 1:11-22.[Medline]
13. Epstein MA, Packer RJ, Porke LB, et al. Vascular malformation with radiation vasculopathy after treatment of chiasmatic/hypothalamic glioma. Cancer 1992; 70:887-893.[CrossRef][Medline]
14. Bowen J, Paulsen CA. Stroke after pituitary irradiation. Stroke 1992; 23:908-911.[Abstract/Free Full Text]
15. Kitano S, Sakamoto H, Fujitani K, Kobayashi Y. Moyamoya disease associated with a brain stem glioma. Childs Nerv Syst 2000; 16:251-255.[CrossRef][Medline]
16. Sawamura Y, Iked J, Shirato H, Tada M, Abe H. Germ cell tumours of the central nervous system: treatment consideration based on 111 cases and their long-term clinical outcomes. Eur J Cancer 1998; 34:104-110.

This Article Abstract Figures Only Full Text (PDF) All Versions of this Article: 2233010822v1 223/3/683    most recent Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Aoki, S. Articles by Araki, T. Search for Related Content PubMed PubMed Citation Articles by Aoki, S. Articles by Araki, T.