Influence of  68 Ga-DOTATOC on sparing of normal tissue for radiation therapy of skull base meningioma: differential impact of photon and proton radiotherapy

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Abstract

Background

To evaluate the impact of ⁶⁸Ga-DOTATOC-PET on treatment planning and sparing of normal tissue in the treatment of skull base meningioma with advanced photons and protons.

Methods

From the institutional database consisting of 507 skull base meningiomas 10 patients were chosen randomly for the present analysis. Target volume definition was performed based on CT and MRI only, as well as with additional ⁶⁸Ga-DOTATOC-PET. Treatment plans were performed for Intensity Modulated Radiotherapy (IMRT) and proton therapy using active raster scanning on both target volumes. We calculated doses to relevant organs at risk (OAR), conformity indices as well as differences in normal tissue sparing between both radiation modalities based on CT/MRI planning as well as CT/MRI/PET planning.

Results

For photon treatment plans, PET-based treatment plans showed a reduction of brain stem D _max and D _median for different levels of total dose. At the optic chiasm, use of ⁶⁸Ga-DOTATOC significantly reduces D _max; moreover, the D _median is reduced in most cases, too. For both right and left optic nerve, reduction of dose by addition of ⁶⁸Ga-DOTATOC-PET is minimal and depends on the anatomical location of the meningioma. In protons, the impact of ⁶⁸Ga-DOTATOC-PET is minimal compared to photons.

Conclusion

Addition of ⁶⁸Ga-DOTATOC-PET information into treatment planning for skull base meningiomas has a significant impact on target volumes. In most cases, PET-planning leads to significant reductions of the treatment volumes. Subsequently, reduced doses are applied to OAR. Using protons, the benefit of additional PET is smaller since target coverage is more conformal and dose to OAR is already reduced compared to photons. Therefore, PET-imaging has the greatest margin of benefit in advanced photon techniques, and combination of PET-planning and high-precision treatment leads to comparable treatment plans as with protons.

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Most cited references 21

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Detection of cranial meningiomas: comparison of ⁶⁸Ga-DOTATOC PET/CT and contrast-enhanced MRI.

Sabine Haufe, Clemens Kratochwil, Stephanie Combs … (2012)

PET imaging with somatostatin receptor ligands, such as (68)Ga-DOTATOC, is a well-established method for detection and target volume definition of meningiomas prior to radiotherapy. Since DOTATOC PET delivers a higher contrast between meningiomas and surrounding tissues than MRI, we conducted a retrospective analysis to compare the diagnostic accuracy of contrast-enhanced MRI (CE-MRI) with (68)Ga-DOTATOC PET/CT in patients with cranial meningiomas prior to radiotherapy. Over a period of 6 years, 134 patients (20-82 years of age, 107 women and 27 men) underwent cranial CE-MRI and (68)Ga-DOTATOC PET/CT. To compare the two methods, the lesions considered typical of meningiomas visually were counted and analysed with respect to their location and SUVmax. In the 134 patients investigated by both modalities, 190 meningiomas were detected by (68)Ga-DOTATOC PET/CT and 171 by CE-MRI. With knowledge of the PET/CT data, the MRI scans were reinvestigated, which led to the detection of 4 of the 19 incidental meningiomas, resulting in an overall detection rate of 92 % of the meningioma lesions that were found by PET/CT. Ga-DOTATOC PET/CT demonstrated an improved sensitivity in meningioma detection when compared to CE-MRI. Tumours adjacent to the falx cerebri, located at the skull base or obscured by imaging artefacts or calcification are particularly difficult to detect by MRI. Therefore (68)Ga-DOTATOC PET/CT may provide additional information in patients with uncertain or equivocal results on MRI or could help to confirm a diagnosis of meningioma based on MRI or could help to confirm MRI-based diagnosis of meningiomas in cases of biopsy limitations. It is possible that not only radiotherapy and surgical planning, but also follow-up strategies would benefit from this imaging modality.

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Improved target volume definition for fractionated stereotactic radiotherapy in patients with intracranial meningiomas by correlation of CT, MRI, and [68Ga]-DOTATOC-PET.

Angelika Bois, Angelika Hoess, D Schulz-Ertner … (2006)

To evaluate the influence of 68-Ga-labeled DOTA (0)-D-Phe (1)-Tyr (3)-Octreotide positron emission tomography ([68Ga]-DOTATOC-PET) for target definition for fractionated stereotactic radiotherapy (FSRT) as a complementary modality to computed tomography (CT) and magnetic resonance imaging (MRI). Because meningiomas show a high expression of somatostatin receptor subtype 2, somatostatin analogs such as DOTATOC offer the possibility of receptor-targeted imaging. Twenty-six patients received stereotactic CT, MRI, and [68Ga]-DOTATOC-PET as part of their treatment planning. Histology was: World Health Organization (WHO) Grade 1 61.5%, WHO Grade 2 7.7%, WHO Grade 3 3.9%, and undetermined 26.9%. Six patients received radiotherapy as primary treatment, 2 after subtotal resection; 17 patients were treated for recurrent disease. Dynamic PET scans were acquired before radiotherapy over 60 min after intravenous injection of 156 +/- 29 MBq [68Ga]-DOTATOC. These PET images were imported in the planning software for FSRT. Planning target volume (PTV)-I outlined on CT and contrast-enhanced MRI was compared with PTV-II outlined on PET. PTV-III was defined with CT, MRI, and PET and was actually used for radiotherapy treatment. PTV-III was smaller than PTV-I in 9 patients, the same size in 7 patients, and larger in 10 patients. Median PTV-I was 49.6 cc, median PTV-III was 57.2 cc. In all patients [68Ga]-DOTATOC-PET delivered additional information concerning tumor extension. PTV-III was significantly modified based on DOTATOC-PET data in 19 patients. In 1 patient no tumor was exactly identified on CT/MRI but was visible on PET. These data demonstrate that [68Ga]-DOTATOC-PET improves target definition for FSRT in patients with intracranial meningiomas. Radiation targeting with fused DOTATOC-PET, CT, and MRI resulted in significant alterations in target definition in 73%.

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Secondary carcinogenesis in patients treated with radiation: a review of data on radiation-induced cancers in human, non-human primate, canine and rodent subjects.

Harald Paganetti, Saveli Goldberg, Eric Hall … (2006)

Concern for risk of radiation-induced cancer is growing with the increasing number of cancer patients surviving long term. This study examined data on radiation transformation of mammalian cells in vitro and on the risk of an increased cancer incidence after irradiation of mice, dogs, monkeys, atomic bomb survivors, occupationally exposed persons, and patients treated with radiation. Transformation of cells lines in vitro increased linearly with dose from approximately 1 to approximately 4-5 Gy. At <0.1 Gy, transformation was not increased in all studies. Dose-response relationships for cancer incidence varied with mouse strain, gender and tissue/organ. Risk of cancer in Macaca mulatta was not raised at 0.25-2.8 Gy. From the atomic bomb survivor study, risk is accepted as increasing linearly to 2 Sv for establishing exposure standards. In irradiated patients, risk of cancer increased significantly from 1 to 45 Gy (a low to a high dose level) for stomach and pancreas, but not for bladder and rectum (1-60 Gy) or kidney (1-15 Gy). Risk for several organs/tissues increased substantially at doses far above 2 Gy. There is great heterogeneity in risk of radiation-associated cancer between species, strains of a species, and organs within a species. At present, the heterogeneity between and within patient populations of virtually every parameter considered in risk estimation results in substantial uncertainty in quantification of a general risk factor. An implication of this review is that reduced risks of secondary cancer should be achieved by any technique that achieved a dose reduction down to approximately [corrected] 0.1 Gy, i.e. dose to tissues distant from the target. The proportionate gain should be greatest for dose decrement to less than 2 Gy.

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Author and article information

Contributors

Falk Stade: Falk.stade@gmail.com

Jan-Oliver Dittmar: o.dittmar@googlemail.com

Oliver Jäkel: o.jaekel@dkfz.de

Clemens Kratochwil: clemens.kratochwil@med-uni.heidelberg.de

Uwe Haberkorn: uwe.haberkorn@med-uni.heidelberg.de

Jürgen Debus: Juergen.Debus@med.uni-heidelberg.de

Stephanie E. Combs: +49-89-4140-4501 , Stephanie.combs@tum.de

Journal

Journal ID (nlm-ta): Radiat Oncol

Journal ID (iso-abbrev): Radiat Oncol

Title: Radiation Oncology (London, England)

Publisher: BioMed Central (London )

ISSN (Electronic): 1748-717X

Publication date (Electronic): 2 April 2018

Publication date PMC-release: 2 April 2018

Publication date Collection: 2018

Volume: 13

Electronic Location Identifier: 58

Affiliations

[1 ]ISNI 0000 0001 0328 4908, GRID grid.5253.1, Department of Radiation Oncology, , University Hospital of Heidelberg, ; Im Neuenheimer Feld 400, 69120 Heidelberg, Germany

[2 ]Deutsches Konsortium für Translationale Krebsforschung (dktk), Partner Site Heidelberg, Heidelberg, Germany

[3 ]ISNI 0000000123222966, GRID grid.6936.a, Department of Radiation Oncology, Klinikum rechts der Isar, , Technische Universität München, ; Ismaninger Straße 22, 81675 Munich, Germany

[4 ]Deutsches Konsortium für Translationale Krebsforschung (dktk), Partner Site Munich, Munich, Germany

[5 ]ISNI 0000 0004 0492 0584, GRID grid.7497.d, Department of Medical Physics in Radiation Oncology, , German Cancer Research Center (DKFZ), ; Im Neuenheimer Feld 280, 69120 Heidelberg, Germany

[6 ]Heidelberg Ion Beam Therapy Center (HIT), Im Neuenheimer Feld 450, 69120 Heidelberg, Germany

[7 ]ISNI 0000 0001 0328 4908, GRID grid.5253.1, Department of Nuclear Medicine, , University Hospital of Heidelberg, ; Im Neuenheimer Feld 400, 69120 Heidelberg, Germany

[8 ]ISNI 0000 0004 0483 2525, GRID grid.4567.0, Institute of Innovative Radiotherapy (iRT), Department of Radiation Sciences (DRS), , Helmholtz Zentrum München, ; Ingolstädter Landstraße 1, 85764 Oberschleißheim, Germany

Article

Publisher ID: 1008

DOI: 10.1186/s13014-018-1008-z

PMC ID: 5880004

PubMed ID: 29606149

SO-VID: 8fcfbcc7-c44b-428c-b6b9-513a24d3aa0a

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 29 August 2017

Date accepted : 23 March 2018

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100001659, Deutsche Forschungsgemeinschaft;

Award ID: KFO 214

Award Recipient : Stephanie E. Combs

Custom metadata

ScienceOpen disciplines: Oncology & Radiotherapy

Keywords: 68ga-dotatoc-pet,skull base meningioma,imrt,proton therapy,oar

Data availability:

ScienceOpen disciplines: Oncology & Radiotherapy

Keywords: 68ga-dotatoc-pet, skull base meningioma, imrt, proton therapy, oar

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