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Volume 93, Issue 2, Pages 234-240 (November 2009)


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Carbon-11 acetate PET/CT based dose escalated IMRT in prostate cancer

Jan SeppäläaCorresponding Author Informationemail address, Marko Seppänenb, Eveliina Arponenb, Paula Lindholma, Heikki Minnab

Received 27 April 2009; received in revised form 31 July 2009; accepted 4 August 2009. published online 22 September 2009.

Abstract 

Purpose

To demonstrate the theoretical feasibility of [11C]acetate PET/CT in delineating the malignant intraprostatic lesions (IPL’s) in prostate cancer and to use the data in external beam radiotherapy to boost the biologically defined target volume (BTV).

Methods and materials

Twelve men with intracapsular prostate carcinoma were imaged with [11C]acetate PET/CT and the data were used to delineate the BTV. Six dynamic IMRT plans were generated to each patient: a standard IMRT (sIMRT) plan with a 77.9Gy dose to PTV (prostate gland with a 6-mm margin) and a simultaneous integrated boost IMRT (SIBIMRT) plan to deliver 77.9Gy, 81Gy, 84Gy, 87Gy and 90Gy to the BTV and 72Gy to the rest of PTV. To study the theoretical dose escalation based on the delineation of BTV, tumor control probabilities (TCPs) and normal tissue complication probabilities (NTCPs) of bladder and rectum were calculated and compared between the treatment plans.

Results

[11C]Acetate was used to delineate the IPL’s of all 12 patients. With every patient the TCP was increased with SIBIMRT without increasing the NTCP of the bladder or rectum. The probability of uncomplicated control (PUC) was increased on average by 28% with the SIBIMRT treatment plans. The highest PUC was achieved with an average dose of 82.1Gy to the BTV.

Conclusions

Our study indicates that [11C]acetate can be used to define the IPL’s and in combination with SIBIMRT the defined areas can theoretically be treated to ultra high doses without increasing the treatment toxicity. These results motivate the formal validation of [11C]acetate PET for biological dose planning in prostate cancer.

a Department of Oncology and Radiotherapy, Turku University Hospital, Turku, Finland

b Turku PET Centre, Turku University Hospital, Turku, Finland

Corresponding Author InformationCorresponding author. Address: Dept of Radiotherapy (821), Turku University Hospital, P.O. Box 52, 20521 Turku, Finland.

PII: S0167-8140(09)00452-6

doi:10.1016/j.radonc.2009.08.010


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