S592 I. J. Radiation Oncology d Biology d Physics Volume 78, Number 3, Supplement, 2010

Conclusions: WLI using tomotherapy reduces RT dose to non-target normal tissues without compromising coverage of PTV. Thismay have a positive impact in minimizing late toxicity including second cancers involving the heart, breast and thyroid.

Author Disclosure: F. Siddiqui, None; T. Mathews, None; B.S. Teh, None; J.A. Kalapurakal, None; E.B. Butler, None; M.Chintagumpala, None; A.C. Paulino, None.

2869 Rotational Errors and Dosimetric Effects for Pediatric Brain Tumor Patients

C. Beltran, A. Pegram, T. E. Merchant

St. Jude Children’s Research Hospital, Memphis, TN

Purpose/Objective(s): To quantify the rotational set-up errors and determine their dosimetric consequence in pediatric braintumor.

Materials/Methods: Twenty pediatric brain tumor patients with a median age of 6.9 years (range, 1 to 18) treated with con-formal or intensity-modulated radiation therapy were included in this study. All patients were enrolled on a prospective in-stitutional daily localization protocol. Each patient was treated in the supine position and immobilized usinga thermoplastic face mask. Ten required daily IV general anesthesia. Prior to each treatment fraction, a cone beam CT(CBCT) was performed to quantify and correct the inter-fraction translational setup error. At the end of every other fraction,a CBCT was performed to quantify intra-fractional motion. For this study, a separate analysis was performed to quantify inter-and intra-fractional rotational (roll, pitch, and yaw) setup errors. Changes in target dose coverage and dose to critical structureswere then quantified by simulating fixed values of rotational error (2 and 5 degrees) about each axis in the treatment planningsystem.

Results: A median of 30 pre and 15 post CBCTs were analyzed for each patient. The mean magnitude (SD) inter-fractionalrotation errors for roll, pitch and yaw, were 0.72 (0.96), 0.66 (1.04), and 0.60 (0.99) degrees, respectively. The intra-fractionrotational errors for roll, pitch and yaw, were 0.53 (0.53), 0.54 (0.61), and 0.63 (0.90) degrees, respectively. Clinically accept-able (\3%) degradation was noted for the 5 degree rotational error simulation when modeling for change in target volumecoverage. There was no meaningful change in critical structure dose in the 2 degree rotational error simulation; however,when modeling for change in critical structure dose using the 5 degree rotational error, the dose to cochlea, spinal cord, brain-stem, optic nerves and chiasm increased from 10 to 25%. For example, the mean dose to the right cochlea for an infratentorialependymoma patient went from 21 to 26 Gy and the generalized equivalent uniform dose of the spinal cord went from 44 to48 Gy.

Conclusions: Pediatric brain tumor patients have small and relatively inconsequential rotation errors (1 + 1 degree) along eachaxis using standardized immobilization procedures with or without anesthesia. The effect of larger rotational errors appears tobecome clinically significant when rotational errors exceed 5 degrees in any axis with the greatest impact in dose to criticalstructures.

Author Disclosure: C. Beltran, None; A. Pegram, None; T.E. Merchant, None.

2870 Tumor and Systemic Cytokine Response in Patients with Pediatric Sarcomas Treated with Limited Margin

3DCRT and IMRT

M. Krasin1, A. Spalding2, F. Navid1, K. Hoth1, C. Hua1, T. Merchant1, S. Wu1

1St. Jude Children’s Research Hospital, Memphis, TN, 2Norton Cancer Radiation Center, Louisville, KY

Purpose/Objective(s): Patterns of serum cytokine profiles prior to, during, and following limited margin RT can be correlated witheither effects of therapy or the treatment of gross disease for pediatric sarcoma patients.

Materials/Methods: A total of 61 children and young adults on a prospective institutional clinical trial of limited margin 3DCRT/IMRT underwent analysis of serum cytokines obtained serially at time points prior to RT (59 pts) and 5 wks (60 pts), 3 and/or 6 mo(57 pts), and 12 mo (47 pts) from initiation of RT. Patients received multimodal therapy for Ewing’s sarcoma (ES, 18 pts), rhab-domyosarcoma (RMS, 37 pts) and soft tissue sarcoma (STS, 6 pts) incorporating chemotherapy (58 pts) and complete surgicalresection (23 pts) in addition to radiation. Millipore 39-Plex Human Cytokine kits were used to process the 251 serum samplesfor 39 cytokines yielding 9789 individual levels. Statistical analysis incorporated modeling of the baseline values (intercept)and the trend over time of the log transformed cytokine values correlating these with the effects of tumor (disease groups) and ther-apy (by the presence or absence of gross disease).

Results: A total of 19 cytokines (IP-10, MDC/CCL22, EGF, Eotaxin, Fractalkine, GM-CSF, IL-1alpha, MIP-1b, FGF-2, GRO, IL-12 (p40), IL-1beta, IL-4, IL-5, IL-8, MCP-3/CCL7, sCD40L, TNFb, VEGF) were found to differ significantly or marginallysignificantly at baseline for patients with the diagnosis of ES or RMS. When only patients with gross primary residual diseasewere considered, 9 cytokines (IP-10, MDC/CCL22, EGF, Eotaxin, Fractalkine, GM-CSF, IL-1alpha, MIP-1b, FGF-2) continuedto differ at baseline suggesting a possible difference in tumor secretion or therapy induced change specific to histology. The base-line levels were universally lower for all cytokines for ES compared to RMS. Only IP-10, MDC/CCL22, and IL-15 demonstrateddifferent trends between ES and RMS over the time of study. Several cytokines demonstrated a significant trend related to diseaserecurrence (FGF-2, INFalpha2) and will require further evaluation.

Conclusions: Serum cytokines may be correlated with disease groups and treatment patterns, both at baseline and over time.RMS patients had increased levels of inflammatory and mitogenic cytokines relative to ES patients which did not decline duringradiation. Defining these relationships will be helpful for future selection of cytokines for analysis in tumor and normal tissueresponse to therapy, as well as rational incorporation of evolving targeted molecular agents for incorporation into multimodalitytrials.

Author Disclosure: M. Krasin, Lance Armstrong Foundation, B. Research Grant; A. Spalding, None; F. Navid, None; K. Hoth,None; C. Hua, None; T. Merchant, None; S. Wu, None.