No abstract

TPS5114 Background: Tumor size and the cell surface glycoprotein CA125 levels have been traditional biomarkers for ovarian carcinoma, but remain suboptimal for assessing patients receiving chemotherapy. Current morphological criteria do not adequately evaluate lesion necrosis from anti-angiogenic therapy when no tumor volume change is measured. The evaluation of functional biomarkers rather than tumor volume may better distinguish responders from non-responders early in treatment with anti-angiogenic therapy. Perfusion CT can evaluate changes in tumor vascularity including blood flow (BF), blood volume (BV), mean transit time (MTT) and capillary permeability surface product (PS) before and after anti-angiogenic therapy with/out decrease in tumor volume. Objectives: The aims of the study are to evaluate the relationship between changes in tumor perfusion parameters and clinical outcomes of progression free survival, overall survival, and standard RECIST anatomic response criteria. A test-retest perfusion CT scan will also be performed to evaluate reproducibility of perfusion parameters in a subset of participants. Methods: In this collaborative trial, participants will be co-enrolled in the GOG-262 treatment trial. Participants will receive doublet chemotherapy of paclitaxel and carboplatin, followed by anti-angiogenic monoclonal therapy at cycle two. Perfusion CT will be performed at three time points: at baseline prior to therapy (T0), between days 18 and 21 of cycle one chemotherapy (T1), and at 8-10 days (T2) in anti-angiogenic monoclonal therapy. Participants with primary epithelial ovarian, peritoneal or fallopian tube cancer with optimally or suboptimally debulked FIGO Stage II, III or IV disease are eligible for the trial. Lesion eligibility will be evaluated by size and attenuation criteria. Accrual: ACRIN 6695 is activated at 12 GOG sites; 4/78 participants have accrued Discussion: Perfusion CT has been readily incorporated into the pre-existing clinical CT protocols and during scheduled RECIST scans. These perfusion CT functional maps of BF, BV, MTT and PS have been generated using vendor provided software without issue. Contact: Please contact Chaan Ng, MD cng@mdanderson.org for additional information.

TPS10635 Background: Glioblastoma (GBM) is an aggressive type of primary malignant brain tumor and despite treatment with surgery, radiation, and temozolomide (TMZ) chemotherapy, median overall survival (OS) remains poor. A pathologic hallmark of GBM is tumor necrosis, a suspected result from endogenous tumor hypoxia. Angiogenesis is stimulated by hypoxia-driven signaling cascades and is required for tumor proliferation. The inefficient blood supply of these hypoxic tumors also limits the efficacy of chemotherapy and radiotherapy. Surviving hypoxic tumor cells may be selected out and proliferate as a more aggressive tumor subtype, therefore hindering OS. 18F-Fluoromisonidazole (FMISO) is a PET radiotracer whose uptake in hypoxic tissues can be measured radiographically. The degree of tumor hypoxia has been negatively associated with time to tumor progression and survival (Spence et al, 2008). Knowledge of the degree/distribution of tumor hypoxia by PET uptake and perfusion MRI parameters may provide prognostic information and help guide therapy for patients with GBM. Methods: In this phase II prospective single arm multi-institution study, patients will undergo baseline FMISO PET and MR imaging two weeks prior to chemoradiotherapy (CRT). A subset of patients will receive a second FMISO PET one week prior to CRT to assess reproducibility. Clinical outcomes of OS and 6-month progression-free survival (PFS-6) will be correlated to PET and MRI parameters. Eligibility: Pathologically confirmed GBM with residual tumor after surgery (including T2/FLAIR hyperintensity consistent with tumor) scheduled to receive standard fractionated radiation therapy and temozolomide alone or with an anti-VEGF agent or PARP inhibitor. Current enrollment: 22 patients of 50 sample size Contact information: Please contact the PI, Elizabeth R. Gerstner, MD ( egerstner@partners.org ) for additional information. Significance: With a better understanding of the extent of tumor hypoxia and changes in hypoxia levels from treatment, more effective therapies could be developed to inhibit GBM growth, target hypoxic areas and individualize patient care.