Medical Specialties Commons^™

A Phase Ii Study Of Acute Toxicity For Celebrex(Tm) (Celecoxib) And Chemoradiation In Patients With Locally Advanced Cervical Cancer: Primary Endpoint Analysis Of Rtog 0128, David K. Gaffney, Kathryn Winter, Adam P. Dicker, Brigitte Miller, Patricia J. Eifel, Janice Ryu, Vilija Avizonis, Mitch Fromm, Kathryn Greven

Department of Radiation Oncology Faculty Papers

Purpose: To determine treatment-related acute toxicity rates in patients with locally advanced cervical cancer treated by oral celecoxib, i.v. cisplatin and 5-FU, and concurrent pelvic radiation therapy.

Methods and Materials: Eligible patients on this RTOG Phase I-II study for advanced cervix cancer included FIGO Stage IIB-IVA or patients with FIGO Stage IB through IIA with biopsy proven pelvic node metastases ortumor size >5 cm. Patients were treated with pelvic radiotherapy and brachytherapy. Celecoxib was prescribed at 400 mg twice daily beginning on day 1 for 1 year. Cisplatin (75 mg/m2) and 5-FU (1g/m2 for 4 days) were administered every 3 …

The Effect Of Hus1 On Ionizing Radiation Sensitivity Is Associated With Homologous Recombination Repair But Is Independent Of Non-Homologous End-Joining, Robert S. Weiss, Xiang Wang, Baocheng Hu, Ya Wang

Department of Radiation Oncology Faculty Papers

Mammalian Hus1 plays an important role in maintaining genomic integrity. Cells lacking mouse Hus1 are hypersensitive to DNA damage inducers including UV and camptothecin (CPT). By using clonogenic assay, we show here that Hus1 deficient mouse cells are hypersensitive to ionizing radiation (IR) compared with their Hus1-positive counterparts. However, these cells show similar induction levels and similar rejoining rates of DNA double strand breaks (DSBs) following IR, indicating that the effect of Hus1 on cell radiosensitivity is independent of non-homologous end-joining (NHEJ). By combining an I-SceI-induced-DNA DSBs system and a siRNA approach, we also show that knocking down Hus1 decreases …

Foreword: Anti-Angiogenic Therapy: Maximizing Therapeutic Gain, Adam P. Dicker

Department of Radiation Oncology Faculty Papers

No abstract provided.

Department Of Radiation Oncology And Kimmel Cancer Center, Thomas Jefferson University, The Intronic G13964c Variant In P53 Is Not A High-Risk Mutation In Familial Breast Cancer In Australia., Anna Marsh, Amanda B Spurdle, Bruce C Turner, Sian Fereday, Heather Thorne, Gulietta M Pupo, Graham J Mann, John L Hopper, Joseph F Sambrook, Georgia Chenevix-Trench

Department of Radiation Oncology Faculty Papers

BACKGROUND: Mutations in BRCA1 and BRCA2 account for approximately 50% of breast cancer families with more than four affected cases, whereas exonic mutations in p53, PTEN, CHK2 and ATM may account for a very small proportion. It was recently reported that an intronic variant of p53--G13964C--occurred in three out of 42 (7.1%) 'hereditary' breast cancer patients, but not in any of 171 'sporadic' breast cancer control individuals (P = 0.0003). If this relatively frequent occurrence of G13964C in familial breast cancer and absence in control individuals were confirmed, then this would suggest that the G13964C variant plays a role in …