title: Radiation induced early necrosis in patients with malignant gliomas receiving temozolomide.
abstract: BACKGROUND
  Temozolomide is the major drug in the treatment of malignant gliomas. Radiation induced necrosis can behave radiologically and clinically like a recurrent tumor. The major problem is the differentiation between recurrence and radiation injury especially in early phases of treatment. The aim of this study was to evaluate the patients receiving temozolomide showing early clinical or radiological progression and impact of early necrosis on follow-up.
  
  
  METHODS
  We retrospectively evaluated medical records of 67 patients with malignant glioma receiving temozolomide. All patients received concomitant radiotherapy and temozolomide followed by adjuvant temozolomide. In case of any radiological or clinical progression, MRI spectroscopy evaluation was used to confirm tumoral progression.
  
  
  RESULTS
  Radiological or clinical progression was observed in 17 (25.4%) patients. Early radiation induced necrosis was diagnosed in 4 of 17 patients (23.5%) by surgery (n=3) and MRI spectroscopy (n=1). The observed incidence of pseudoprogression was 4 in 67 (6%) patients. Patients with diagnosis of early radiation injury had median progression-free survival of 7 months compared to 5 months in patients without radiation damage (p=0.004). However, there was no statistically significant difference in terms of overall survival between groups.
  
  
  CONCLUSIONS
  Temozolomide can cause early radiation induced injury which can mimic progressive tumor. Although the discrimination between two entities results in the accurate evaluation of response to therapy and benefits those patients, it did not affect overall survival. MRI spectroscopy is a valuable tool to define early radiation necrosis and should be further evaluated in larger prospective studies.
authors.affiliation: Department of Medical Oncology, Mersin State Hospital, Mersin, Turkey. emel.yaman@gmail.com
authors.forename: Emel
authors.initials: E
authors.lastname: Yaman
authors.forename: Suleyman
authors.initials: S
authors.lastname: Buyukberber
authors.forename: Mustafa
authors.initials: M
authors.lastname: Benekli
authors.forename: Yusuf
authors.initials: Y
authors.lastname: Oner
authors.forename: Ugur
authors.initials: U
authors.lastname: Coskun
authors.forename: Muge
authors.initials: M
authors.lastname: Akmansu
authors.forename: Banu
authors.initials: B
authors.lastname: Ozturk
authors.forename: Ali Osman
authors.initials: AO
authors.lastname: Kaya
authors.forename: Dogan
authors.initials: D
authors.lastname: Uncu
authors.forename: Ramazan
authors.initials: R
authors.lastname: Yildiz
mesh_terms: D000328:Adult; D000368:Aged; D018906:Antineoplastic Agents, Alkylating / Q000009:adverse effects* / Q000627:therapeutic use; D001932:Brain Neoplasms / Q000150:complications / Q000188:drug therapy* / Q000532:radiotherapy / Q000601:surgery; D003131:Combined Modality Therapy / Q000009:adverse effects; D003606:Dacarbazine / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000627:therapeutic use; D018572:Disease-Free Survival; D005260:Female; D005910:Glioma / Q000150:complications / Q000188:drug therapy* / Q000532:radiotherapy / Q000601:surgery; D006801:Humans; D053208:Kaplan-Meier Estimate; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D009336:Necrosis / Q000139:chemically induced / Q000175:diagnosis; D011832:Radiation Injuries / Q000139:chemically induced / Q000473:pathology*; D011878:Radiotherapy / Q000009:adverse effects; D012189:Retrospective Studies; D000077204:Temozolomide; D055815:Young Adult
chemical_list: D018906:Antineoplastic Agents, Alkylating; D003606:Dacarbazine; D000077204:Temozolomide