title: Invasion is not an independent prognostic factor in high-grade glioma.
abstract: OBJECTIVE
  The role of invasion as a prognostic factor in high-grade gliomas (HGG) remains controversial. An apparent increase in invasiveness following anti-angiogenic therapy makes this question clinically relevant. The goal of this study is to assess survival differences in patients with newly diagnosed HGG who present with diffuse invasive disease compared to those who did not, but went on to develop diffuse invasive disease following bevacizumab therapy.
  
  
  METHODS
  Twenty-three patients presented as newly diagnosed diffuse invasive HGG. All patients underwent surgical resection with radiation therapy and temozolomide for one year. Progression-free survival (PFS) and overall survival (OS) were compared to a control of 58 patients with focal high-grade glioma who received similar therapy, but that included bevacizumab at 10 mg/kg given every two weeks.
  
  
  RESULTS
  The patient characteristics were similar in each group. The median PFS and OS for invasive HGG patients were 6 and 13 months and for the focal HGG patients, 11 and 24 months, respectively (P=0.092 and P=0.071). In the subgroup of invasive HGG that showed significant angiogenesis, the median PFS and OS were 3 and 9 months, respectively. 56% of the focal HGG patients recurred as diffuse invasive relapse. For patients with focal HGG who recurred as invasive disease, the median PFS and OS were 9 and 21 months respectively.
  
  
  CONCLUSIONS
  Presence of diffuse invasive disease not accompanied by angiogenesis either prior to therapy or subsequent to anti-angiogenic therapy does not seem to have prognostic significance. However, invasion accompanied by angiogenesis in newly diagnosed HGG may confer a poor prognosis.
authors: Department of Radiation Oncology and Neurosurgery, New York University Langone Medical Center, New York, NY 10016, USA. narayana@nyumc.org
authors: Ashwatha
authors: A
authors: Narayana
authors: Donato
authors: D
authors: Perretta
authors: Saroj
authors: S
authors: Kunnakkat
authors: Deborah
authors: D
authors: Gruber
authors: John
authors: J
authors: Golfinos
authors: Erik
authors: E
authors: Parker
authors: Praveen
authors: P
authors: Medabalmi
authors: David
authors: D
authors: Zagzag
authors: R N
authors: RN
authors: Pat Eagan
authors: Michael
authors: M
authors: Gruber
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D020533:Angiogenesis Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000008:administration & dosage / Q000627:therapeutic use; D000068258:Bevacizumab; D001932:Brain Neoplasms / Q000188:drug therapy / Q000401:mortality / Q000473:pathology* / Q000532:radiotherapy; D002648:Child; D003131:Combined Modality Therapy; D003606:Dacarbazine / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000627:therapeutic use; D018572:Disease-Free Survival; D005260:Female; D005910:Glioma / Q000188:drug therapy / Q000473:pathology* / Q000532:radiotherapy / Q000601:surgery; D006801:Humans; D008297:Male; D008875:Middle Aged; D009361:Neoplasm Invasiveness; D009364:Neoplasm Recurrence, Local; D009389:Neovascularization, Pathologic; D011379:Prognosis; D000077204:Temozolomide
chemical_list: D020533:Angiogenesis Inhibitors; D061067:Antibodies, Monoclonal, Humanized; D000068258:Bevacizumab; D003606:Dacarbazine; D000077204:Temozolomide