title: Impact of p53 status to response of temozolomide in low MGMT expression glioblastomas: preliminary results.
abstract: OBJECTIVE
  This study was designed to assess the clinical outcomes of MGMT low expression glioblastomas with different p53 statuses to the treatment of temozolomide capsule chemotherapy.
  
  
  METHODS
  In this retrospective study, glioblastomas with low MGMT expression receiving surgical resection, radiotherapy and temozolomide capsule chemotherapy were divided into high and low mutant p53 expression groups. Patient age, gender, KPS score and extent of resection were analysed between the two groups by t-test and Fisher's exact test, respectively. Correlation between p53 status and control of tumor growth was analysed by survival analysis.
  
  
  RESULTS
  In total, 30 patients were included in the study. No statistically significant differences in age, gender, KPS score or extent of resection existed between the two groups. Patients with both low mutant p53 expression and low MGMT had much longer progression-free survival time to temozolomide capsule than those with high mutant p53 expression and low MGMT (p<0.05) Overall survival time did not reach statistical significance between the two groups.
  
  
  CONCLUSIONS
  p53 in addition to MGMT plays a role in chemotherapy resistance to temozolomide. Glioblastoma patients with both low MGMT and low mutant p53 expression have higher progression-free survival time and may have longer term prognosis compared with those patients with both low MGMT and high mutant p53 expression.
authors.affiliation: Department of Neurosurgery, No. 1 Hospital of Harbin Medical University, Harbin 150001, China.
authors.forename: Shouwei
authors.initials: S
authors.lastname: Li
authors.forename: Tao
authors.initials: T
authors.lastname: Jiang
authors.forename: Guilin
authors.initials: G
authors.lastname: Li
authors.forename: Zhongcheng
authors.initials: Z
authors.lastname: Wang
mesh_terms: D000328:Adult; D018906:Antineoplastic Agents, Alkylating / Q000627:therapeutic use*; D016022:Case-Control Studies; D017024:Chemotherapy, Adjuvant / Q000379:methods; D015254:DNA Modification Methylases / Q000378:metabolism*; D045643:DNA Repair Enzymes / Q000378:metabolism*; D003606:Dacarbazine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D005260:Female; D005500:Follow-Up Studies; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects / Q000235:genetics; D005909:Glioblastoma / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism; D006801:Humans; D008297:Male; D009154:Mutation; D011878:Radiotherapy / Q000379:methods; D012189:Retrospective Studies; D000077204:Temozolomide; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*; D025521:Tumor Suppressor Proteins / Q000378:metabolism*
chemical_list: D018906:Antineoplastic Agents, Alkylating; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; D003606:Dacarbazine; D015254:DNA Modification Methylases; C515491:MGMT protein, human; D045643:DNA Repair Enzymes; D000077204:Temozolomide