title: [Time factor and repopulation during fractionated radiotherapy. Comparison between two xenografted human squamous cell carcinoma].
abstract: BACKGROUND
  A series of experiments were performed to determine the local tumour control of two human squamous cell carcinoma lines in nude mice. An accelerated-fractionated radiation therapy regime is compared to a conventional-fractionated therapy regime.
  
  
  METHODS
  KB is a well established human nasopharyngeal squamous cell carcinoma line (ATCC CCL 17). In nude mice KB grows as an low differentiated carcinoma. PEC MB is an undifferentiated squamous cell carcinoma of the maxillary sinus, which was successfully established in nude mice by our group 1993. Both tumors were serially passaged in nude mice. Local irradiation was given without anaesthesia under ambient conditions to air breathing animals using 18 MeV electrons of an linear accelerator (Mevatron 77, Siemens, Munich). Each dose level group consists of six to eight animals. The radiation treatments were given in ten equals fractions using graded dose levels of 2, 3, 4.5, 6 and 8 Gy. The interfraction time interval was 6 hours in the accelerated-fractionated group and 24 hours in the conventional-fractionated group (Figure 1). In the conventional-fractionated group a therapy break was given after 5 fractions for 72 h. The endpoint of the experiments was the dose, which was necessary to control 50% of the tumors (TCD(50)). The TCD(50) values were calculated after 60 days (Tables 1a and 1b).
  
  
  RESULTS
  The experiments show, that with increasing overall treatment time of 8 3/4 days using the same number of fractions under ambient conditions the tumor control dose of the tumor KB increases from 36.3 Gy (95% CI 30.9...42.7) to 44.3 Gy (38.3...51.2) (Figure 2a). For the tumor PEC MB the tumor control dose increases from 39.5 Gy (33.4...46.7) to 45.5 Gy (37.0...56.0 (Figure 2b).
  
  
  CONCLUSIONS
  This observed increase of the dose necessary to control the squamous cell carcinoma KB and PEC MB can be caused by repopulation of clonogenic tumors cells, however, other mechanism such as an increasing fraction of hypoxic tumor cells can not be ruled out.
authors.affiliation: Klinik und Poliklinik für Strahlentherapie - Radioonkologie, Universitätsklinikum Münster, Germany. hessels@uni-muenster.de
authors.forename: Stefan
authors.initials: S
authors.lastname: Hesselmann
authors.forename: Katja
authors.initials: K
authors.lastname: Lindel
authors.forename: Kirsten
authors.initials: K
authors.lastname: Horn
authors.forename: Stefan
authors.initials: S
authors.lastname: Könemann
authors.forename: Andreas
authors.initials: A
authors.lastname: Schuck
authors.forename: Normann
authors.initials: N
authors.lastname: Willich
authors.forename: Christian
authors.initials: C
authors.lastname: Rübe
mesh_terms: D000818:Animals; D002294:Carcinoma, Squamous Cell / Q000473:pathology / Q000532:radiotherapy*; D002455:Cell Division / Q000528:radiation effects*; D002470:Cell Survival / Q000528:radiation effects*; D019583:Dose Fractionation, Radiation; D004307:Dose-Response Relationship, Radiation; D006801:Humans; D051379:Mice; D008819:Mice, Nude; D009368:Neoplasm Transplantation; D014407:Tumor Cells, Cultured / Q000473:pathology / Q000528:radiation effects*