title: Radiation-induced cell cycle response in lymphocytes is not related to clinical side-effects in breast cancer patients.
abstract: BACKGROUND
  We examined whether development of radiation-induced lung injury after irradiation for breast cancer correlates with lymphocyte radiosensitivity (LRS) in vitro.
  
  
  METHODS
  Patients were selected from a cohort of 177 patients, who were treated with adjuvant postoperative radiotherapy (RT) for loco-regional breast cancer, and included 14 patients who had severe early lung injury measured as respiratory symptoms caused by RT and treated with corticosteroids (i.e. "cases") and a corresponding 14 control patients without such symptoms. LRS was measured as the postirradiation fraction of mitogen-stimulated blood lymphocytes in S- and G2-phase. Plasma levels of TGF-beta 1 and thiols, both suggested to be involved in the pathogenesis of radiation-induced lung injury, were also analysed.
  
  
  RESULTS
  The result showed that cells from the controls responded to a higher extent to mitogen stimulation than cells from the cases (p < 0.05). Analysis of the fraction of S- and G2-phase cells after irradiation showed no significant difference between the two groups (p = 0.57 and 0.31, respectively). There was no difference in plasma levels of TGF-beta 1 and thiols in patients who did or did not develop pulmonary injury after RT. Tamoxifen administered before or at RT did not influence the incidence of pulmonary reactions.
  
  
  CONCLUSIONS
  No differences in LRS were found between breast cancer patients with lung complications after RT and matched control patients without complications.
authors.affiliation: Department of Oncology-Pathology, Karolinska Institutet and Hospital, SE-171 76 Stockholm, Sweden. roger.tell@cck.ki.se
authors.forename: Roger
authors.initials: R
authors.lastname: Tell
authors.forename: Margareta R
authors.initials: MR
authors.lastname: Edgren
authors.forename: Asgerdur
authors.initials: A
authors.lastname: Sverrisdottir
authors.forename: Juan
authors.initials: J
authors.lastname: Castro
authors.forename: Tommy
authors.initials: T
authors.lastname: Fornander
authors.forename: Lars-Olof
authors.initials: LO
authors.lastname: Hansson
authors.forename: Sven
authors.initials: S
authors.lastname: Skog
authors.forename: Rolf
authors.initials: R
authors.lastname: Lewensohn
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001943:Breast Neoplasms / Q000097:blood* / Q000532:radiotherapy*; D002453:Cell Cycle / Q000528:radiation effects; D003208:Concanavalin A / Q000494:pharmacology; D005260:Female; D006801:Humans; D008171:Lung Diseases / Q000097:blood / Q000209:etiology*; D008213:Lymphocyte Activation / Q000187:drug effects; D008214:Lymphocytes / Q000187:drug effects / Q000528:radiation effects*; D008875:Middle Aged; D011832:Radiation Injuries / Q000097:blood* / Q000209:etiology; D011836:Radiation Tolerance; D013438:Sulfhydryl Compounds / Q000097:blood; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D016212:Transforming Growth Factor beta / Q000097:blood; D053773:Transforming Growth Factor beta1
chemical_list: D013438:Sulfhydryl Compounds; C508960:TGFB1 protein, human; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D003208:Concanavalin A; D013755:Tetradecanoylphorbol Acetate