title: Different susceptibilities of lymphokine-activated killer cells (LAK cells) among primary and metastatic renal cell carcinoma derived from the same patient.
abstract: OBJECTIVE
  To investigate the susceptibility of primary renal cell carcinoma (RCC) and metastatic RCC to lymphokine-activated killer (LAK) cells using three RCC cell lines derived from the primary and metastatic tumours in a male patient with advanced RCC.
  
  
  METHODS
  Three RCC cell lines (named HANKS) were derived from a 44-year-old man with advanced RCC. HANKS-Pr, HANKS-Lu and HANKS-LN were established from the primary lesion and the metastatic lung and lymph node lesions, respectively. The susceptibility of HANKS cell lines to 18 different LAK cells obtained from either patients with urological cancer or from healthy volunteers was studied. The three groups of LAK cells were divided as follows: (A) LAK cells from RCC patients (n = 6); (B) LAK cells from patients with transitional cell carcinoma (TCC)/prostatic carcinoma (CaP) (n = 4) and (C) healthy volunteers (n = 8). A 51Cr-releasing cytotoxic assay was used to determine susceptibility.
  
  
  RESULTS
  The mean percentage lysis of the HANKS cell lines to the 18 allogenic LAK cells were 28.1% in HANKS-Pr, 20.2% in HANKS-Lu and 10.4% in HANKS-LN. The susceptibility of HANKS-LN to LAK cells was significantly lower than that of HANKS-Pr and HANKS-Lu in all three groups (P < 0.05). In contrast, the susceptibility of HANKS-Pr was significantly higher than HANKS-Lu in group A only (P < 0.01).
  
  
  CONCLUSIONS
  This is the first report to describe the different susceptibilities of primary RCC and metastatic RCC derived from the same patient. HANKS-LN itself might be the least susceptible to LAK cells because it was not related to the source of LAK cells. Furthermore, RCC may affect the cytotoxicity of LAK cells to HANKS-Pr. These data indicate there are at least two different types of mechanisms leading to the different susceptibilities of HANKS cells to LAK cells.
authors.affiliation: Department of Urology, Nippon Medical School, Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Hattori
authors.forename: M
authors.initials: M
authors.lastname: Satoh
authors.forename: T
authors.initials: T
authors.lastname: Nishimura
authors.forename: N
authors.initials: N
authors.lastname: Kawamura
authors.forename: M
authors.initials: M
authors.lastname: Akimoto
mesh_terms: D000328:Adult; D002292:Carcinoma, Renal Cell / Q000276:immunology*; D002295:Carcinoma, Transitional Cell / Q000276:immunology; D003602:Cytotoxicity, Immunologic; D006801:Humans; D007680:Kidney Neoplasms / Q000276:immunology*; D015979:Killer Cells, Lymphokine-Activated / Q000502:physiology*; D008285:Major Histocompatibility Complex / Q000276:immunology; D008297:Male; D011471:Prostatic Neoplasms / Q000276:immunology; D014407:Tumor Cells, Cultured