title: [Study on the origin of H/RS cell and their biological behavior in Hodgkin lymphoma by using multiple mark techniques].
abstract: OBJECTIVE
  To investigate the apoptosis-related genes and protein expression patterns in relation to classical Hodgkin lymphomas (CHL) and the origin of H/RS cell.
  
  
  METHODS
  Sixty-two cases of CHL were retrieved from Shanxi Tumor Hospital files. An ABC method was used to detect the expression of bcl-2, CD3, CD20, CD30, CD15 and CD10, a double immunohistochemical method to study the H/RS cells P53 expression, a double immunohistochemical ABC-DNA end labeling technique to detect the apoptosis, a double immunohistochemical ABC- in situ hybridization technique to detect the expression of kappa mRNA and lambda mRNA, and a multiple mark techniques to detect the distribution of background non-neoplastic T and B cells.
  
  
  RESULTS
  Of 62 CHL, 14 (22.58%) were p53 positive and 35 (56.45%) bcl-2 positive. Apoptosis was found in the background non-neoplastic cells in all of the cases, but in H/RS cells in only 10 of 62 cases. There was a significant reverse correlation between bcl-2 expression and apoptosis in H/RS cells (P = 0.02). CD30 positive H/RS cells were observed in all cases, whereas CD15 positive in only 41 cases, and CD20 positive in 8 cases. None was positive for CD3, MPO, bcl-6, CD10, kappa RNA and lambda RNA in H/RS cells. The H/RS cells were surrounded by non-neoplastic T cells looked like a rosette and the outer periphery was B cells.
  
  
  CONCLUSIONS
  The H/RS cell of classical Hodgkin lymphoma has a great variety of B lineage markers. The characteristic distributions of T, B and H/RS cells may serve as a reference for the diagnosis. Multiple marker technique is able to highlight the critical cells, and facilitate the study of H/RS cells. Abnormal expression of P53 may not play a major role in CHL. Over expression of bcl-2 may be linked to blockage of apoptosis in CHL.
authors.affiliation: Department of Pathology, Shanxi Tumor Hospital, Taiyuan 030013, China.
authors.forename: Jin-fen
authors.initials: JF
authors.lastname: Wang
authors.forename: Yan-feng
authors.initials: YF
authors.lastname: Xi
authors.forename: Li-xia
authors.initials: LX
authors.lastname: Wang
authors.forename: Wei-dong
authors.initials: WD
authors.lastname: Yin
authors.forename: Jin-wen
authors.initials: JW
authors.lastname: Zhang
authors.forename: Fang-chun
authors.initials: FC
authors.lastname: Gong
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D018951:Antigens, CD20 / Q000235:genetics / Q000378:metabolism; D017209:Apoptosis; D014408:Biomarkers, Tumor / Q000235:genetics / Q000378:metabolism*; D017252:CD3 Complex / Q000235:genetics / Q000378:metabolism; D002648:Child; D002675:Child, Preschool; D006689:Hodgkin Disease / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D020287:In Situ Nick-End Labeling; D017730:Ki-1 Antigen / Q000235:genetics / Q000378:metabolism; D016256:Lewis X Antigen / Q000235:genetics / Q000378:metabolism; D008875:Middle Aged; D015260:Neprilysin / Q000235:genetics / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D016539:Reed-Sternberg Cells / Q000378:metabolism / Q000473:pathology*; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism; D055815:Young Adult
chemical_list: D018951:Antigens, CD20; D014408:Biomarkers, Tumor; D017252:CD3 Complex; D017730:Ki-1 Antigen; D016256:Lewis X Antigen; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D015260:Neprilysin