title: Proliferative index and CD15 expression in pediatric classical Hodgkin lymphoma.
abstract: BACKGROUND
  This study was conducted to assess the clinical and prognostic significance of lack of CD15 expression, proliferative index (PI), and expression of tumor suppressor protein p53 in pediatric classical Hodgkin lymphoma (CHL).
  
  
  METHODS
  Pre-treatment lymph node (LN) biopsies were studied by immunohistochemistry for immunophenotyping of the lymphoma and with Ki-67 (PI) and p53 antibodies. Expression of CD15 antigen on the Hodgkin and Reed-Sternberg (H-RS) cells, proliferation, and apoptosis parameters were correlated with clinical stage, response to chemotherapy alone, overall (OS) and failure-free survival (FFS).
  
  
  RESULTS
  One hundred and twenty-one children with CHL were studied. Expression of Ki-67 and p53 in H-RS cells was seen in 100% and 89.9% of the cases, respectively. Loss of CD15 expression, seen in 12 (9.9%) cases, was significantly associated with p53 negativity and was an independent prognostic factor for poor OS and poor FFS. PI </= 74% was an independent prognostic factor for poor FFS.
  
  
  CONCLUSIONS
  Loss of CD15 expression in CHL might be related to p53 dysregulation. High PI in HL might reflect a high level of endomitosis within tumor cells, and could lead to higher sensitivity to chemotherapy. Low pre-treatment PI and lack of CD15 expression were found to be predictive factors for poor FFS in pediatric CHL.
authors.affiliation: Department of Pediatrics, All India Institute of Medical Sciences, New Delhi, India. verodinand@fastem.com
authors.forename: Veronique
authors.initials: V
authors.lastname: Dinand
authors.forename: Ajay
authors.initials: A
authors.lastname: Malik
authors.forename: Rajani
authors.initials: R
authors.lastname: Unni
authors.forename: Laxman S
authors.initials: LS
authors.lastname: Arya
authors.forename: R M
authors.initials: RM
authors.lastname: Pandey
authors.forename: Ramesh
authors.initials: R
authors.lastname: Dawar
mesh_terms: D000293:Adolescent; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000008:administration & dosage / Q000627:therapeutic use; D001761:Bleomycin / Q000008:administration & dosage; D048708:Cell Growth Processes / Q000502:physiology; D002648:Child; D002675:Child, Preschool; D003520:Cyclophosphamide / Q000008:administration & dosage; D003606:Dacarbazine / Q000008:administration & dosage; D018572:Disease-Free Survival; D004317:Doxorubicin / Q000008:administration & dosage; D005260:Female; D006689:Hodgkin Disease / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism* / Q000473:pathology*; D006801:Humans; D016130:Immunophenotyping; D053208:Kaplan-Meier Estimate; D019394:Ki-67 Antigen / Q000096:biosynthesis; D016256:Lewis X Antigen / Q000096:biosynthesis*; D008297:Male; D009367:Neoplasm Staging; D011241:Prednisone / Q000008:administration & dosage; D011344:Procarbazine / Q000008:administration & dosage; D012189:Retrospective Studies; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis; D014747:Vinblastine / Q000008:administration & dosage; D014750:Vincristine / Q000008:administration & dosage
chemical_list: D019394:Ki-67 Antigen; D016256:Lewis X Antigen; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53; D001761:Bleomycin; D011344:Procarbazine; D014750:Vincristine; D014747:Vinblastine; D003606:Dacarbazine; D004317:Doxorubicin; D003520:Cyclophosphamide; D011241:Prednisone