Characterization of a novel HHV-8-positive cell line reveals implications for the pathogenesis and cell cycle control of primary effusion lymphoma

Leukemia. 2000 Jul;14(7):1301-9. doi: 10.1038/sj.leu.2401802.

Abstract

Primary effusion lymphoma (PEL) represents a peculiar type of B cell lymphoma which associates with HHV-8 infection and preferentially grows in liquid phase in the serous body cavities. In this report, we provide the detailed characterization of a newly established PEL cell line, termed CRO-AP/6. The cell line was obtained from the pleural effusion of a HIV-positive patient with PEL. Its derivation from the tumor clone was established by immunogenotypic analysis. Detailed phenotypic investigations defined that CRO-AP/6 reflects pre-terminally differentiated B cells expressing the CD138/syndecan-1 antigen. Karyotypic studies of CRO-AP/6 identified several chromosomal abnormalities, whereas genotypic studies ruled out the involvement of molecular lesions associated with other types of B cell lymphoma. Both CRO-AP/6 and the parental tumor sample harbored infection by HHV-8. Conversely, EBV infection was present in the parental tumor sample although not in CROAP/6, indicating that CRO-AP/6 originated from the selection of an EBV-negative tumor subclone. The pattern of viral (HHV-8 v-cyclin) and cellular (p27Kip1) regulators of cell cycle expressed by CRO-AP/6, together with the results of growth fraction analysis, point to abrogation of the physiological inverse relationship between proliferation and p27Kip1 expression. Also, both CRO-AP/6 and the parental tumor sample display biallelic inactivation of the DNA repair enzyme gene O6-methylguanine-DNA methyltransferase (MGMT) by promoter methylation. Overall, the CRO-AP/6 cell line may help understand cell cycle control of PEL cells, may clarify the relative contribution of HHV-8 and EBV to the disease growth and development and may facilitate the identification of recurrent cytogenetic abnormalities highlighting putative novel cancer related loci relevant to PEL.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antigens, Viral / biosynthesis
  • Antigens, Viral / genetics
  • Cell Cycle
  • Chromosome Aberrations
  • Clone Cells / pathology
  • Clone Cells / virology
  • Cyclins / biosynthesis
  • Cyclins / genetics
  • DNA Methylation
  • Enzyme Activation
  • Epstein-Barr Virus Infections / pathology
  • Epstein-Barr Virus Infections / virology
  • Gene Expression Regulation, Neoplastic
  • Gene Expression Regulation, Viral
  • Genes, Tumor Suppressor
  • Herpesviridae Infections / genetics
  • Herpesviridae Infections / pathology*
  • Herpesviridae Infections / virology
  • Herpesvirus 4, Human / immunology
  • Herpesvirus 4, Human / isolation & purification
  • Herpesvirus 4, Human / pathogenicity
  • Herpesvirus 8, Human / immunology
  • Herpesvirus 8, Human / isolation & purification
  • Herpesvirus 8, Human / pathogenicity*
  • Humans
  • Immunophenotyping
  • Lymphoma, AIDS-Related / etiology
  • Lymphoma, AIDS-Related / genetics
  • Lymphoma, AIDS-Related / pathology*
  • Lymphoma, AIDS-Related / virology
  • Lymphoma, B-Cell / genetics
  • Lymphoma, B-Cell / pathology
  • Lymphoma, B-Cell / virology*
  • Neoplasm Proteins / biosynthesis
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / physiology*
  • O(6)-Methylguanine-DNA Methyltransferase / deficiency*
  • O(6)-Methylguanine-DNA Methyltransferase / genetics
  • O(6)-Methylguanine-DNA Methyltransferase / physiology
  • Pleural Effusion, Malignant / genetics
  • Pleural Effusion, Malignant / pathology*
  • Pleural Effusion, Malignant / virology
  • Promoter Regions, Genetic
  • Proto-Oncogenes
  • Tumor Cells, Cultured / virology*
  • Tumor Virus Infections / genetics
  • Tumor Virus Infections / pathology*
  • Tumor Virus Infections / virology
  • Viral Proteins / biosynthesis
  • Viral Proteins / genetics
  • Virus Latency

Substances

  • Antigens, Viral
  • Cyclins
  • Neoplasm Proteins
  • Viral Proteins
  • O(6)-Methylguanine-DNA Methyltransferase