Mantle cell lymphoma-a spectrum from indolent to aggressive disease

Sander B., Quintanilla-Martinez L., Ott G., Xerri L., KUZU I., Chan J. K. C., ...Daha Fazla

VIRCHOWS ARCHIV, cilt.468, sa.3, ss.245-257, 2016 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Derleme
  • Cilt numarası: 468 Sayı: 3
  • Basım Tarihi: 2016
  • Doi Numarası: 10.1007/s00428-015-1840-6
  • Dergi Adı: VIRCHOWS ARCHIV
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.245-257
  • Anahtar Kelimeler: Mantle cell lymphoma, Morphology, Immunophenotype, Genetic aberrations, FISH, Indolent, Aggressive, LEUKEMIA/SMALL LYMPHOCYTIC LYMPHOMA, IN-SITU, GENE-EXPRESSION, SOX11 EXPRESSION, CYCLIN D1, CHROMOSOMAL-ABNORMALITIES, PROGNOSTIC INFORMATION, MONOCLONAL-ANTIBODIES, PERIPHERAL-BLOOD, CCND2 GENE
  • Ankara Üniversitesi Adresli: Evet

Özet

Mantle cell lymphoma (MCL) is a distinctive lymphoma type generally characterized by the presence of CCND1 translocation and overexpression of cyclin D1. MCL usually presents with advanced stage and rapid clinical progression. The diagnosis is in most instances uncomplicated but cases with variant morphologies or immunophenotypes, especially cyclin D1-negative cases, may cause diagnostic difficulties. During the mantle cell lymphoma (MCL) session at the European Association of Haematopathology/Society for Hematopathology workshop 2014 held in Istanbul, Turkey, submitted cases illustrated interesting features such as unusual morphology or immunophenotypes. In several submitted cases of cyclin D1-positive MCL, CCND1 rearrangement could not be detected by t(11;14)(q13;q32) dual-color dual-fusion FISH but was suggested by CCND1 break-apart probes, and advantages and disadvantages of different FISH probes were highlighted. Three cyclin D1-negative MCL cases were submitted. These were identified by SOX11 immunohistochemistry and found to carry CCND2 translocations and/or to express high levels of cyclin D2 mRNA. Features associated with aggressive clinical course were presented including high expression of p53 protein and MYC aberrations. The need to integrate histological, immunophenotypic, genetic, and clinical data to arrive at the correct diagnosis was emphasized.