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Neutral glycosphingolipid expression in B‐cell neoplasms
Author(s) -
Kalisiak Angela,
Minniti J. Gerald,
Oosterwuk Egbert,
Old Lloyd J.,
Scheinberg David A.
Publication year - 1991
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910490607
Subject(s) - chronic lymphocytic leukemia , glycosphingolipid , biology , chromosomal translocation , leukemia , lymphoma , phenotype , cancer research , microbiology and biotechnology , immunology , genetics , gene
The expression of neutral glycosphingolipids (GSL) in 37 B‐cell neoplasms [7 acute lymphocytic leukemia (ALL), 5 Burkitt's lymphoma (BL), 7 chronic lymphocytic leukemia (CLL), 5 diffuse, poorly differentiated lymphoma (DPDL), 6 diffuse histiocytic lymphoma (DHL), 3 hairy‐cell leukemia (HCL), and 4 multiple myeloma (MM)] was examined. Patterns of expression of simple (GlcCer, LacCer) and globo‐series GSL (Gb 3 , Gb 4 ,) were found for each tumor type. In addition, pre‐B ALL expressed the neo‐lacto series GSL, paragloboside, which was not significantly seen at later stages of maturation. As a group, leukemias expressed about 10 times higher ratios of simple GSL to Globo‐series GSL as compared to lymphomas, regardless of stage of differentiation. Significant amounts of GSL of other series were not found except in one CLL which contained asialo‐GM2. GSL phenotype in these cells was not grossly affected by cell genotype since pre‐B ALL containing Philadelphia chromosome t(9q;22q) translocations were similar to other ALL; and DHL with t(8q;14q) translocations had GSL patterns similar to other DHL samples and dissimilar to GSL patterns found in Burkitt's lymphomas with t(8q;14q). Differences in GSL expression among the different types of B‐cell neoplasm suggested that GSL patterns form a phenotypic map that may complement the traditional glycoprotein immunophenotypic map and contribute to our understanding of the biology of these diseases and B‐cell differentiation.