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From the Departments of Pathology*
and Bacterial
Infection,§
Institute of Medical Science,
University of Tokyo, Tokyo, Japan; the First Department of Internal
Medicine
and the Department of
Pathology,¶
Faculty of Medicine, University of
Tokyo, Tokyo, Japan; the Developmental Oncology/Hematology and Leukemia
Unit,
Department of Medical Oncology, Centro
di Riferimento Oncologico, I.R.C.C.S., Aviano, Italy; the Clinical
Laboratory,||
National Children’s Hospital, Tokyo, Japan;
and the Fourth Department of Internal Medicine,**
Kitasato University, School of Medicine, Kanagawa, Japan
We earlier identified a variant of CD30 (CD30v) that retains only
the cytoplasmic region of the authentic CD30. This variant is expressed
in alveolar macrophages. CD30v can activate the nuclear factor-
B
(NF-B) as CD30, and its overexpression in HL-60 induced a
differentiated phenotype. To better understand the physiological and
pathological functions of CD30v, expression of this variant was
examined using a multiple approach to examine 238 samples of human
malignant myeloid and lymphoid neoplasms. Screening by reverse
transcriptase-polymerase chain reaction (RT-PCR) revealed expression of
CD30v transcripts in 52 of 72, 7 of 11, 63 of
90, and 7 of 30 samples of acute myeloid leukemia
(AML), myeloid blast crisis of myeloproliferative disorders
(MBC), and lymphoproliferative disorders (LPDs) of B- and
T-cell origin, respectively. CD30v expression was high in
monocyte-oriented AMLs (FAB M4 and M5), B-cell chronic
lymphocytic leukemia (B-CLL), and multiple myeloma (MM). Using
the specific antibody HCD30C2, prepared using a peptide
corresponding to the nine amino acids of the amino-terminal
CD30v, expression of CD30v protein was detected in 10 of 25 and
2 of 10 AML and ALL samples, respectively. In AMLs,
immunocytochemical detection of CD30v revealed the presence of loose
clusters of CD30v-expressing cells dispersed amid a population of
CD30v-negative blasts. Finally, the parallel expression of
CD30v mRNA and protein, as evidenced by Northern and Western
blotting, was confirmed in selected cases of AMLs and LPDs. A
significant correlation was found between expressions of CD30v and CD30
ligand transcripts in AML and LPD (P =
0.02, odds ratio = 3.2). The association of CD30v with
signal-transducing proteins, tumor necrosis factor
receptor-associated factor (TRAF) 2, and TRAF5 was demonstrated
by coimmunoprecipitation analysis, as was demonstrated for
authentic CD30 protein. Expression of transcripts for TRAF1,
TRAF2, TRAF3, and TRAF5, as demonstrated by
RT-PCR, was noted in leukemic blasts that express CD30v.
Collectively, frequent expression of CD30v along with TRAF
proteins in human neoplastic cells of myeloid and lymphoid origin
provide supportive evidence for biological and possible pathological
functions of this protein in the growth and differentiation of a
variety of myeloid and lymphoid cells.
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  M. Watanabe, M. Sasaki, K. Itoh, M. Higashihara, K. Umezawa, M. E. Kadin, L. J. Abraham, T. Watanabe, and R. Horie JunB Induced by Constitutive CD30-Extracellular Signal-Regulated Kinase 1/2 Mitogen-Activated Protein Kinase Signaling Activates the CD30 Promoter in Anaplastic Large Cell Lymphoma and Reed-Sternberg Cells of Hodgkin Lymphoma Cancer Res., September 1, 2005; 65(17): 7628 - 7634. [Abstract] [Full Text] [PDF]
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