|
|
 Previous Article | Table of Contents | Next Article 
Blood, 15 August 2000, Vol. 96, No. 4, pp. 1388-1392
HEMATOPOIESIS
Intramedullary apoptosis of hematopoietic cells in
myelodysplastic syndrome patients can be massive: apoptotic cells
recovered from high-density fraction of bone marrow
aspirates
Vilasini Shetty,
Seema Hussaini,
LaTanya Broady-Robinson,
Krishnan Allampallam,
Suneel Mundle,
Raphael Borok,
Eileen Broderick,
Lucia Mazzoran,
Francesca Zorat, and
Azra Raza
From the Rush Cancer Institute, Rush-Presbyterian-St
Luke's Medical Center, Chicago, IL.
A higher percentage of apoptotic cells (apoptotic index or
AI) is consistently found in bone marrow (BM) biopsies compared to BM
aspirates of patients with myelodysplastic syndrome (MDS). Most studies
have only investigated the low-density fraction (LDF) mononuclear
cells from BM aspirates following density separation for AI
determination. In the present study, both LDF and high-density fraction (HDF) cells for AI were examined by electron microscopy (EM)
in 10 MDS patients and 4 healthy donors. Matched BM biopsies were
subjected to AI detection by in situ end labeling (ISEL) of
fragmented DNA. The results indicate that in LDF and HDF cells, AI is consistently higher in MDS patients (8.5% vs 1.5%,
respectively; P = .039) compared to healthy donors (27%
vs 4%, respectively; P = .004). The BM biopsy AI
was also higher in MDS patients than in healthy donors (3+ vs 0+,
respectively; P = .036). In addition, in MDS patients,
more apoptotic cells were found in HDF cells than in LDF cells
(27% vs 8.5%, respectively;P = .0001). All stages of maturation, ranging from blasts to terminally mature cells belonging
to all 3 lineages, were represented in the dying cells in both
compartments. Using EM, typical Pelger-Huett-type cells appeared to
be apoptotic granulocytes. Both LDF and HDF cells should be
examined for an accurate estimation of apoptotic cells because
AI would be underestimated if only the LDF cells were studied.
Ultrastructural studies consistently show a higher AI in BM biopsies
compared to BM aspirates despite the correction factor of HDF
cells provided by AI. This may represent the actual extant
state, which could conceivably be due to a higher
concentration of proapoptotic signals in the biopsies.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
B. Novotna, R. Neuwirtova, M. Siskova, and Y. Bagryantseva
DNA instability in low-risk myelodysplastic syndromes: refractory anemia with or without ring sideroblasts
Hum. Mol. Genet.,
July 15, 2008;
17(14):
2144 - 2149.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Braun, G. Carvalho, A. Coquelle, M.-C. Vozenin, P. Lepelley, F. Hirsch, J.-J. Kiladjian, V. Ribrag, P. Fenaux, and G. Kroemer
NF-{kappa}B constitutes a potential therapeutic target in high-risk myelodysplastic syndrome
Blood,
February 1, 2006;
107(3):
1156 - 1165.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. Mirandola, G. Gobbi, C. Ponti, I. Sponzilli, L. Cocco, and M. Vitale
PKC{epsilon} controls protection against TRAIL in erythroid progenitors
Blood,
January 15, 2006;
107(2):
508 - 513.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Campioni, P. Secchiero, F. Corallini, E. Melloni, S. Capitani, F. Lanza, and G. Zauli
Evidence for a Role of TNF-Related Apoptosis-Inducing Ligand (TRAIL) in the Anemia of Myelodysplastic Syndromes
Am. J. Pathol.,
February 1, 2005;
166(2):
557 - 563.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. Suarez, M.-B. Vidriales, J. Garcia-Larana, G. Sanz, M.-J. Moreno, A. Lopez, S. Barrena, R. Martinez, M. Tormo, L. Palomera, et al.
CD34+ Cells from Acute Myeloid Leukemia, Myelodysplastic Syndromes, and Normal Bone Marrow Display Different Apoptosis and Drug Resistance-Associated Phenotypes
Clin. Cancer Res.,
November 15, 2004;
10(22):
7599 - 7606.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
U. Schmidt, E. van den Akker, M. Parren-van Amelsvoort, G. Litos, M. de Bruijn, L. Gutierrez, R. W. Hendriks, W. Ellmeier, B. Lowenberg, H. Beug, et al.
Btk Is Required for an Efficient Response to Erythropoietin and for SCF-controlled Protection against TRAIL in Erythroid Progenitors
J. Exp. Med.,
March 15, 2004;
199(6):
785 - 795.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
W.-K. Hofmann, S. de Vos, M. Komor, D. Hoelzer, W. Wachsman, and H. P. Koeffler
Characterization of gene expression of CD34+ cells from normal and myelodysplastic bone marrow
Blood,
November 15, 2002;
100(10):
3553 - 3560.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Albitar, T. Manshouri, Y. Shen, D. Liu, M. Beran, H. M. Kantarjian, A. Rogers, I. Jilani, C. W. Lin, S. Pierce, et al.
Myelodysplastic syndrome is not merely "preleukemia"
Blood,
July 18, 2002;
100(3):
791 - 798.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. L. Greenberg, N. S. Young, and N. Gattermann
Myelodysplastic Syndromes
Hematology,
January 1, 2002;
2002(1):
136 - 161.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
V. T. Shetty, S. D. Mundle, and A. Raza
Pseudo Pelger-Huet anomaly in myelodysplastic syndrome: hyposegmented or apoptotic neutrophil?
Blood,
August 15, 2001;
98(4):
1273 - 1275.
[Full Text]
[PDF]
|
|
|
|
|
