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Marrow cytokine transcripts and the secondary hematologic disorders

  • Harvey D. Preisler(corresponding author)
    ,
  • Xue Zhi Gao
    ,
  • Tao Ming
    ,
  • Biarou Li
    ,
  • Sucai Bi
    ,
  • Emmanuelle Devemy
*Corresponding author for this work
  • Rush Cancer Institute
Scholary Output:
Contribution to journal
Article
Peer-review

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

A comparison was made of the cytokine transcripts in normal, monoclonal, MDS, and AML marrow aspirates. While both normal and monoclonal marrow aspirates contain transcripts for SCF, few MDS or AML marrow aspirates contain these transcripts. Similarly, IL1ra transcripts are found with reduced frequency in MDS and AML marrow aspirates. The fall in SCF transcripts between monoclonal and MDS marrow aspirates parallels the appearance of apoptosis and the reduced in vitro proliferative ability which are characteristics of MDS marrow aspirate cells. The frequent IL1β production by MDS and AML marrow aspirate cells, with few marrow aspirates producing IL1ra transcripts, suggests that unbalanced IL1β effects may contribute to the proliferative advantage of MDS and AML cells over their normal counterparts.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 297-302 (6 pages)

Journal (Volume, Issue Number)

Leukemia and Lymphoma (Volume 35, Issue 3-4)

Publication milestones

  • Published - 1999

Publication status

Published - 1999

ISSN

1042-8194

Publication IDs

  • Scopus: 0032732823
  • PubMed: 10706453

Publication metrics

Metrics

SciVal
citations
1
SciVal
FWCI
0.11
SciVal
Author count
8
SciVal
Paper percentile
29
Fractional count
1
Fractional count
0.13
Fractional count
7
Fractional count
0.88
Fractional count
1
Fractional count
1
Scopus
citations

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Funding Details

This work was supported by a grant from the National Institutes of Health/National Cancer Institute Po-1 7560603 and R01 CA60086.
FundersFunding numbers
NIH
-
NCI
Po-1 7560603, R01CA060086