Glucocorticoid-induced apoptosis and treatment sensitivity in acute lymphoblastic leukemia of children

M. Csóka, J. Bocsi, A. Falus, C. Szalai, V. Klujber, B. Szende, D. Schuler

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Sensitivity of leukemic blasts to steroid therapy is one of the prognostic factors in acute lymphoblastic leukemia (ALL) in children. We examined the number of steroid receptors and the increase in the apoptotic index in peripheral blast cells after administration of prednisolone monotherapy in 21 children with ALL. A new diagnostic method was established based on determination of the apoptotic index in peripheral blood lymphoblasts to evaluate the steroid sensitivity of leukemic cells during the first day of therapy. The increase in apoptotic ratio, analyzed by morphologic and/or flow cytometric studies, was most expressed in the first 6 hours of treatment. The apoptotic ratio showed a good correlation with the clinical response. The number of steroid receptors (gcRs) on the blast cells was also examined, but it proved to be less informative than the in vivo steroid response itself.

Original languageEnglish
Pages (from-to)433-442
Number of pages10
JournalPediatric Hematology and Oncology
Volume14
Issue number5
Publication statusPublished - Sep 1997

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Cell death
Precursor Cell Lymphoblastic Leukemia-Lymphoma
Glucocorticoids
Steroid Receptors
Steroids
Apoptosis
Blood
Prednisolone
Therapeutics
Therapy
Factors
Diagnostics

Keywords

  • Apoptosis
  • Glucocorticoid receptors
  • Glucocorticoid therapy
  • Leukemia
  • Prognosis

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Hematology
  • Oncology
  • Cancer Research
  • Management of Technology and Innovation

Cite this

Glucocorticoid-induced apoptosis and treatment sensitivity in acute lymphoblastic leukemia of children. / Csóka, M.; Bocsi, J.; Falus, A.; Szalai, C.; Klujber, V.; Szende, B.; Schuler, D.

In: Pediatric Hematology and Oncology, Vol. 14, No. 5, 09.1997, p. 433-442.

Research output: Contribution to journalArticle

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