The phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) was tested for its ability to induce phenotypic changes in the human non-T,. non-B ALL cell line REH. Cells were cultured with nanogram concentrations of TPA for up to 48 hr, and were analyzed by indirect immunofluorescence with a panel of monoclonal antibodies and an antibody to the enzyme terminal deoxynucleotidyl transferase (TdT). TPA induced REH cells to express the leukemia-associated antigen, p24 (detected with monoclonal antibody BA-2; p24/BA-2) by 8 hr of culture, with induction complete by 24 hr. TPA-treated cells also underwent a concomitant decrease in the expression of TdT when analyzed enzymatically or by immunofluorescence. Analysis of TPA-treated cells with monoclonal antibodies BA-1 (detecting a B cell-associated antigen), 7.2 (detecting a monomorphic HLA-DR antigen), or OKT11 (detecting a structure closely associated with the E receptor) showed no change compared to controls. In addition there was no detectable cytoplasmic immunoglobulin in control or TPA-treated cells. These results show clearly that TPA is capable of inducing phenotypic changes in REH cells. Such changes may reflect the differentiation-linked expression of antigens present in normal bone marrow lymphoid progenitor cells.

Download full-text PDF

Source

Publication Analysis

Top Keywords

reh cells
12
tpa-treated cells
12
non-t non-b
8
lymphoid progenitor
8
phenotypic changes
8
monoclonal antibodies
8
cells
7
phorbol ester-induced
4
ester-induced differentiation
4
differentiation non-t
4

Similar Publications

This study investigates the interrelationship between human telomerase reverse transcriptase (hTERT) and ferroptosis in precursor-B (pre-B) acute lymphoblastic leukemia (ALL), specifically examining how hTERT modulation affects ferroptotic cell death pathways. Given that hTERT overexpression characterizes various cancer phenotypes and elevated telomerase activity is observed in early-stage and relapsed ALL, we investigated the molecular mechanisms linking hTERT regulation and ferroptosis in leukemia cells. The experimental design employed Nalm-6 and REH cell lines under three distinct conditions: curcumin treatment, hTERT siRNA knockdown, and their combination.

View Article and Find Full Text PDF

Retinal diseases often lead to degeneration of specific retinal cell types with currently limited therapeutic options to replace the lost neurons. Previous studies have reported that overexpression of or combinations of proneural factors in Müller glia (MG) induce regeneration of functional neurons in the adult mouse retina. Recently, we applied the same strategy in dissociated cultures of fetal human MG and although we stimulated neurogenesis from MG, our effect in 2D cultures was modest and our analysis of newborn neurons was limited.

View Article and Find Full Text PDF

Retinal degeneration in mammals causes permanent loss of vision, due to an inability to regenerate naturally. Some non-mammalian vertebrates show robust regeneration, via Muller glia (MG). We have recently made significant progress in stimulating adult mouse MG to regenerate functional neurons by transgenic expression of the proneural transcription factor Ascl1.

View Article and Find Full Text PDF
Article Synopsis
  • L-asparaginases are enzymes that convert L-asparagine into L-aspartic acid and ammonia, and they are important in the pharmaceutical industry, particularly for cancer treatments.
  • Scientists are exploring yeast-derived L-asparaginases as an alternative to bacterial ones, which can cause adverse immune responses.
  • The study focuses on a specific yeast enzyme, Lachancea thermotolerans, demonstrating that a mutant form of this enzyme shows increased activity and significant antileukemic potential compared to commercial bacterial versions.
View Article and Find Full Text PDF
Article Synopsis
  • Endogenous reprogramming of glial cells, specifically Müller glia, shows potential for neuron restoration in the adult retina by using strategies adapted from regenerative species.
  • The transcription factor Ascl1 can induce some Müller glia to regenerate neurons, but this process is hindered by neuroinflammation from infiltrating monocytes from the peripheral immune system.
  • Preventing monocyte infiltration enhances the neurogenic capacity of Müller glia, suggesting that targeting peripheral immune responses could improve neuronal regeneration therapies in the central nervous system.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!