The presence of bcl-2 in myeloid leukemias has been associated with a decrease in therapy-induced apoptosis, reduced patient survival and in vitro autonomous growth of leukemic cells. The present study focuses on the quantitation of resistance to increasing doses of 1-beta-d-arabinofuranosylcytosine (Ara-C) by using hematological tumors expressing different levels of bcl-2. Scanning densitometry of Western blots demonstrated that the myeloid U-937 cells express low levels of bcl-2 (RD = 0.008), whereas the follicular lymphoma RL-7 expressed very high levels (RD = 3.084). Colony formation was also examined following incubation with Ara-C and RL-7 cells demonstrated a higher clonogenic survival (LD50 = 0.5 microns) when compared with U-937 cells (LD50 = 0.005 microM). Similarly, the level of bcl-2 expression in each cell line was also related to apoptosis with U-937 cells demonstrating increased DNA fragmentation when compared with RL-7 cells. To further evaluate the effect of upregulated bcl-2 on Ara-C treatment, U-937 cells were transfected with a retroviral vector carrying the murine bcl-2 or vector alone. Upregulation of bcl-2 by myeloid leukemic cells increased the resistance by 3 logs to Ara-C when comparing LD50 values from clonogenic assays, and decreased apoptosis by at least 3 logs when measuring dUTP positive cells by flow cytometry.

Download full-text PDF

Source
http://dx.doi.org/10.1111/j.1600-0609.1996.tb01353.xDOI Listing

Publication Analysis

Top Keywords

u-937 cells
16
leukemic cells
12
cells
10
quantitation resistance
8
myeloid leukemic
8
bcl-2
8
bcl-2 myeloid
8
levels bcl-2
8
rl-7 cells
8
resistance cytosine
4

Similar Publications

Article Synopsis
  • The study highlights the urgent need for improved treatments for chronic myeloid leukemia (CML), given the high incidence and mortality rates among men and women.
  • It investigates the potential enhanced effects of combining inecalcitol with existing therapies imatinib and dasatinib on various cancer cell lines.
  • Results showed that while some cell lines were resistant, AR-230 and LAMA-84-s exhibited significant cell-killing effects, suggesting that the effectiveness of combined treatments varies depending on the specific cell type.
View Article and Find Full Text PDF

Effects of ERK1/2 Inhibitors on the Growth of Acute Leukemia Cells.

Anticancer Res

December 2024

Department of Laboratory Medicine, Institute of Science Tokyo, Tokyo, Japan

Background/aim: Extracellular signal-regulated kinases (ERK)1/2 are important regulatory proteins that control cell proliferation and survival, playing a significant role in cancer progression, metastasis, and chemoresistance. This study investigated the effects of ERK1/2 inhibitors on the in vitro growth of acute leukemia cell lines.

Materials And Methods: Three ERK1/2 inhibitors were used: SCH772984, temuterkib (LY3214996), and ulixertinib (BVD-523).

View Article and Find Full Text PDF

The objective of this study was to assess fibrinogen (FIB) co-modified with citrulline (CIT) and/or malondialdehyde-acetaldehyde (MAA) initiates macrophage-fibroblast interactions leading to extracellular matrix (ECM) deposition that characterizes rheumatoid arthritis-associated interstitial lung disease (RA-ILD). Macrophages (Mϕ) were stimulated with native-FIB, FIB-CIT, FIB-MAA or FIB-MAA-CIT. Supernatants (SN) (Mϕ-SN [U-937-derived] or MϕP-SN [PBMC-derived]) or direct antigens were co-incubated with human lung fibroblasts (HLFs).

View Article and Find Full Text PDF

Licochalcone A (Lico A), a naturally bioactive flavonoid, has shown antitumor activity in several types of cancers. However, few studies have focused on its effect on acute myeloid leukemia (AML). Cell viability and colony formation potential were detected by CCK-8 assay and colony formation assay, respectively.

View Article and Find Full Text PDF

All immune cells must transit from the blood to distal sites such as the lymph nodes, bone marrow, or sites of infection. Blood borne monocytes traffic to the site of inflammation by adhering to the endothelial surface and migrating along endothelial intracellular adhesion molecule 1 (ICAM-1) by their ligand's macrophage 1 antigen (Mac-1) and lymphocyte functional antigen 1 (LFA-1) to transmigrate through the endothelium. Poor patient prognoses in chronic inflammation and tumors have been attributed to the hyper recruitment of certain types of macrophages.

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!