Lectin-binding properties of Burkitt's lymphoma cell lines: application to bone marrow purging.

Exp Hematol

Department of Bone Marrow Transplantation, Hadassah University Hospital, Jerusalem, Israel.

Published: January 1990

The efficacy of binding of several lectins to different Burkitt's lymphoma (BL) cell lines was investigated. Soybean agglutinin (SBA), peanut agglutinin (PNA), wheat germ agglutinin (WGA), and Sambucus nigra agglutinin (SNA) bound strongly to all BL cell lines. Because SBA has been used safely in clinical bone marrow transplantation (BMT) as part of the procedure for T-cell depletion and hence does not bind to the stem cells, we chose this lectin to establish a model for purging BL cells from human bone marrow. Using a two-step purging procedure with tumor cell agglutination by SBA in solution, a 2-log depletion could be accomplished. Using SBA-coated magnetic beads, we could improve BL cell depletion to greater than 4 logs. Because SBA seems to have a broad specificity for BL cells with concomitant enrichment in hematopoietic progenitor cells, the use of SBA-coated magnetic beads could be of interest for autologous BMT for lymphomas as well as other hematological malignancies and solid tumors with positive binding to SBA.

Download full-text PDF

Source

Publication Analysis

Top Keywords

cell lines
12
bone marrow
12
burkitt's lymphoma
8
lymphoma cell
8
sba-coated magnetic
8
magnetic beads
8
cell
5
sba
5
lectin-binding properties
4
properties burkitt's
4

Similar Publications

Efficient synthesis of coumarin based triazole linked O-glycoconjugates as new bio-active glycohybrids.

Carbohydr Res

January 2025

Glycochemistry Laboratory, School of Physical Sciences, Jawaharlal Nehru University, New Delhi, 110067, India. Electronic address:

Glycohybrids are biologically significant molecules with variety of biological functions and are found as structural motifs in numerous natural products. Here, we report the synthesis of various new coumarin-based O-glycoconjugates as glycohybrids that are chirally enriched and bridged by 1,2,3-triazoles ring system. The1,2,3-triazoles bridging was done via CuAAC click-chemistry.

View Article and Find Full Text PDF

Adaptive immune resistance in cancer describes the various mechanisms by which tumors adapt to evade anti-tumor immune responses. IFN-γ induction of programmed death-ligand 1 (PD-L1) was the first defined and validated adaptive immune resistance mechanism. The endoplasmic reticulum (ER) is central to adaptive immune resistance as immune modulatory secreted and integral membrane proteins are dependent on ER.

View Article and Find Full Text PDF

One hallmark of cancer is the upregulation and dependency on glucose metabolism to fuel macromolecule biosynthesis and rapid proliferation. Despite significant pre-clinical effort to exploit this pathway, additional mechanistic insights are necessary to prioritize the diversity of metabolic adaptations upon acute loss of glucose metabolism. Here, we investigated a potent small molecule inhibitor to Class I glucose transporters, KL-11743, using glycolytic leukemia cell lines and patient-based model systems.

View Article and Find Full Text PDF

Background: Ovarian cancer (OC), particularly high-grade serous ovarian carcinoma (HGSOC), is the leading cause of mortality from gynecological malignancies worldwide. Despite the initial effectiveness of treatment, acquired resistance to poly(ADP-ribose) polymerase inhibitors (PARPis) represents a major challenge for the clinical management of HGSOC, highlighting the necessity for the development of novel therapeutic strategies. This study investigated the role of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), a pivotal regulator of glycolysis, in PARPi resistance and explored its potential as a therapeutic target to overcome PARPi resistance.

View Article and Find Full Text PDF

Background: Pathogenic or null mutations in WRN helicase is a cause of premature aging disease Werner syndrome (WS). WRN is known to protect somatic cells including adult stem cells from premature senescence. Loss of WRN in mesenchymal stem cells (MSCs) not only drives the cells to premature senescence but also significantly impairs the function of the stem cells in tissue repair or regeneration.

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!