| 1. |
- Fioretos, Thoas, et al.
(författare)
-
Regional localization and developmental expression of the BCR gene in rodent brain
- 1995
-
Ingår i: Cellular & molecular biology research. - 0968-8773. ; 41:2, s. 97-102
-
Tidskriftsartikel (refereegranskat)abstract
- The BCR gene is implicated in the development of Ph-positive leukemia through its fusion with the nonreceptor tyrosine kinase gene ABL. The normal 160 kDa Bcr protein has several functional domains, and recently one specific role for Bcr was established in the regulation of respiratory burst activity in white blood cells. Bcr expression levels are relatively constant throughout mouse development until adulthood in brain and in hematopoietic tissues, a pattern that is distinctly different from that of the functionally related n-chimerin gene. In the present study, RNA in situ hybridization was used to explore the normal cellular function of Bcr in rodent brain and hematopoietic organs. The data pinpoint the high bcr expression in the brain to the hippocampal pyramidal cell layer and the dentate gyrus, and to the piriform cortex and the olfactory nuclei, reflecting a potentially interesting function for Bcr in these highly specialized brain regions.
|
|
| 2. |
- Bum-Erdene, Khuchtumur, et al.
(författare)
-
Novel Selective Galectin-3 Antagonists Are Cytotoxic to Acute Lymphoblastic Leukemia
- 2022
-
Ingår i: Journal of Medicinal Chemistry. - : American Chemical Society (ACS). - 0022-2623 .- 1520-4804. ; 65:8, s. 5975-5989
-
Tidskriftsartikel (refereegranskat)abstract
- Galectin-3 is a β-galactoside-specific, carbohydrate-recognizing protein (lectin) that is strongly implicated in cancer development, metastasis, and drug resistance. Galectin-3 promotes migration and ability to withstand drug treatment of B-cell precursor acute lymphoblastic leukemia (BCP-ALL) cells. Due to high amino acid conservation among galectins and the shallow nature of their glycan-binding site, the design of selective potent antagonists targeting galectin-3 is challenging. Herein, we report the design and synthesis of novel taloside-based antagonists of galectin-3 with enhanced affinity and selectivity. The molecules were optimized by in silico docking, selectivity was established against four galectins, and the binding modes were confirmed by elucidation of X-ray crystal structures. Critically, the specific inhibition of galectin-3-induced BCP-ALL cell agglutination was demonstrated. The compounds decreased the viability of ALL cells even when grown in the presence of protective stromal cells. We conclude that these compounds are promising leads for therapeutics, targeting the tumor-supportive activities of galectin-3 in cancer.
|
|
| 3. |
- Fioretos, Thoas, et al.
(författare)
-
Standpoint on imprinting of BCR and ABL
- 1995
-
Ingår i: Leukemia. - 1476-5551. ; 9:4, s. 743-744
-
Tidskriftsartikel (refereegranskat)abstract
- Cytogenetic studies of Ph-positive leukemic patients and their parents have indicated that chromosome 22 involved in the formation of the t(9;22) is of maternal origin, whereas chromosome 9 is preferentially of paternal origin. These data have suggested that the two genes BCR and ABL, which become fused through the translocation, might be imprinted, ie expressed in a parental-specific manner. Recent molecular genetic studies however, have shown that BCR and ABL are expressed on both alleles and that the maternal and paternal ABL genes contribute equally often to the BCR-ABL fusion messenger. The findings make imprinting of these genes unlikely as an explanatory model and necessitate a combined cytogenetic and molecular genetic study.
|
|
| 4. |
|
|
