Acute leukemia in bcr/abl transgenic mice

Article Abstract:

The Philadelphia chromosome is a chromosomal abnormality where a part of chromosome 9 is translocated, or moved, to chromosome 22 and a part of chromosome 22 is translocated to chromosome 9. The Philadelphia chromosome is seen in patients with certain leukemias such as chronic myelocytic leukemia and acute lymphoblastic leukemia. The oncogene (gene which can cause cancer), known as 'abl', and located on chromosome 9, is moved next to another oncogene, known as 'bcr', on chromosome 22. In patients with acute lymphoblastic leukemia, there are two areas of the chromosomes where the deoxyribose nucleic acid (DNA) breaks and the genes join with the other genes. One area is in a cluster of breakpoints, the other is in a part of the bcr gene. When the DNA breaks in the part of the bcr gene, two genes (bcr and abl) code for a protein which is a combination of two proteins, known as the bcr/abl fusion protein, p190. The fusion protein has abnormal functions, including the addition of phosphate molecules to other molecules and to itself. Transgenic mice were injected with a gene that codes for the bcr/abl p190 fusion protein. The progeny of the mice were either born dead, or died within 10 to 58 days after birth, after developing acute myeloid or lymphoid leukemia. These findings support the theory that the Philadelphia chromosome is involved in the development of leukemia. This animal model for human leukemia, containing the Philadelphia chromosome, will result in a better understanding of the disease and provide further opportunities for testing treatments. (Consumer Summary produced by Reliance Medical Information, Inc.)

Models, Causes of, Lymphocytic leukemia, Genetically modified mice, Acute leukemia, Myeloblastic leukemia, Human chromosome abnormalities

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Parental origin of chromosomes involved in the translocation t(9;22)

Article Abstract:

The translocated chromosome 9 in cases of Philadelphia-chromosome-positive leukemia is inherited paternally whereas the translocated chromosome 22 is inherited maternally. Thus the chromosomes implicated in predisposing people to hematological and other tumors are characterized by genomic marking, which is the identification of some genetic materials as either maternal or paternal in derivation. The finding that genomic marking characterizes some leukemias suggests that imprinting may influence inherited tumor-specific chromosome variations.

Genetic aspects, Human chromosomes, Myeloid leukemia, Philadelphia-positive, Philadelphia-positive myeloid leukemia

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Regulation of focal adhesion-associated protein tyrosine kinase by both cellular adhesion and oncogenic transformation

Article Abstract:

The protein pp120 has the same molecular structure and function as the cell adhesion-associated protein tyrosine kinase pp125FAK. Moreover, pp120's tyrosine phosphorylation is regulated by cell adhesion and the transformation of another protein, pp60V-SPC. These findings regarding pp120's role as a phosphoprotein illuminate how cell adhesion receptors aid in controlling the growth and differentiation of cells and their alteration by oncogenes.

Molecular biology, Cell differentiation, Protein tyrosine kinase, Protein-tyrosine kinase, Phosphorylation, Cell adhesion

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