Identification of a transcriptionally inactive p53 mutant by functional analysis of separated alleles in yeasts (FASAY) in a child osteosarcoma tumor: a case report.

Tumor suppressor gene p53 is one of the most specific genetic alterations occurring in osteosarcoma pathogenesis. It is thought to be an early and key step in the tumorigenesis of osteosarcoma. However, whether the p53 status is a marker predictive of response to therapy and a marker of prognostic value remains controversial.

Introduction of a normal retinoblastoma (Rb) gene into Rb-deficient lymphoblastoid cells delays tumorigenicity in immunodefective mice.

Inactivation of the Rb susceptibility gene occurs in various human cancers and has been associated with tumorigenicity. Rb gene is inactivated in 30% of acute leukaemias. The effect of Rb protein expression was assessed in the lymphoblastoid cell line IM-9 defective for Rb protein, after stable transfection with a wild-type Rb gene.

Promoter function of the human glucose-6-phosphate dehydrogenase gene depends on two GC boxes that are cell specifically controlled.

Human glucose-6-phosphate dehydrogenase is expressed in all cells by a housekeeping gene whose regulatory 5'-flanking sequence includes at least nine GC boxes. By transient transfection of HeLa and HepG2 cells with constructs containing glucose-6-phosphate dehydrogenase gene regions linked to a reporter gene, we have now delineated the core promoter and have located upstream stimulatory and inhibitory sequences. By mutational analysis, we demonstrate that the activity of the core promoter requires two out of seven GC boxes.

Discrepancies between histological and physical methods for trace element mapping in the rat brain.

This paper contains a comparison between four experimental methods for the detection of trace metals in biological tissues, e.g. autoradiography, dithizone-, Timm-staining and microPIXE (Particle Induced X-ray Emission).

Autoradiographic demonstration of the copper-accumulating tissues in mice with a defect homologous to Menkes' Kinky Hair disease.

Mutated Brindled mice have a genetic defect homologous to the human disorder Menkes' or Kinky Hair disease. These animals were used to survey the tissues in which copper accumulates as result of this defect. Heterozygous and unaffected animals were i.