Suppression of tumorigenicity of rat liver epithelial tumor cell lines by a putative human 11p11.2-p12 liver tumor suppressor locus

We have previously identified and mapped a locus within human chromosome 11p11.2-p12 that suppresses the tumorigenic potential of a rat liver tumor cell line (termed GN6TF) which contains well defined chromosomal aberrations involving rat chromosomes 1, 4, 7, and 10. In the present study, we investigated the potential of this human 11p11.2-p12 liver tumor suppressor locus to suppress the tumorigenic potential of two other rat liver tumor cell lines (GN3TG and GP10TA) following microcell-mediated introduction of human chromosome 11. These tumor cell lines are aneuploid and contain chromosomal abnormalities that are similar to the GN6TF tumor line. The tumorigenic potential and other phenotypic characteristics of GN3TG-11neo and GP10TA-11neo microcell hybrid (MCH) cell lines were variable, and dependent upon the status of the introduced human chromosome 11. MCH cell lines that retained the region of 11p11. 2-p12 delineated by microsatellite markers D11S1385 and D11S903 exhibited suppression of tumorigenicity in vivo (decrease in tumorigenicity and/or elongation of latency), whereas, the tumorigenic potential of one MCH line that lacked markers in this region of human 11p11.2-p12, but retained flanking markers, was not changed from that of the parental tumor cell line. The chromosomal interval between microsatellite markers D11S1385 and D11S903 encompasses the previously localized minimal liver tumor suppressor region, suggesting that a common locus is responsible for tumor suppression among the rat liver tumor cell lines examined. The results of the present study have verified the presence of a liver tumor suppressor locus within human 11p11.2-p12, and have identified a substantial number of microsatellite markers that are closely linked to this tumor suppressor region. These chromosomal markers will facilitate positional cloning of candidate genes from this region, and may prove useful for determining the involvement of this locus in the pathogenesis of human liver cancer.     

Density and crystallinity of poly (3-hydroxybutyrate/3-hydroxyvalerate) copolymers

Bacteria can produce a range of optically active copolymers of (R)-3-hydroxybutyrate (HB) and (R)-3-hydroxyvalerate (HV). These copolymers have aroused much scientific interest because of their high crystallinity at all HB ∶ HV compositions which suggests the possibility of inclusion of HB and HV in the same crystal. In this paper we look at the assessment of crystallinity by density measurements taking into account the possible changes in crystal and amorphous densities caused by the rejection or inclusion of HV from the crystallites. The approach developed is applicable to crystallization of copolymers and blends whatever the composition of the crystals and makes a distinction between mass fraction and mole fraction crystallinities for cases where the average molar mass of residues in the crystal and amorphous phases differs. While it is impossible to give values for crystallinity without knowing the degree of inclusion of HV into the crystals it is possible to say that the previous suggestions that the crystallinity remains constant independent of HV content and that there is equal concentration of HV in the crystal and amorphous phases are incompatible with the measured sample densities. We also show that the crystallization temperature is an important factor in the balance between the crystallinity and HV content of crystals.