The Food Systems Summit's Failure to Address Corporate Power.

Based on analysis of documentation associated with the UN Food Systems Summit process, we identify three main ways in which the Summit failed to address the problem of corporate power in food systems in a meaningful way. First, the Summit was 'strategically silent' on the problem of corporate power, mentioning the problem only very infrequently and in a way that failed to identify corporations as holding disproportionate power in food systems. Second, it advanced technology and innovation-based solutions that benefit large agrifood companies rather than seeking structural transformation of food systems.

Metastatic conversion of chemically transformed human cells.

A linear model for human cell metastasis has been developed in vitro from chemically transformed normal human cells. The chemically transformed cells are nontumorigenic in nude mice, but can be converted to a tumorigenic phenotype by transfection with a nondirectional cDNA library or antisense cDNA to the ML-1 gene. The primary transfected cell line (TR1T) forms localized, progressively growing tumors in nude mice that do not invade into the surrounding tissue.

Changes in levels of normal ML-1 gene transcripts associated with the conversion of human nontumorigenic to tumorigenic phenotypes.

Evaluation of malignant human tumors in a xenobiotic nude mouse system has demonstrated that not all cells in tumors exhibit the capacity to form progressively growing tumors. However, nontumorigenic cells isolated from human tumors can be converted to a tumorigenic phenotype in nude mice by treatment with chemical carcinogens or by transfection with antisense to tumor suppressor genes. A newly discovered gene, designated ML-1, appears to be associated with tumorigenesis, because an ML-1 antisense cDNA construct, transfected into nontumorigenic, anchorage-independent growth (AIG) cells, was sufficient to convert these cells into a tumorigenic phenotype.

Expression of molecular biomarkers in primary breast tumors implanted into a surrogate host: increased levels of cyclins correlate with tumor progression.

Background: The overexpression or amplification of tumor suppressor and proto-oncogenes are important factors in the progression of breast cancer. Recent attention has focused on the cyclin genes, whose involvement in signal transduction pathways regulate cell cycle progression. The amplification of the cyclins D1 and D3 genes usually leads to loss of normal growth control and is thought to play an important growth regulatory role in tumor development and progression.