Autophagy in Pancreatic Cancer

Pancreatic adenocarcinoma (PDAC) is a devastating disease with an extremely poor life expectancy and no effective treatment. Autophagy is a process of degradation of cytoplasmic component capable of recycling cellular components or eliminate specific targets. The presence of autophagy in PDAC has been demonstrated. However, the implicated cellular pathways are not fully understood and, more importantly, the role of autophagy in PDAC is matter of intensive debate. This review summarizes recently published data in an attempt to clarify the importance of autophagy in this disease and try to reconcile apparently contradictory results.

Incorporation of Protease K into Larval Insect Membrane Vesicles Does Not Result in Disruption of Integrity or Function of the Pore-Forming Bacillus thuringiensisδ-Endotoxin

ABSTRACT Bacillus thuringiensis δ-endotoxins insert into the brush border membranes of insect larval cells to form ion channels. A possible interaction of these toxins with a cytoplasmic component was examined by preloading vesicles from insect larval cells with protease K followed by incubation with toxin. There was no evidence for toxin antigens smaller than the intact toxin in extracts of solubilized vesicles, nor was there an effect of the inclusion of protease K on either of two functional properties, the formation of toxin aggregates or of ion pores. These toxins, physically and functionally, appear to be confined to the membrane.

Staining of the Midbody by an Anti-digoxin-specific Antibody

Using RNA in situ hybridization to reveal cytoplasmic localization patterns of mRNAs in cultured cells, we noted unexpected staining of a cytoplasmic component in telophase cells. Control experiments revealed that the anti-digoxin-specific antibody was responsible for this staining. Because the staining was observed only at a position where both daughter cells are still connected, we identified the stained component as the midbody. This was confirmed by double staining of cells with anti-digoxin and antia -tubulin antibodies. We concluded that anti-digoxin-specific antibody shows crossreactivity with a component present in the midbody.