Researchers have gained new insights into the structure of the killer protein Bax. The protein induces programmed cell death, the method by which the body disposes of cells that are no longer needed or have been pathologically altered. Since Bax is constantly changing its location in the cell, its structure is difficult to investigate. (Mehr in: Cancer News — ScienceDaily)
How does a cytostatic like cisplatin or carboplatin actually get into the cell? Scientists have now succeeded in showing that the volume-regulated anion channel VRAC is 50 % responsible for active substance uptake. If one of the VRAC subunits LRRC8A or LRRC8D is down-regulated, cells take up considerably less of the anti-cancer drug. In addition to this finding, programmed cell death or apoptosis is also significantly disturbed when LRRC8A is missing. The researchers have thus identified a potential cause for therapy resistance, they suggest. (Mehr in: Cancer News — ScienceDaily)
Tübingen researchers have studied the formation of membrane pores that are critical to start the apoptosis program (Mehr in: Pressemitteilungen – idw – Informationsdienst Wissenschaft)
High-grade serous ovarian cancer often responds well to the chemotherapy drug carboplatin, but why it so frequently comes back after treatment has been a medical mystery. Now a team of researchers has discovered that a subset of tumor cells that don’t produce the protein CA125, a biomarker used to test for ovarian cancer, has an enhanced ability to repair their DNA and resist programmed cell death — which allows the cells to evade the drug and live long enough to regrow the original tumor. (Mehr in: Cancer News — ScienceDaily)
Lung cancer researchers have discovered a novel strategy to exploit apoptosis, a form of programmed cell death, for the treatment of lung cancer. The protein Bcl-2 is a known target for cancer treatment since it allows cancer cells to evade cell death via apoptosis. (Mehr in: Cancer News — ScienceDaily)
Cancer is a group of almost 200 diseases that involve variety of changes in cell structure, morphology, and physiology. Cancer phenotype is underlying several alterations in cellular dynamics with three most critical features, which includes self-sufficiency in growth signals and insensitivity to inhibitory signals, evasion of programmed cell death and limitless replicative potential with a potential for the invasion of other organs. Cancer disease is widespread among metazoans. Some properties of cancer cells such as uncontrolled cell proliferation, lack of apoptosis, hypoxia, fermentative metabolism and free cell motility, i.e. metastasis, resemble a prokaryotic lifestyle, which leads to the assumption of a reversal like evolution from eucariotic back to proteobacterial state. This phenotype matches the phenotype of the last universal common ancestor (LUCA) that resulted from the endosymbiosis between archaebacteria and α-proteobacteria, which later became the mitochondria.