Cancer Research Center.
Cancer Research Center.

Cancer Research Center.



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Deubiquitinating enzyme regulating hepatitis, fibrosis and cancer

On June 12, Cancer Cell magazine reported that deubiquitinating enzyme, inactivation of cylindrical matosis (CYLD) tumor suppressor can lead to liver cell apoptosis, inflammation, fibrosis and cancer. Cylindrical matosis (CYLD) tumor suppressor can inhibite activation pathway of NFκB and mitotic mitogen-activated protein kinase (MAPK) by deubiquitination upstream factor. This study shows that , liver-specific blocking of CYLD triggered the death of liver cells ,which is around the hepatic portal vein area ,by spontaneous or chronic activation of TGF-β activated kinase 1 (TAK1) and c-Jun N-terminal kinase (JNK). Subsequently, the hepatic stellate cells and Kupper cells is activated, thus contributing to the progressive liver fibrosis, inflammation and production of tumor necrosis factor (TNF), and lead hepatocyte apoptosis toward venous central .At a later stage, compensatory proliferation leads to the generation of the cancerous center. The cancerous center re-express -specific genes of carcinoembryonic liver cells and stem cell typically. These results confirm that the CYLD as an important liver cell homeostasis regulator in the liver, , can protect cells from harm of spontaneous apoptosis,by the prevention of TAK1 and JNK activation that is not controlled.
28.7.12 07:52


Telomere damage mediated formation of the tetraploid and then precipitate cancerous

On June 12, Cancer Cell magazine reported on the latest research about the relationship among telomere imbalance , abnormal karyotype cells and tumors . Tumor cells with Subtetraploid karyotype originated from tetraploid precursor cells ,but the cause of tetraploid’s formation is not clear. Previously, research has shown that replication in the mouse nucleus is adjoint with persistent telomere dysfunction and genome-wide DNA damage. A study found that, when telomere in human adult fibroblasts and breast epithelial cells is in crisis, there will be replication in nuclear and mitosis disorders. The researchers also found that p53 and Rb can inhibit the tetraploid formation. Using inducible system to cause telomere’s short-term damage, the researchers found that telomere-driven formation of tetraploid enhance the formation of cancerous transformation of mouse cells. Genetic caused tumor, is similar to human solid tumors, can develop to the sub-tetraploid karyotype. These data confirm that the particularly short telomeres induced telomere-driven formation of tetraploid. It has the potential to promote tumorigenesis in early cancerous damage.
28.7.12 07:26

How to study Cell cycle progression

As all we know the cell cycle goes through interphase(which is divided into G1,S and G2 stage) and M phase.But How can we tell what stage a cell has reached in the cell cycle? We have several methods make sure which stage the cells are in.To begin with, Observation with a mcroscope may be called to your mind.Before observation,we have to lable the cells to be detected.during cell culture,with certain reagent,such as BrdU. For example,BrdU-labled epithelia cells of the zebrafish gut is become golden yellow ,which indicates the cells are in S phase. BrdU-labled RKO cells may become purple,which imply that the purple cells is in S phase too.Secondly,we can use the method of fluorescent-activated cell sorter(FACS) to measure the DNA content with a flow cytometer.The relative amount DNA in per cell may tell us that the cells are in a certain stage.Thirdly,we can use methods of immunology,such as antibody-antigen reaction may be used.
28.7.12 06:52

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