Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The expression of tissue factor (TF) in tumors reportedly exacerbates the aggressiveness of several types of cancers. The shedding of TF-containing membrane particles is believed to influence the ability of tumors to expand and metastasize, and these microparticles may also be harmful in the onset of disseminated intravascular coagulation in specific cancers. Furthermore, the intracellular signaling that is elicited after the formation of the TF / coagulation factor VIIa complex at the cell membrane modulates the activity of adhesion molecules and mitogen-activated protein (MAP) kinases. To evaluate whether TF overexpression in tumor cells modulates its shedding and neighboring stromal cells by its catalytic or intracellular activity, TF-GFP (green fluorescent protein) and a tailless form (TFDeltaC-GFP) were stably expressed in the rat Morris hepatoma and human HT1080 fibrosarcoma cell lines. Both TF proteins were efficiently produced by tumor cells and functionally active, and their clotting activity could be blocked by the active site-inhibited factor VIIa (ASIS). TF-expressing tumorigenic cells produced a soluble factor that increased the migration of arterial smooth muscle cells in vitro. This effect was abrogated by ASIS and the PAR-1 receptor antagonist ATAP-2, showing that it is dependent on the proteolytic activity of the TF ligand factor VIIa and the thrombin-activated cell membrane receptor. We propose that TF-containing microparticles that are released in the culture medium by tumor cells influence the migratory behavior of neighboring stromal cells, thus aiding the cancer cell's tumorigenic potential.
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PMID:Tumor cells expressing tissue factor influence the migration of smooth muscle cells in a catalytic activity-dependent way. 1979 20

Aggressive natural killer (NK)-cell leukemia (ANKL) is a very rare oncohematological disease among youngsters in Latin America. Its clinical picture imitates a variety of syndromes and diseases due to its pathophysiology. Its diagnosis is relatively simple due to the prominence of NK malignant cells in peripheral blood and its clinical aggressiveness. In certain circumstances though, the presence of blast NK cells and the natural course of the disease can be so modified by the treatment of one of the imitated diseases, especially when using steroids, that it becomes very difficult to diagnose early in its course. We present a case of a 16-year-old Mexican male who initiated symptoms imitating dengue to severe dengue for which he received steroids, apparently inducing a partial remission; he was then diagnosed as having community acquired pneumonia, then sepsis, septic shock w/disseminated intravascular coagulation, primary hemophagocytic syndrome, severe hepatitis, lupus and finally hyper IgE. It was not until 1 day before dying of hemorrhagic shock, a month after initiating symptoms, when the (re)emergence of blast NK cells in peripheral blood allowed the correct diagnosis to be made. Knowledge of ANKL pathophysiology may raise awareness of this multifaceted malignancy and may open up possibilities for its therapy. Gained knowledge can also be used for guiding NK cell evident aggressiveness against other malignancies.
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PMID:Non-EBV-Related Aggressive NK-Cell Leukemia: An Oncohematological Great Imitator. 3230 Apr 33