Cancer Research Center.
Cancer Research Center.

Cancer Research Center.



   recombinant cd40
   Epitope Mapping
   nextgen sequencing
   organic synthesis
   HUman tissue

  Letztes Feedback
   3.10.12 09:15
    lig6oq fnzdmjowthnc, [u
   3.10.12 15:15
    IUCqym    4.06.13 05:30
Click For Info
   10.08.13 20:50
       13.08.13 06:56
   20.12.13 08:52
    Ich wollte einfach einen

Gratis bloggen bei

The target inflammation precipitating factor prevention and treatment of cancer

August 24, 2012 - / biological Valley BIOON / - Georgia Health Sciences University Cancer Center researchers found a gene that can destroy the liver cancer-related inflammation. Laboratory mice that lack this gene missing promote inflammatory protein TREM-1 makes its own exposure to carcinogens freedom from suffering from liver cancer. The study, published in the Journal of Cancer Research of the American Association for Cancer Research The GHSU Cancer Centre immunologist Dr. Anatolij Horuzsko, said: The study may be beneficial to develop cancer drugs targeting TREM-1. Horuzsko said: We have always thought that chronic inflammation in the initial stage of the cancer is a very powerful tool to promote tumor development or metastatic cancer. We focus on molecules that control the inflammatory response, in order to better understand how this process is to play a catalytic role in the tumor. We found that one important inflammatory trigger TREM-1 receptor. TREM-1 primarily in viral or bacterial infection, such as against the trigger inflammation, and play an important role in the maintenance of normal tissue function. However, Horuzsko research team found that liver function damage caused under normal circumstances, such as abuse of alcohol or other irritants, TREM-1 generation is out of control. TREM-1 leads to the generation of other inflammatory factors resulting in a chronic, low phase of the inflammatory response, which will result in more damage to the cells, causing the cells to mutate. Then these mutant cells will lead to the occurrence of cancer proliferation and growth. Of TREM-1 role in the last 14 months of the study period, Horuzsko and his team used a mouse model of liver cells in mice life is about three years, the length of study time set to imitate the human hepatoma 20 30-year stage. Experimental design the two groups of mice, a group of the TREM-1 knockout, a group of normal, two groups of mice were exposed to a carcinogenic agent diethylnitrosamine, diethyl nitrosamine is present in tobacco smoke chemical substances. Injection of diethylnitrosamine just 48 hours, the control group of mice liver cells damage and death in the Kupffer cells TREM-1 expression at a high level. These particular liver cells destroy bacteria and damaged red blood cells. 8 months later, these mice also appeared in a large area of ​​the liver tumors. However, excluding the TREM-1 gene in mice remain healthy, the symptoms appear very little, if any and subject to eight months time slowly tumor. The only difference between the two groups of Kupffer cells in the existence of TREM-1. Horuzko team hope for TREM-1 results as well as a potential cancer therapeutic strategy can also be applied to other cancers. TREM-1 may be a treatment of inflammation-related cancer target. Horuzsko said: In the future, we can use the targeting TREM-1 drug in the body to treat cancer. Currently we have been working in this direction. The state-of-the-art cancer treatment drugs is a growing field of research, immunotherapy is an important part of cancer treatments. In addition, the Horuzsko the research team also found that another potential drug therapeutic targets that liver cell damage and death of the product of HMGB1. HMGB1 is a previously unknown stimulus Kupffer cells produce the activating ligand of the TREM-1 protein and start the process of inflammation.

24.8.12 10:21
Letzte Einträge: Iatrogenic false aneurysm treatment use ultrasound-guided thrombin injection in during the five years, Enhancement effect function of T cell CD8 from healthy controls and patients with HIV infection is through the activation of thrombin receptor 1 protease activity., Thrombin cracking fragment in malignant osteopontin is overexpressed glial tumors, and provides a molecular niche and survival advantage, Macrophages, epithelial cells of the CCL2 help rhinovirus induced high reactivity and inflammation in a mouse model of air allergic disease., Differential regulation of CD4 + T cell adhesion to the brain microvascular endothelial & # 946; The CCL2 and CCL3 chemokines, Increased urinary CCL2: Cr ratio in 6 months later the renal allograft loss.


bisher 0 Kommentar(e)     TrackBack-URL

E-Mail bei weiteren Kommentaren
Informationen speichern (Cookie)

 Smileys einfügen

Verantwortlich für die Inhalte ist der Autor. Dein kostenloses Blog bei! Datenschutzerklärung