EGFR Blockade Enriches for Lung Cancer Stem–like Cells

Erlotinib can be effective in the treatment of special gene changes in patients with advanced lung cancer, but when the same drugs for the treatment of early stage lung cancer patients, treatment effect was not effective. Recently, published a report in the l Journal Cancer Research, researchers from Ohio State University Cancer Center, it has carried on the analysis to the reasons of the occurrence of the above results.

Oncologists use of erlotinib for epidermal growth factor receptor (Egfr) mutation in patients with lung cancer. Gene mutation which patients are often will accelerate the deterioration, and erlotinib can block the molecular activities of the body excessive. The study revealed, when erlotinib promote tumor atrophy smaller at the same time, the drug also increased invasion tumor therapy. Therefore, termination cancer growth could accelerate, leading to an unknown secondary effect the reason may because by inhibition of EGFR.

Professor David Carbone says, erlotinib blocking EGFR could activate the expression of a sub signal molecule Notch3, the activation of pathways will lead to cancer stem cell development, and accelerate the growth of tumor. This study may explain why clinical erlotinib can make patients with early-stage lung cancer survival rate decreases dramatically.

This study in the use of non small cell lung cancer cell lines was studied to reveal whether the inhibition of EGFR molecules can enhance the activity of the Notch signaling pathway. The results show that once the Notch signal activation, mutant EGFR will direct inhibition of the Notch signal, and the use of erlotinib inhibits EGFR will remove the restrictions on the Notch signal to activate the Notch pathway. This result show that the bidirectional target special role may overcome the negative effects on the body.

The key point of this study are as follows: 1) in two non small cell lung cancer cell lines, erlotinib therapy can be respectively killed 84% and 75% cells, in the survival of the cells, 23% and 70% of all the cells become a stem cell like cells; 2) erlotinib therapy can increase the growth potential of survival of lung cancer cells by activating Notch3 receptors and increase the number of stem cell like cells.

Bacterial infection can cause the body's problems, when the patient often has weakened immune function. But complicates the problem is, given after antibiotic therapy, can reduce or prevent infection, to life in the body mainly in the gut health promoting bacteria produce negative influence. If the microflora balance is broken, can cause harmful bacteria dominated, and antibiotic resistant strains.

In view of this, scientists are more interested in, clear body is how against pathogens, but not eliminate benign bacteria. The researchers believe that to understand this point may lead to new ways to enhance the body's natural defense against bacterial infection ability. Now researchers have identified an unusual mechanism of human body, using its mechanism can sense the presence of pathogenic bacteria and destroy them. Its mechanism is not the direct detection of microorganism, but each cell can monitor interference with mitochondrial bacteria.

Some intestinal bacteria causing mitochondrial dysfunction may contribute to infection. MSK cell biologist Cole Haynes said: as a response to the perceived some time when cells mitochondria function is disturbed, they open the promoter on bacterial attack. Haynes explained that this mechanism may have evolved to enable cells to detect harmful bacteria from the beneficial bacteria.

The Haynes team is the main research stress response; stress response is a natural mechanism of cell protection and maintenance of mitochondria. Mitochondria provide energy, allowing the cells to perform its normal function. Mitochondrial dysfunction seems to play a role in cancer and aging process. In recent years, Dr Haynes and his colleagues have focused on a protein called ATFS-1 protection. When cells are under stress, accumulation of ATFS-1 in the nucleus and the opening of a series of genes that contribute to restoring mitochondrial function. But the researchers found that ATFS-1 also opened related to fight bacterial genes. The researchers assume that maybe this stress response and innate immunity together, help the body to detect disrupted mitochondrial bacteria, and eliminate pathogens.

Numerologist Warda is hooked on OG-L002 fishing, collecting. And lastly her encouragement comes from socializing along with her companions.