Parkinson’s disease is a neurodegenerative disorder that affects Dopaminergic neurons, which are nerve cells in the brain responsible for producing dopamine. Dopamine functions as a neurotransmitter...
It seems that everyday research comes up with great ideas, facts, and promises that could help the cancer patient. The problem is, we never see it come to pass. Hopefully that will change one day.
As published in an article by Ana Sandoiu and fact checked by Carolyn Robertson, there is now new research that throws a wrench in cancer’s deception plans. They have designed a molecule that is designed to stop cancerous cells from tricking the immune system into sustaining their growth.
There are many sly ways in which Cancer tricks the immune system into sparing it or into boosting its spread. One way is the so-called myeloid cells that are a key weapon in the immune system’s armory. These cells are crucial for the body’s immune response and its adaptive response against many pathogens.
The myeloid cells should attack invaders such as the abnormal cells. The cancerous cells trick the myeloid cells into thinking the cancer cells are actually a part of the body that something has damaged. Then the tumor cells rope the myeloid cells into helping them to divide and grow. They have now found a way to fool cancer’s plans which they have published in the journal Nature Communications. It reveals a novel target for immunotherapy that can stop cancer from recruiting myeloid cells.
Vineet Gupta, Ph.D., is a professor and vice chairperson for research and innovation in the Department of Internal Medicine at Risk Medical College in Chicago, Il, who jointly led the new research with Judith Varner, Ph.D., of the Moores Cancer Center at the University of California in San Diego.
They used two types of genetically modified mice and unraveled the mechanism by which the cancerous cells deceive the immune system. A protein called CD11b usually helped myeloid cells to transform into a sub-type of myeloid cell called M1 macrophages that can stop tumor growth. It revealed that cancerous cells interfere with the activity of CD11b and turned them into M2 macrophages rather than by turning myeloid cells into M1 macrophages. M2 macrophages boost this process instead of suppressing tumor growth by keeping the immune T cells at bay. Therefore, myeloid cells promote tumor growth and suppress the activity of T cells. Drugs that activate T cells can be effective in controlling tumor growth.
They looked for an agent that would enhance the activity of CD11b to stop myeloid cells changing into M2 macrophages. Effects of CD11b was studied in mice and they found transplanted tumors grew faster and larger in mice without the gene for CD11b. The majority of myeloid cells in the tumors were M2 macrophages. Next a molecule called Leukadherin-1 (LA-1) was developed to boost the activity of CD11b, which drastically reduced tumors in the mice having the treatment. The boost in CD11b activity in the mouse with the point mutation mimics the one imparted on CD11b in normal mice with administration of LA-1 and the results were the same. The tumors shrank drastically, meaning that activating CD11b is a valid new drug target in cancer immunotherapy.
The designed molecule LA-1 is a promising drug, but they caution it may take years before it translates into a widely available safe treatment for cancer.
Dr Fredda Branyon