A Novel Stem Cell Therapy Is Up To Good For Adamant Cancer Cells
Every one of us knows what functions does our immune system offer to our bodies. It builds a sturdy defensive mechanism against all the foreign intruders, making us immune to a wide range of diseases. Not only does it protect us from a common cough and cold, but it has a huge potential to restrict the glares of some forms of cancers in our bodies too.
How The Immune System Works?
The immune system works as a warrior as it offers the first line of defense for us. The key component of the immune system is a white blood cell, otherwise known as a macrophage. It is for the macrophage, we are protected round the clock as it keeps strolling around our various systems and combating those wicked, infected and cancerous cells.
Why Cancer Cells Become So Aggressive?
Have you ever thought if that white blood cell works round the clock in our bodies, how do we fall victims to those hard-to-treat cancer cells?
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That’s because cancer cells have a protein called ‘CD47’ on their surfaces, while a protein called SIRPalpha binding to macrophages works in alliance with ‘CD47’ protein. The combination of these proteins helps cancer cells to avoid the clutches of the macrophages by emitting a signal ‘don’t eat me’, and thus, cancer cells escape their engulfing grasp.
However, this unique ability of cancer cells can be outperformed by a novel stem cell therapy designed by scientists at the Stanford University. Researchers Irv Weismann and his associate Ravi Majeti developed the new stem cell therapy through a preclinical development trial using funds from the California Institute of Regenerative Medicine (CIRM) and Forty Seven Inc. The clinical trials backed by the Stanford University raise hopes to deactivate the performance of CD47 and develop new therapies for acute myeloid leukemia (AML), solid tumors and also colon cancers.
How The Therapy Appear To Be Affective On CD47?
The stem cell therapy consisting of the two monoclonal antibodies such as 5F9 and Rituximab can bind to the surface of CD47 and SIRPalpha and deactivates the signal “don’t eat me” from cancerous stem cells. Therefore, cancer cells can no longer exert their functions to impact the immune system. Interestingly, the cancer cells are infused with cancer stem cells, and therefore they can proliferate at a faster rate and cause tumor relapses.
The Results Of The Therapy
The therapy along with antibodies and Rituximab resulted in a drop of remission by 50% for patients with relapse in the clinical trials. The trials are still underway, but it is hard to say that this therapy offers a greater efficacy to kill cancer cells by blocking CD47 protein signal only.
Scientists found that blocking the action of CD47 is not everything to make macrophage fight aggressive cancer cells. Despite macrophages killing cancer stem cells, some stubborn cancer cells can easily cloak themselves and remain active in the body.
Even though ‘don’t eat me’ signal is turned off, the cancer cells seem to follow some other signal to survive.
And therefore, the high levels of MHI or Major Histocompatibility Complex class I became an essential tool for the detection of cancer cells’ resistance to macrophages. It guides another immune system in the body to detect the happenings in the body. When the cells of another immune system like T and B cells find something disturbing, they can destroy them.
However, MHI class I protein binds to a protein known as LILRB1 on macrophages and protect cancer cells by triggering ‘don’t eat me’ signal. Thereby, when either of the functions of MHI Class I or LILRB1’s signals is turned off, the macrophages get their strength back and fight cancer cells all over again. The entire observation was carried out in a petri dish or an animal model.
The therapy can prove to be effective to fight the stubborn tumor growth and cancer stem cells in the real clinical settings one day. The wait is there only for the clinical trial so that it can get the success on the participants as well.
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