According to studies conducted on mice, certain cancer cells that facilitate the spread of cancer and are responsible for the majority of deaths caused by the illness may possess a fatal weakness. Cancer cells have a dependence on certain fats to fuel their invasion of healthy parts of the body.
What is cancer?
Cancer is simply an abnormal growth of cells. Somatic cells divide in a process called mitosis. Due to a mutation, cells will divide swiftly and unhealthily, and they crowd out healthy, normal cells. Cancer cells continue to grow and make new cells. This makes it extremely difficult for the body to work the way it should. Cancerous cells have the capability to leave their primary site and spread throughout the body. Cancerous cells move and invade other parts of the body and can form lumps. If this happens, the cancer has formed a severe and threatening malignant tumor.
In order for cancer to spread throughout the body, a cancer cell must split from its current location, travel through the bloodstream in a process called metastasis, and dominate another part of the body. Researchers have struggled to interpret how and what cells can manage this process.
Scientists identified a population of oral tumor cells that are capable of making the journey in mice. These cells may feed on and rely on fats as fuel for their trip. In order to discover this, Salvador Aznar Benitah and his colleagues from the Institute for Research in Biomedicine at the Barcelona Institute of Science and Technology, located in Spain, examined oral cancer cells in mice for those that could trigger tumors. Some of the cells contained high levels of the molecule CD36. This molecule is responsible for assisting cells in taking lipids from their environment.
Because lipids compactly store energy, tumor cells can use them as an energy source. As metastasis requires a lot of energy, the tumor cells may depend on lipids for energy. This phenomenon makes sense since cells learn to adapt to their environment.
Why is this important?
Researcher Benitah and his team found that high CD36 content was essential for metastasis in mice. There are antibodies that work against CD36. These antibodies completely prevented metastasis by eliminating the cancer cell’s interaction with the fatty acids in lipids, thus taking away their energy source. However, these antibodies had no beneficial effect on the development of primary tumors, where the cancer begins to grow.
Not surprisingly, the scientists found that high levels of the CD36 molecule were related to poor final results for those affected by bladder, lung, breast, etc. cancer. Due to the antibodies’ vital role in inhibiting metastasis in mice, Salvador Aznah Benitah’s team continue to try to develop antibodies that can stop the harmful, sometimes fatal, effect of CD36 in cancer patients. Over at least four more years, Benitah approximates, the antibodies will be put to use in clinical trials. As mentioned earlier, the antibodies were only advantageous once the cancer was trying to spread. So, the antibody therapy would only be efficacious when metastasis is on the verge of starting and spreading cancer to other parts of the body. The experimental antibodies Benitah and his peers created effaced metastatic tumours, or tumors formed due to metastasis, 15% of the time. The other metastatic tumours went through a size reduction of at least 80%.
In addition, the team is examining the effect of a high-fat diet on the tumor growth in mice. According to the data collected, providing the mice with a high-fat diet led to additional growth and larger tumors in the lymph nodes and lungs, a sign of metastasis, in comparison with mice on normal diets.
Benitah’s team continues to further their research process by conducting a study that will inspect 1,000 people with cancer, profiling lipids in their blood to search for any links to the pervasiveness of cancer cells. Because this study is still very new, it is too early to tell cancer patients to avoid fatty foods, as cancer patients generally need high-energy diets, which include fats.
Ashna Kumar ’20
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