From David Railton, Medical News Today. Comments from Patrick J. Ward, MD, PhD, co-director of research at OHC, and David M. Waterhouse, MD, MPH, co-director of research at OHC
September 13, 2018
Cancer never rests — and neither do those who have devoted their lives to finding new ways to battle this disease. There are so many exciting new findings being discovered every day in cancer research. Here is a brief summary of some of the most promising cancer research studies worldwide from August 2018.
Stopping cancer in its tracks.
Metastasis occurs when cancer cells break away, traveling through the body and multiplying in new areas. This spreading of cells creates significant challenges for cancer doctors attempting to locate and destroy tumors.
Researchers behind a new study examined a natural process called autophagy, wherein damaged components of metastatic cancer cells are broken down with the help of cellular structures called lysosomes. The scientists tried turning off the activity of the lysosomes. When they did, they found that the cancerous cells couldn’t survive the process of metastasis.
“This is science stopping cancer in its metabolic tracks,” said Patrick J. Ward, MD, PhD, co-director of research at OHC.
Acidity matters.
Making cancer cells more acidic could stop their ability to multiply. This was the conclusion that researchers in the United States and Spain came to after they used a computer model to study the conditions that affect metabolic pathways in cancer cells. The model showed that cancer cells need a more acidic environment to multiply. It also helped identify some enzymes that work better in the more acidic environment to promote cancer.
“This is exciting because new treatments could be developed to target these enzymes and stop cancer growth,” noted David M. Waterhouse, MD, MPH, co-director of research at OHC.
The study paper is now published in the journal, Nature Communications. Study co-author Miquel Duran-Frigola says the work is still very academic but some of the targets identified are ready to be tested.”
And so does protein.
Another recent study investigated the role that Wnt proteins play in cancer development. Wnt proteins control the proliferation of cells.
Researchers already know that a process involving these proteins called Wnt signaling enables cells to divide. When it goes wrong, it can cause malignant cells to divide, resulting in cancer. The researchers found that there are protrusions on cells involved in Wnt signaling, and that the process can be interrupted by preventing protrusions from forming. They believe that new therapies targeting the formation of these protrusions may then be effective against cancer.
Say “good night” to cancer.
Would putting cancer cells “to sleep” work? Apparently so, according to researchers from Australia, who developed a new class of compounds that appear to block the activity of cancer cells.
“This new class of anticancer drugs puts cancer cells into a permanent sleep,” said study author Anne Voss, from the Walter and Eliza Hall Institute in Parkville, Australia. “This new class of compounds stops cancer cells from dividing by switching off their ability to ‘trigger’ the start of the cell cycle. The cells are not dead, but they can no longer divide and multiply.”
There is still a lot of work to be done, but their discovery suggests these drugs could be particularly effective as a type of consolidation therapy to kill any cancer cells that may be left in the body after initial treatment.
What are Sprouty 1 and 2?
Some cancer studies have looked at how the body’s natural defense mechanisms might be improved to fight cancer better. One study, for instance, found that immune cells are more effective at attacking cancerous cells if two key molecules, Spry 1 and Spry 2 (delightfully called “Sprouty 1 and Sprouty 2”), are deleted.
Deleting these genes improved the survivability of CD8 T cells, which are a powerful weapon of the immune system for dealing with cancerous cells. The removal of these genes also allowed the CD8 T cells to “memorize” their cancerous cells, so if the body encounters these cells again in the future, the immune system is quicker and more effective at reacting to them.
“Any time we can provide a treatment that continues to attack future cancer cells, it’s like an added bonus to the treatment,” explained Dr. Ward. “Another emerging treatment, called CAR T-cell therapy, is similar in that T cells are reprogrammed to attack and kill cancers cells, and because they continue to multiply in the patient’s body, they attack new cancer cells.”
Missing the instructions.
Scientists from the University of California, San Diego recently investigated how some genes support cancer development. They discovered that shards of DNA called enhancer RNAs (eRNAs) — which had previously been considered by scientists to have no functional purpose — contain “instructions” for making molecules that help cancer spread. The study found that when eRNAs were depleted, the tumor-promoting genes were less effective.
Causing cancer to self-destruct.
Researchers identified a chemical compound that causes brain cancer to “self-destruct.” The compound cut off the energy supply of malignant cells in mice who had a highly aggressive type of brain cancer called glioblastoma.
Cancerous cells’ energy supply consists of tiny organelles called mitochondria. Scientists found that a compound called KHS101 prevented the mitochondria from turning nutrients into energy, effectively killing the glioblastoma cells.
“The excitement with this study includes the researchers’ discovery that this approach of cutting off the energy supply was effective at treating a number of genetic variations of glioblastoma cells, not just one,” said Dr. Waterhouse.
The authors explained that this step is the first in a long process that could pave the way for drug developers to start investigating the uses of KHS101 and extend people’s lives.
Why are elephants less susceptible to cancer?
Approximately 17 percent of people die from cancer. Interestingly, less than five percent of elephants in captivity die from cancer. This is surprising because they live for an average of 70 years and have roughly 100 times as many cells. Living a long life and having more cells can make cancer more likely to appear. This is due to the fact that each time a cell divides, its DNA is copied, which increases the possibility of errors. As these errors mount up over a long life, cancer is more likely to develop. If we can understand how elephants’ cells outsmart tumors, perhaps we can use that knowledge to help reduce humanity’s odds of cancer.
Now a new study suggests an explanation.
Scientists previously discovered that elephants each have at least 20 copies of a gene called p53 that suppresses tumors, compared with one copy of this gene that humans and most other animals carry. In the new study, researchers found that p53 contains the “pseudogene” LIF6, which has the ability to “come back to life” and reactivate. When it is reactivated, LIF6 ceases to be a pseudogene and starts to attack and kill damaged DNA by starving them of energy, and preventing them from potentially becoming cancerous.
Co-author Juan Manuel Vazquez says large, long-lived animals must have evolved robust mechanisms to either suppress or eliminate cancerous cells in order to live as long as they do and reach their adult sizes. Next, the team plans to investigate LIF6, focusing on exactly how it triggers cell death.
“These studies demonstrate the immeasurable benefits of cancer research,” added Dr. Waterhouse. “Dr. Ward and I and our colleagues at OHC are very active in cancer research because we are witnessing studies and successes that keep putting us another step closer to eradicating cancer. And, let us face it – who doesn’t love elephants?”
OHC is pleased to be able to offer cancer patients access to the newest treatments through its nationally recognized clinical trials program. For a list of open trials, please visit https://ohcare.com/patient-resources/clinical-trials/available-trials/ or call 1-888-649-4800.
