A horrified astronaut utters over the radio, “Uh…Houston, we have a problem. Someone just hacked our computers. Now, we are viewing a message that states we must pay a ransom of 20,000 bitcoins or lose our top-20 karaoke playlist! Please advise.” I bet this conversation never occurred during lunar missions from the 60’s and 70’s.
Today, our beloved cell phones carry more computational capacity than the computers used to get men to the moon (NASA, 2017). As we become even more dependent on phones and other computers to help navigate our everyday lives, we become more vulnerable to malicious hackers or malware that can render them useless, or worse, steal valuable data.
Cancer, a biological equivalent to hackers and malware, can overtake our bodies and create such havoc that it disrupts our day-to-day lives or even ends them. As in the computer technology sector, large resources are being poured into figuring out how the hacks occur and how to remedy the situation. Recently in Nature, two articles were published detailing hacking methods used by some cancers that involve taking over how cells normally communicate with one another and control cell fate.
In a typical scenario, cells communicate with one another using proteins that decorate the outer surface of the cell or are excreted (Perrimon, Pitsouli, & Shilo, 2012). These proteins will bind to another protein (known as a receptor) found on the surface of another cell. This binding event triggers a cascade of internal events that can cause a cell to carry out a specific function, such as transforming into a different cell. Pending how the involved proteins have been modified (e.g., by sugars, phosphates or other chemical compounds added to the proteins), the resulting cascade can have very different outcomes. For instance, this type of cellular communication can tell an embryonic cell to become part of a hand, foot, heart, brain, etc.
When cancer hacks the system, normal cell fates are compromised. In lung adenocarcinoma for example, Tammela et al. found that the tumor cells can differentiate into two types (Tammela et al., 2017). One type is a typical tumor cell. The second cell type almost appears like a “normal” cell, but it is producing proteins that can fuel the cancer (think of adding gasoline to a raging fire). In another study, Lim et al. also saw how cancer cells can fuel their own fire (Lim et al., 2017). In small-cell lung cancer, neuroendocrine tumor cells, which produce hormones (messages to other cells) in response to signals received from the nervous system, switch to a different cell type upon activation of a pathway that can suppress tumor growth. These new cancer cells tend to be resistant to chemotherapy, and produce signals that encourage proliferation of the original neuroendocrine tumor cells. In these two studies, the authors suggest that these hacking strategies could be the source for new biomarkers or targets for new therapeutics.
As our understanding of this malicious hacker/malware improves, we can develop better diagnostics or patches (therapeutics) that can protect our most valuable asset, our health. How nice would it be to go to a doctor’s office, take a blood test and learn that we need the anticancer patch v2.0? This is already a reality for our phones and computers. Only time will tell if it becomes reality for the doctor office equivalent. If we can get a person to the moon with technology that fits (in most cases) in our back pocket, then maybe the time is getting closer?
Lim, J. S., Ibaseta, A., Fischer, M. M., Cancilla, B., O'Young, G., Cristea, S., . . . Sage, J. (2017). Intratumoural heterogeneity generated by Notch signalling promotes small-cell lung cancer. Nature, 545(7654), 360-364. doi:10.1038/nature22323
National Aeronautics and Space Administration (NASA). Do-It-Yourself Podcast: Rocket Evolution. Retrieved on June 17, 2017 at https://www.nasa.gov/audience/foreducators/diypodcast/rocket-evolution-index-diy.html
Perrimon, N., Pitsouli, C., & Shilo, B. Z. (2012). Signaling mechanisms controlling cell fate and embryonic patterning. Cold Spring Harb Perspect Biol, 4(8), a005975. doi:10.1101/cshperspect.a005975
Tammela, T., Sanchez-Rivera, F. J., Cetinbas, N. M., Wu, K., Joshi, N. S., Helenius, K., . . . Jacks, T. (2017). A Wnt-producing niche drives proliferative potential and progression in lung adenocarcinoma. Nature, 545(7654), 355-359. doi:10.1038/nature22334