Robyn is a biomedical genetics student & healthcare worker. She shares what she learns so that more people can be informed too.
Who is cancer?
How about - a terrifyingly miraculous disease involving cell heterogeneity, manipulation of cellular mechanisms, and the overall hijacking of the human genome.
Intro to… me?
Ugh, hi. You may be wondering - who is this random gal on the internet writing articles about cancer genomics? It me. I am not a doctor or a scientist…. Yet. But I am earning a graduates degree in biomedical genetics and I’ve recently found myself enthralled by the cancer material we’ve been covering. Thus, the creation of this article. So anyways, feel free to read this if you’ve ever wanted to live out your aspiring geneticist dreams…. Or if you’re just curious. That’d be cool, too.
The Emperor of all Maladies?
“Down to their innate molecular core, cancer cells are hyperactive, survival-endowed, scrappy, fecund, inventive copies of ourselves.”
— Siddhartha Mukherjee // Author of “The Emperor of All Maladies: A Biography of Cancer”
Why is cancer tricky?
So this past week I watched the docu-series based on a novel called “The Emperor of All Maladies: A Biography of Cancer.” First of all, 10/10 highly recommend if you yearn to learn something new about cancer.
Second, this series opened my eyes to many facets of cancer I hadn’t considered before, so I was inspired to compile some of what I’ve learned in my genetics classes regarding cancer thus far.
On the surface level, cancer seems like this disease that we should know so much more about by now. I mean, cancer as we know it has plagued our world for millennia, yet despite our best efforts we still haven’t found that magic medication or therapeutic regimen that cures the disease consistently. So, why is that?
The answer is very complex, but I’d like to break it down into some key factors that have been emphasized in the literature.
1) Genome-wide sequencing studies (GWAS) have identified numerous sources of mutations that could contribute to cancer development. Not only that, but additional studies that focus on expression quantitative trait loci (eQTLs) have discovered that it‘s often not only just one gene variation in the human genome that contributes to cancer development, but several. Often, it can be very many genes that have been perfectly mutated to work in sync. It’s crazy, but genes can do that. Although our genetic code theoretically stays the same throughout our life time, certain facets of it can be altered due to a variety of things in our environment. This influential portion of our genome, if you will, is called the epigenome. This is what people talk about when they say things like smoking causes lung cancer. You aren’t born with mutated cells in your lungs, but being a consistent smoker is more likely to induce mutational changes that cause cancer to grow in your lungs.
Didn’t think it could get more complex, huh? Well “hold on to your butts,” as they say in the original Jurassic park film.
2) Recent years of research have unveiled even more complex findings regarding cancer. For example, sometimes its not even our bodily cells that are specifically being affected by genetic mutations, but the cellular mechanisms. This becomes even harder to track, because how do you measure or quantify to what extent a cellular mechanism has been altered? And once you’ve figured that out… to what extent is this mechanistic alteration contributing to the cancer itself? Sometimes scientists think they’ve found an answer, only to realize that the mechanism in which they thought was influencing the cancer growth actually isn’t the primary cause of its growth. To break this down, think of it this way. Our cells are reproducing constantly at a steady rate in an effort to replace damaged cells. Our cells also have mechanisms for repairing themselves in the event that they are injured, but sometimes these repair systems go rogue. If the mechanisms that maintain cellular life become broken, then the cells can essentially start reproducing at an uncontrollable rate. This is how abnormal cells start accumulating in the body and them sometimes once its accumulated enough, it can be spread to other locations of the body via blood or lymphatic fluids. This is how metastasized cancer develops.
So, yeah. Cancer sucks.
“History repeats, but science reverberates.”
— Siddhartha Mukherjee
Now for the identity part
So we’ve established how much cancer sucks. But what do I mean when I say it has its own identify?
So here’s the thing. Cancer is very complex, that is one thing we don’t underestimate. But, we are also very smart. One thing we’ve learned is that cancer tissue tends to be extremely heterogenous, which basically means its composed of a symphony of many different cells, as opposed to the tissue containing only one variety of abnormal cell growth. Although this sounds scary, we are slowly making progress in exploiting this finding. What I mean is, by tracking the variety of cells and genetic mutations across the board and compiling this information into databases for comparison, we are beginning to design algorithms in which targeted treatment therapies can be used based on the cancer’s specific characteristics. Basically, if we can see specifically which cells, cellular mechanisms, or genetic variants are being affected in cancer tissue, then we can use this information to begin tracking which medications or therapeutic regimens would be most successful in treating that cancer.
It’s a novel idea, but its in the making. So yeah, cancer has its own identity containing an array of special factors. But the good part is we are learning how to use this to our advantage.
Cancer remains, for now. But hopefully soon, the day will come to overthrow the emperor.
© 2022 Robyn