Why Is There Still No Cure For Cancer?

Why Is There Still No Cure For Cancer?

Cancer: The sexiest of the diseases.
No, I don’t mean literally, but if anybody says they work in cancer research, you’re almost obligated to reply with a ‘wooow that’s amazing.’ As opposed to renal disease, asthma, or diabetes which get a rather underwhelming ‘oh, that’s cool.’

Over about a century of research, billions of dollars have been poured into finding the cure for cancer, so why don’t we have one? We could make COVID-19 vaccines in less than a year, so why don’t we have a ‘cancer vaccine’? Are scientists just hoarding our hard-earned tax dollars and making sharks with friggin laser beams attached to their friggin heads instead? Hopefully, you’ve picked up on my sarcasm by now, but the answer is unequivocally and unquestionably no.

The unfortunate reality is, cancer is responsible for one in six deaths globally, and is unlike any other disease we know of. It presents in hundreds of different forms, and is incredibly difficult to understand, study, and treat.

So, what is cancer, and what makes a cell cancerous?

Cancer, unlike many other diseases, is not a foreign pathogen invading the body using you as their pawn in the evolutionary war of which superbug will reign supreme. Cancer is actually a mass of our own cells that, for one reason or another, have uncontrolled cell growth and division, inadequate or non-functioning cell death mechanisms, and the ability to rapidly acquire genetic mutations. Amazingly, cancerous cells can mutate so rapidly, that there is more genetic variation between two types of cancers (lung vs kidney, for example), than there are between two people – so much for one disease, one cure, right?

Cell biology, being the wondrously and at times incomprehensibly complicated field, has proven there are countless ways DNA could be damaged or mutated, meaning there are many, many different ways a tumour could form. Being a very individual-specific disease, those DNA mutations could have arisen through a completely different pathway between two people, even though they have the same type of cancer. Oh, also, there are only about 2-5 genes (called oncogenes) that actually make us susceptible to cancer out of the roughly 20,000 that make up the human genome. So if only 0.01% of our genes make us susceptible to cancer, how in the world do we treat or prevent it from happening, and why does it happen so frequently?

Our cells replicate and divide throughout our entire life, and it’s not a perfect process. Mutations accumulate pretty frequently but are often recognised by the cell itself, or by the immune system. If those mutations are harmful, those cells are targeted for destruction (apoptosis), but if they’re harmless, then the cell may continue to function normally. However, when it goes unchecked, that’s when cancer can form.

Thankfully, we know quite a lot about the path from genetic mutation to tumour growth – lung cancer is a great example. A lot of lung cancer-causing mutations are tightly linked to smoking cigarettes, and some of the treatment options can be tailored quite ‘easily’ depending on your smoking history.

Chemotherapy, a form of systemic cancer treatment, is a common treatment method for various types of cancers. By targeting rapidly diving cells, which cancer definitely is, chemo (for the most part) targets cancer cells, leaving the majority of your cells happy and intact. Of course, I say this with a degree of caution, because chemo has plenty of side effects, and often targets other non-cancerous, rapidly diving cells such as hair follicles and germ cells. And that’s the tradeoff with chemotherapy – it’s about finding the right Achilles heel for the right cancer in the right patient.

Another treatment option is to target the protein, that the mutated cancer gene produced. Here’s the theory: If gene X codes for protein X, and protein X prevents the cell from undergoing apoptosis, then perhaps a vaccine targeting and inhibiting protein X will prevent those cells from becoming cancerous. Research is ongoing in this area, and some inhibitors have been found, which are currently undergoing clinical trials.

While oncologists have several treatment options, they are hardly as cancer-specific as we’d like them to be. If we remind ourselves of how rapidly cancers can divide and mutate, they can also move throughout the body (a process known as metastasis; check out this great TED-ed talk on metastasis), which can then change the treatment regime. Once the cancer has moved, from say the ovary to the liver, this may require a different cocktail of chemotherapy and pharmaceuticals to target the new mutations and new form of cancer – cancer precision medicine is cutting edge stuff, and clearly very, very difficult (maybe oncologists do deserve an oh wowww).

While we may be able to stop some cancers from getting out of control once you have it, preventing it from happening in the first place or killing the cancerous cells without killing your own and before it has metastasised is the tricky part.

Have we gotten anywhere?
I’ve been pretty doom and gloom so far, and I apologise. Because it isn’t all doom and gloom, and we’ve learned an extraordinary amount about this extremely complicated, evasive disease. For example, in the past 50 years, breast cancer survival rates have skyrocketed. In 1975, there was a bleak 15-20% survival rate within 5-years of diagnosis, whereas in 2018 it sits closer to 90%, and overall cancer survival in the UK has doubled in 40 years from 25% to 50% – how incredible is science?

This is thanks to the amazing oncologists around the globe studying cancers but also the inherently collaborative nature of research. While cancer can generally be described as a localised disease (unless metastasised), we also need to understand everything we can about the healthy tissues or organs the cancerous cells stem from. This is why oncology overlaps with just about every other biological/medical field there is, and why underlying organ function can significantly influence cancer survival rates.

So, will we ever get a cure?
Here I go being doomy and gloomy again, but it’s very unlikely to be any time soon. Technically, we’ve only cured (eradicated completely) two diseases, and both are the result of vaccine development (smallpox and rinderpest).

Cancer researchers have picked a very difficult career filled with experimental and clinical strife. However, scientists have a remarkable ability to stay resolved and committed to their research, even in times of hardship. And, as I said earlier, science is inherently collaborative and the solutions to our problems may not be in the most obvious of places.

For example, have you heard of Peto’s paradox? Essentially, as larger animals have more cells than smaller ones, they should be much more prone to cancer than smaller animals. Makes sense, right? More cells, higher probability of genetic mutations, higher probability of cancer.

But, here’s where the paradox comes in. Large animals get cancer far, far less than they ‘should’. In fact, blue whales don’t really seem to get cancer at all…Why? Is the cure for cancer hidden in a blue whale’s stomach? Well, there are two main theories here: Evolution and hypertumours. Put simply, larger animals may have evolved to naturally have a higher number of tumour-suppressive genes, and therefore require more mutations for cancer to develop. They’re not ‘immune’, but it’s just very, very rare.

Now the more sinister-sounding theory, hypertumours, employs a cancer cell’s own mutative speed against them. Over time, some of those cells in the tumour can break away and form their own, genetically distinct tumour, which then competes with the original tumour for resources (the whale). This fight to the death between tumours may ironically leave the whale relatively unscathed, just like how Mr Burns got every disease known to man and was ‘indestructible’. So, in a weird way, the hypertumour situation keeps all the tumours in check, preventing them from getting large enough to be noticeable or troublesome for the animal. After all, a 2g tumour to a mouse is roughly 10% of its body weight, 0.002% of a human, and 0.000002% of a blue whale – see my point?

For a more in-depth, animated version of the Peto’s paradox, I highly recommend checking out a video by Kurzgesagt – In a Nutshell.

So, what have we learned?
Cancer is impressively difficult to kill, extremely virulent, and can come in hundreds of different forms with each requiring its own unique treatment regime.

We’ve come a long way in cancer research, and cancer survival rates have never been so high. But where to next? Are blue whales the ‘next big thing’ in cancer research? Are the tumour-suppresive genes inside a blue whale the key to a cancer cure? The only thing I can say with confidence is wooow, that’s amazing.