Clarice Stumpf | January 26, 2026

Cancer is one of the leading causes of death worldwide, and scientists spend millions of hours and dollars trying to understand it. But if we’ve been researching cancer for so long, why don’t we have a “cure”? 

To answer that, we need to take a step back and talk about what cancer actually is.

What is cancer? A quick explanation

Your body is made up of trillions of cells, and they follow some strict rules: grow when you’re told to grow, stop when you’re told to stop. 

Cancer happens when some cells decide to ignore all those signals. They divide and divide, piling up into a mass called a tumor (Fig 1). 

Figure 1. Photo of breast cancer cell growth. (Source: National Cancer Institute.)

Some tumors stay put. These are benign tumors. This is like a sick person quarantining by themselves; they’re sick, but they won’t get anyone else sick.

Other tumors are malignant, meaning the cancer cells move through the body. They do this through the lymphatic network, a series of vessels that run throughout your body and act as a transportation system. Once cancer cells get into these channels, they can move anywhere and set up new tumors in distant organs. [1] 

Think of a malignant tumor as a sick person visiting a crowded shopping mall, they can spread illness far and fast. As the tumor cells spread around the body, they are able to set up shop and grow new tumors which worsens the condition of the patient. 

A stage 1 cancer means the tumor cells are confined to one place, by stage 4, the cancer has spread widely and has grown in multiple places. The stages measure the spread of cancer cells throughout the body. [1] The more cancer spreads, the harder it is to treat. 

The different kinds of cancer 

You’ve probably heard people talk about lung cancer, breast cancer, prostate cancer, and dozens of others. These aren’t just different locations, they’re completely different diseases that happen to share one behavior: uncontrolled cell growth. 

A lung cell that becomes cancerous behaves differently from a breast cell that becomes cancerous. These cancers rely on distinct signaling pathways, accumulate different mutations, and often respond to treatments in different ways. A signaling pathway allows a cell to receive a command from the body. You can think of it like a baseball and a glove. The pathway throws a ball or signal which the cell receives with its glove or “receptor.” However, cells have completely different shaped receptors meant to catch different balls. [2,3,4] 

Because receptors recognize completely different molecules, a drug that works for one cancer may be useless for another. Scientists aren’t curing one disease; they’re researching a whole bunch of slightly different diseases. 

Even within one type of cancer, two people’s tumors can behave differently. One person’s breast cancer might respond well to a drug, while another person’s barely reacts. That’s because cancer is shaped by your genetics, your environment, random chance, and the specific mutations the tumor picks up along the way. [1] 

So why can’t we cure cancer? 

Part of the answer is that “cancer” isn’t a single disease, it’s an umbrella term for hundreds of slightly different, but related diseases. But there’s another challenge that’s just as important: Cancer cells are not foreign invaders. They’re your own cells gone rogue. This is what makes cancer uniquely difficult. When you’re fighting a virus or a bacteria, your body can recognize it as “not self.” Antibiotics or antivirals can attack the invader without harming most healthy cells. 

But with cancer cells? They started as normal human cells. They still look mostly like normal cells. They use the same nutrients, the same pathways, the same signals. They simply grow when they’re not supposed to. Because they’re so similar to healthy cells, it’s very hard to create a treatment that only kills the cancer and leaves everything else untouched. [1]

That’s why treatments like chemotherapy have side effects. Chemotherapy works by targeting fast-growing cells. Cancer cells grow fast, but so do some healthy cells, such as: hair-producing cells, stomach cells in the digestive lining, and bone marrow cells that make blood. Chemo can’t distinguish between normal and cancerous, so it will affect both. That’s why people can lose their hair, feel sick, or become tired and immunocompromised during treatment. [5] 

Modern treatments like targeted therapy and immunotherapy try to focus on specific weaknesses or traits that are unique to cancer cells. However, these traits differ not only between cancer types, but sometimes even between individual cells within the same tumor. For example, about 20% of breast cancer cells rely on HER2 receptors for growth signaling. Drugs like Herceptin and Perjeta target the HER2 receptor. They are monoclonal antibodies that work via a lock and key system. They bind very specifically to the HER2 receptor, which blocks growth signals the cell needs to survive and flag it for attack by the immune system. [6] However these treatments will not work on the 80% of cancer cells that do not overexpress HER2. Those cancers require alternate treatments with their own targets. You can see why this is so difficult. 

The real challenge isn’t destroying cancer cells. It’s destroying only cancer cells. 

If we could flip a switch and remove every cancer cell without hurting healthy tissue, cancer would be easy to cure. The difficulty lies in finding a way to precisely target something that is, in so many ways, still part of the body. 

Although we haven’t found a universal cure for cancer, recent decades have brought huge improvements in cancer treatment. Advances in cancer detection mean tumors are caught much earlier, when they are still localized and can often be removed surgically without the need for additional treatment. [7] Doctors have begun using “personalized” treatments, in which a patient’s DNA and tumor genetics are analyzed to predict which therapies will be most effective. [8] Targeted treatments such as the monoclonal antibodies Herceptin and Perjeta were developed only within the past few decades. [6] As research continues to advance, cancer survival rates continue to improve alongside it. 

References: 

1. Cooper GM. The Cell: A Molecular Approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000. The Development and Causes of Cancer. Available from: https://www.ncbi.nlm.nih.gov/books/NBK9963/ 

2. Nature Education. (2010). Cell Signaling | Learn Science at Scitable. Nature.com. https://www.nature.com/scitable/topicpage/cell-signaling-14047077/

3. Choudhary, N., Bawari, S., Burcher, J. T., Sinha, D., Tewari, D., & Bishayee, A. (2023). Targeting Cell Signaling Pathways in Lung Cancer by Bioactive Phytocompounds. Cancers, 15(15), 3980. https://doi.org/10.3390/cancers15153980 

4. Ortega, M. A., Fraile-Martínez, O., Asúnsolo, Á., Buján, J., García-Honduvilla, N., & Coca, S. (2020). Signal Transduction Pathways in Breast Cancer: The Important Role of PI3K/Akt/mTOR. Journal of oncology, 2020, 9258396. 

https://doi.org/10.1155/2020/9258396

5. Amjad MT, Chidharla A, Kasi A. Cancer Chemotherapy. [Updated 2023 Feb 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK564367/ 

6. Stanowicka-Grada, M., & Senkus, E. (2023). Anti-HER2 Drugs for the Treatment of Advanced HER2 Positive Breast Cancer. Current treatment options in oncology, 24(11), 1633–1650. https://doi.org/10.1007/s11864-023-01137-5

7. Madar, S., Amor, R. E., Furman-Assaf, S., & Friedman, E. (2025). Innovative Approaches to Early Detection of Cancer-Transforming Screening for Breast, Lung, and Hard-to-Screen Cancers. Cancers, 17(11), 1867. https://doi.org/10.3390/cancers17111867

8. Hoeben, A., Joosten, E. A. J., & van den Beuken-van Everdingen, M. H. J. (2021). Personalized Medicine: Recent Progress in Cancer Therapy. Cancers, 13(2), 242. https://doi.org/10.3390/cancers13020242