Cancer is a disease that many people think they understand, but its true nature is complex and often misunderstood. By exploring some frequently asked questions about cancer’s origins, risk factors, and behavior, we can shed some light on cancer’s true colors.
What causes cancer?
Cancer is caused by changes or mutations in our DNA that allow cells to grow and divide uncontrollably. These changes can be inherited or acquired over our lifetime. Many factors can contribute to the DNA mutations that lead to cancer, including tobacco use, excessive sun exposure, radiation exposure, chemicals, and infectious diseases.
Cancer-causing mutations affect genes involved in cell growth and division or those that help cells live longer. As cells accumulate more mutations over time, they are more likely to evade normal growth controls and become cancerous. However, cancer is a multi-step process – no single mutation can cause cancer alone.
What are the main types of cancer?
There are over 100 different known cancers that are characterized based on the type of cell they originate from. The main cancer types are:
- Carcinoma – cancer that begins in epithelial cells that line or cover internal and external surfaces of the body
- Sarcoma – cancer that originates in connective tissue like bones, muscles, and fat cells
- Leukemia – cancer of the body’s blood-forming tissues, including bone marrow
- Lymphoma and Myeloma – cancers that begin in the cells of the immune system
- Central nervous system cancers – cancers that begin in tissues of the brain and spinal cord
Some of the most common cancers are breast, lung, prostate, colon, skin melanoma, lymphoma, leukemia, and cancers of the pancreas, thyroid, kidney, liver, and bladder.
What causes cancer cells to spread?
Cancer cells can spread from their original site to other parts of the body through a process called metastasis. This occurs when cancer cells break away from the primary tumor, enter the bloodstream or lymphatic system, and establish new tumors elsewhere in the body.
Several cellular changes enable metastasis, including:
- Increased motility – cancer cells can move on their own due to cytoskeleton changes
- Invasiveness – cancer cells can degrade proteins and push through extracellular matrix and tissues
- Change in cellular adhesion – cancer cells lose connections to adjacent cells and can break off from the tumor
- Entry into blood vessels – cancer cells can enter capillaries by passing through vessel walls
Once cancer spreads, it becomes much more difficult to treat. Detecting metastasis early and understanding what enables it to occur are important areas of cancer research.
Do all cancers form solid tumors?
No, not all cancers form solid tumors or masses. Cancers like leukemia involve cancerous cells circulating through the bloodstream while cancers like lymphoma involve tumors that form from lymph nodes or other lymphatic tissue. Myeloma involves cancerous plasma cells collecting in the bone marrow.
Solid tumor cancers, also called carcinomas, are characterized by clustered cancer cells that form an abnormal mass. Breast, prostate, lung, and colon cancer are some of the most common solid tumor cancers. These cancers usually form tumors in the organs or tissues where the cancer began.
Both solid tumors and blood cancers are dangerous, but solid tumors present some unique challenges. As they grow, they take up space which can press on organs, nerves, and vessels. Solid tumors also have distinct regions that complicate treatment – areas with poor blood flow or necrotic centers with dead cells.
What allows cancer cells to evade the immune system?
Cancer cells employ several methods to avoid detection and attack by immune cells that would normally seek out and destroy aberrant cells:
- Reduced antigen expression – Cancer cells have fewer molecular markers that identify them as abnormal
- Resisting cell death – Cancer cells avoid apoptosis and programmed cell death mechanisms
- Immune suppressing signals – Cancer cells release cytokines that inhibit immune cells in the tumor environment
- Evading recognition – Cancer cells downregulate major histocompatibility receptors needed for an immune response
- Adaptation – Cancer cells can stop expressing targeted antigens or become insensitive to immune attacks over time
Understanding how cancers bypass immune surveillance is an important area of focus for immunotherapy development, where researchers aim to artificially boost patients’ immune defenses against cancer.
How do cancer cells differ from healthy cells?
Cancer cells differ from healthy cells in several key ways:
| Healthy Cells | Cancer Cells |
|---|---|
| Regulated cell growth and division | Uncontrolled cell growth and division |
| Programmed cell death capability | Resist cell death |
| Differentiated, specialized cells | Loss of cell specialization |
| organized cell structure | Disorganized cell structure |
| Respond to signals to stop dividing | Ignore or self-generate growth signals |
| Stable genome | Genome instability and mutations |
| Normal metabolism | Altered metabolism |
Learning more about the unique attributes of cancer cells continues to reveal new molecular targets for potential cancer treatments.
Do all cancers progress the same way?
No, cancers do not necessarily progress in the same linear fashion. Cancer growth and progression depends on factors like:
- Cancer type and site of origin
- Number and types of mutations
- Age, health, and genetics of the patient
- Whether the cancer is driven by hormones or is a result of inflammation
- If the patient has a compromised immune system
- Whether the cancer cells remain at the primary site or have metastasized
While some cancers follow a more predictable path of progression, many demonstrate a lot of variability. Cancers are extremely complex diseases. Even tumors of the same diagnostic classification can exhibit different risk factors, molecular profiles, behaviors, and responses to treatment from one patient to the next.
What allows some cancers to grow resistant to treatment?
Cancer cells are genetically unstable and prone to mutations, which enables some cancers to eventually resist treatments that they were initially sensitive to. Common resistance mechanisms include:
- Target mutation – Cancer cells mutate the specific proteins targeted by a drug
- Altering signaling pathways – Cancer cells activate alternate cell growth pathways not impacted by the drug
- Drug metabolism changes – Cancer cells increase expulsion of drugs through efflux pumps
- DNA repair – Cancer cells adapt to overcome drug-induced DNA damage
- Growth signaling self-sufficiency – Cancer cells switch to growth signal independence
- Anti-cell death blocking – Cancer cells disrupt apoptotic cell death mechanisms
Combination therapies and new drugs that hit multiple targets or work through diverse mechanisms are strategies to combat treatment resistance in cancers.
How do cancers form blood vessels?
Cancers need to form new blood vessels in order to grow beyond a certain size, obtain oxygen and nutrients, and metastasize. This process is called angiogenesis. Cancer cells recruit surrounding blood vessels via signaling proteins that induce vessel growth toward and into tumors.
Proteins involved in tumor angiogenesis include:
- Vascular endothelial growth factor (VEGF) – stimulates new vessel growth
- Fibroblast growth factor (FGF) – helps new blood vessels form
- Platelet-derived growth factor (PDGF) – recruits connective tissue and smooth muscle cells to help vessel walls
- Transforming growth factor beta (TGF-β) – regulates vessel wall integrity
- Angiopoietins – guide maturation and stability of vessels
Anti-angiogenesis therapeutics that block these signals are an effective treatment approach for some cancers. Disrupting the blood supply to tumors helps limit cancer progression.
What allows cancer cells to live indefinitely?
Normal cells have a finite lifespan, after which they stop dividing through a process called senescence. Cancer cells acquire mutations that allow them to continue replicating indefinitely without entering senescence. Common alterations include:
- Overexpression of telomerase – maintains protective telomeres on chromosome ends
- Evading growth suppressors – disables proteins that inhibit cell proliferation
- Activating oncogenes – mutations causing constant growth signal production
- Disabling cell death pathways – blocks programmed cell death mechanisms
- Altering cell metabolism – less sensitivity to antigrowth signals triggered by oxygen or nutrient deficiency
Understanding how cancer cells escape senescence continues to reveal new potential therapeutic targets and treatments focused on restricting the replicative potential of cancer cells.
Conclusion
Cancer has many complex facets, but exploring questions about its origins, risk factors, progression, and behavior sheds light on cancer’s true colors. While cancers have diverse causes and presentations, the disease ultimately results from an accumulation of mutations that lead to uncontrolled cell growth and division, evasion of cell death, and acquisition of invasive and metastatic potential. Ongoing research to unravel cancer’s complexity continues to reveal new molecular targets for therapies and preventive interventions.
