Oncology: How Cancer Works
Cancer is not one disease. It is a process. One cell stops obeying the body’s rules and starts dividing on its own. This chapter follows that process from the first mutation to a spreading tumor. You will see how a normal cell turns malignant. You will learn how we tell a harmless lump from a dangerous one, how cancer travels, what sets it off, and how it is graded, staged, and treated.
By the end of this chapter you can
- Explain how a normal cell becomes cancer. Mutated oncogenes and tumor-suppressor genes drive it.
- Compare benign and malignant tumors. Use the -oma, carcinoma, and sarcoma names.
- Describe how cancer invades. Name the routes and common sites of metastasis.
- Name the major carcinogens. Say what p53 and BRCA do.
- Tell grading from staging (TNM). Spot tumor lysis syndrome.
Section 1From a normal cell to cancer
Every cell in your body lives by a simple rule: divide only when you are told to, and stop when the job is done. A healthy cell reads chemical signals from its neighbors. It copies its DNA with care. It checks that copy for errors. Then it either keeps going or quietly retires. Genes control that balance between growing and stopping. When those control genes get damaged, the balance tips. A normal cell can then turn, slowly, into a cancer cell. Cancer is not an invader from outside. It is one of your own cells that has lost its instructions.
The accelerator and the brakes
Think of cell division like driving a car. Two sets of genes keep it under control. Proto-oncogenes are the accelerator. They normally tell the cell when it is time to grow and divide. Tumor-suppressor genes are the brakes. They slow division, fix damaged DNA, or order a broken cell to self-destruct. In a normal cell these two work together. So growth happens only when it should.
Mutations break this system in two different ways. When a proto-oncogene mutates, it becomes an oncogene. That is a stuck accelerator. It screams "grow!" even with no signal. This is a gain of function. Usually only one copy of the gene needs to change. When a tumor-suppressor gene mutates, the brakes fail. This is a loss of function. Here, both copies must usually be knocked out before protection is lost. The famous tumor suppressor p53 is often called the "guardian of the genome." It normally halts a damaged cell and triggers apoptosis, the cell’s self-destruct program. When p53 fails, damaged cells survive and keep dividing.
The multistep journey: how tissue changes over time
Cancer does not appear overnight. Tissue drifts through stages we can recognize as mutations pile up:
- Hyperplasia: too many cells, but they still look normal and stay in order.
- Dysplasia: cells start to look abnormal, with odd shapes, odd sizes, and messy arrangement. This is pre-cancerous, but it can still reverse.
- Carcinoma in situ: cells look fully cancerous, but they stay above the basement membrane. Nothing has spread yet, so cure rates are high.
- Invasive cancer: cells break through the basement membrane into nearby tissue. They can then travel to distant sites (metastasis).
What makes a cancer cell dangerous: the hallmarks
Researchers describe cancer through a set of shared "hallmark" behaviors. Put simply, cancer cells learn to do these things:
- Divide without permission: the stuck accelerator and failed brakes problem. They multiply even when the body signals stop.
- Evade apoptosis: normal cells with broken DNA are told to die. That ordered death is programmed cell death. Cancer cells silence the signal, often by disabling p53. Damaged cells then refuse to die.
- Grow their own blood supply: a process called angiogenesis. Once a tumor grows past roughly 1 to 2 mm, it starves for oxygen. So it releases signals that pull in new blood vessels to feed it. Later those vessels give cancer cells a highway to spread.
Tumor is not the same as cancer
These two get mixed up all the time. A tumor (or neoplasm) is simply a lump. It is an abnormal mass of cells. Cancer means the tumor is malignant: it invades and can spread. A benign tumor, like a lipoma, is a lump that stays put.
| Feature | Benign tumor | Malignant tumor (cancer) |
|---|---|---|
| Growth | Usually slow | Often fast |
| Border | Clear edge, often inside a capsule | Ragged edge, grows into nearby tissue |
| Cell appearance | Looks like normal tissue (well-differentiated) | Odd and disordered (poorly differentiated) |
| Spread (metastasis) | No | Yes, through blood or lymph |
| Danger | Usually harmless unless it presses on something | Deadly if not treated |
Explore the figure below. Watch a cell move from normal, through adaptation, into dysplasia. It is the same stepwise drift described here.
- Proto-oncogenes are the accelerator. Tumor-suppressor genes are the brakes. Cancer needs a stuck accelerator (an oncogene, one hit) and failed brakes (a tumor suppressor, usually two hits).
- Cancer builds in steps: hyperplasia to dysplasia to carcinoma in situ to invasive cancer, as mutations pile up over time.
- Hallmark behaviors: uncontrolled division, evading apoptosis (often by disabling p53), and angiogenesis, which means growing its own blood supply.
- A tumor is any lump. Only a malignant tumor is cancer. What defines it is the power to invade and metastasize.
- Invasion means breaking through the basement membrane. That is the line between contained disease and spreading disease.
Section 2Benign vs malignant
Your body makes new cells all the time. Skin, gut lining, and blood cells are always being replaced. Normally this runs under tight control. Cells divide only when signaled. They mature into a specific job. Then they stop dividing once the tissue is repaired. This maturing process is called differentiation. A well-differentiated cell looks and acts like the tissue it came from. A neoplasm (literally "new growth") is a lump of cells that has escaped normal growth controls. It keeps dividing when it should not. The big clinical question is always the same. Is this growth benign or malignant?
Benign growths: slow, walled-off, and well-behaved
A benign tumor grows slowly and stays put. Because it grows slowly, the tissue around it often has time to build a fibrous capsule. The mass is then encapsulated, so a surgeon can usually shell it out cleanly. Its cells are well-differentiated. That means they still look much like the normal tissue of origin, and they often still do that tissue’s job. Benign tumors do not invade nearby structures. They also do not metastasize, which means spread to distant sites. Under the microscope the cells look orderly. The nuclei are normal in size, and few cells are dividing (a low mitotic rate).
Malignant growths: fast, invasive, and mobile
Malignant tumors (true cancer) behave the opposite way. They grow fast, so they rarely build a tidy capsule. Instead they send out finger-like projections that invade and destroy nearby tissue. That is why the cut surface can look crab-like, which is where the word "cancer" comes from. Their cells are poorly differentiated or undifferentiated. They no longer look like the parent tissue or act like it. Most important, malignant cells can break away. They travel through blood or lymph and seed new tumors elsewhere. That spread is metastasis. It is the feature that makes cancer so dangerous and so hard to cure.
| Feature | Benign | Malignant |
|---|---|---|
| Growth rate | Slow | Fast, often uneven |
| Border | Inside a capsule, clear edge | Invades, edge is unclear |
| Differentiation | Well-differentiated | Poorly differentiated to anaplastic |
| Metastasis | Never | Common |
| Comes back after removal | Rare | Common |
How tumors are named
Naming follows a pattern worth memorizing. The ending -oma usually means a benign tumor, named for the tissue it came from. A lipoma is a benign fat tumor. An adenoma is a benign gland tumor. A leiomyoma is a benign smooth-muscle tumor, which is a uterine "fibroid." Malignant tumors get one of two labels, based on the tissue they came from: carcinomas from epithelial tissue, sarcomas from connective (mesenchymal) tissue. A carcinoma starts in epithelial tissue, which lines skin, glands, and organs. It is by far the most common group, and it includes adenocarcinoma of the colon or breast. A sarcoma starts in connective tissue such as bone (osteosarcoma), cartilage, muscle, or fat. A few dangerous "-oma" names break the rule. Melanoma and lymphoma are malignant, despite the friendly ending.
Differentiation and anaplasia
Pathologists describe cancers by how far the cells have drifted from normal. Grading measures differentiation. A well-differentiated (low-grade) cancer still looks like its tissue of origin. It usually behaves less aggressively. Anaplasia is the far opposite. The cells are so primitive and disordered that they barely look like any tissue. Anaplastic cells show pleomorphism, which means they vary in size and shape. They have large dark nuclei with a high nucleus-to-cytoplasm ratio. They also show many mitoses, some of them abnormal. In general, the less differentiated the cell, the more aggressive the tumor and the worse the outlook.
When "benign" still hurts you
Benign does not always mean harmless. A tumor that would be minor elsewhere can be deadly because of where it sits. A benign meningioma in the skull has nowhere to expand. As it grows it raises intracranial pressure and presses on brain tissue. That brings headaches, seizures, or lost nerve function. A benign adenoma can also make hormones. One example is insulin from a pancreatic tumor, which drives dangerous hypoglycemia, or low blood sugar. A benign mass can also block a hollow organ or press on a vital vessel. Location, hormone release, and pressure drive the risk, not just the label.
Try the dial below. One lump slides from calm to wild, and the growth rate, the capsule, the edge and the cells all move together.
- Benign tumors are slow, encapsulated, well-differentiated, and they stay put. Malignant tumors are fast, invasive, poorly differentiated, and they metastasize.
- Metastasis is the defining danger of malignancy. It is the main reason cancer is hard to cure.
- Naming: -oma usually means benign, carcinoma means malignant epithelial, sarcoma means malignant connective tissue. Watch the exceptions, melanoma and lymphoma.
- Differentiation drives grade. Anaplasia, with primitive, pleomorphic, fast-dividing cells, signals the most aggressive tumors.
- A benign tumor can still be deadly, because of its location, its hormone release, or the pressure it makes. The classic case is a meningioma raising intracranial pressure.
Section 3How cancer grows and spreads
Normally your tissues are beautifully organized. Cells stay in their own neighborhood. A thin, tough sheet called the basement membrane holds them in place. It separates the surface layer (epithelium) from the deeper connective tissue below. Cells also respect their neighbors. They stop dividing when they touch, which is called contact inhibition. They anchor down where they belong. And they call for new blood vessels only when the body truly needs them. Cancer is what happens when a cell breaks every one of these rules at once. So how cancer grows and travels is really the story of a cell that has forgotten how to stay put. Explore it below as we walk through each step.
Local invasion: breaking through the basement membrane
A tumor usually starts as a well-behaved lump. It stays on its own side of the basement membrane. As long as it has not crossed that barrier, we call it carcinoma in situ, which means "in place." This stage is often curable, because nothing has gone anywhere yet. The dangerous turning point is local invasion. Cancer cells release enzymes called matrix metalloproteinases (MMPs). These enzymes digest the basement membrane and the extracellular matrix around it. Once that fence dissolves, the cells lose their normal stickiness. They turn down E-cadherin, the "glue" protein, and crawl into the deeper tissue. This is the moment a cancer becomes invasive. It is also why pathologists care so much whether the basement membrane is intact.
Metastasis: how cancer travels to distant sites
Metastasis is the spread of cancer from the first (primary) tumor to a distant site. It is the single biggest reason cancer becomes life-threatening. There are three main routes.
- Lymphatic spread: cells enter lymph vessels and travel to nearby lymph nodes first. This is the classic route for carcinomas, the epithelial cancers such as breast and colon. It is why lymph nodes are examined. It is also why we biopsy the sentinel lymph node, the first node that drains a tumor, to see whether spread has begun.
- Hematogenous spread: cells invade blood vessels and ride the bloodstream to far-off organs. This is the favored route for sarcomas, the connective-tissue cancers. It explains tumors that show up in distant organs.
- Seeding of body cavities: cells shed off the tumor surface and scatter across a cavity lining. Peritoneal seeding in ovarian cancer is the classic case. This can cause malignant ascites, a fluid buildup in the belly, or fluid around the lungs (pleural effusions).
| Feature | Lymphatic spread | Hematogenous spread |
|---|---|---|
| Typical cancer type | Carcinomas (epithelial) | Sarcomas (connective tissue) |
| First stop | Nearby (regional) lymph nodes | Distant organs |
| Clinical clue | Large, firm nodes | Masses in lung, liver, bone, brain |
| Checked by | Sentinel node biopsy | CT or PET imaging, bone scan |
Where cancer tends to land
Metastases are not random. Cells often lodge in the first capillary bed they reach. Certain organs also make good "soil" for tumor cells to settle in. That idea is called the seed-and-soil hypothesis. The four most common landing sites are lung, liver, bone, and brain. The lung and liver catch a large share of traveling cells, because they work as filters with dense capillary networks. The liver receives portal blood, and the lungs filter all the blood coming back from the veins. Bone metastases are common in breast and prostate cancer. They often cause deep pain, pathologic fractures, and high calcium levels (hypercalcemia). Brain metastases can raise intracranial pressure. That brings headaches, seizures, or new nerve problems.
Angiogenesis: the tumor builds its own supply lines
A clump of cancer cells can only grow to about 1 to 2 mm on its own. After that the cells in the center start to starve. They sit too far from any blood vessel to get oxygen and nutrients by diffusion. To keep growing, the tumor pulls off a striking trick called angiogenesis. It releases chemical signals, above all vascular endothelial growth factor (VEGF). Those signals coax nearby blood vessels to sprout new branches straight into the tumor. This "angiogenic switch" gives the tumor its own supply line for more growth. Sadly, it also gives escaping cells an on-ramp into the bloodstream for metastasis. These new vessels are usually leaky and poorly built. That adds to swelling and makes drug delivery hard to predict. Because VEGF is so central, several cancer drugs block it to try to starve the tumor. Bevacizumab is one of these anti-angiogenic agents.
Now pick a starting cancer and a route out of it. The road decides which organs can light up, and the funnel shows how few traveling cells ever take hold.
- Cancer turns invasive when it uses enzymes (MMPs) to break through the basement membrane. Before that, carcinoma in situ is often curable.
- Metastasis spreads by three routes: lymphatic (typical of carcinomas), hematogenous through the bloodstream (typical of sarcomas), and seeding of body cavities.
- The most common landing sites are lung, liver, bone, and brain. New bone pain in a cancer patient is a red flag for metastasis.
- Angiogenesis, driven by VEGF, lets a tumor recruit its own blood supply and grow past 1 to 2 mm. It also opens a route for cells to escape and spread.
Section 4What causes cancer
Every day your body makes billions of new cells. Old cells wear out, get injured, or reach the end of their life. So a healthy cell divides to make a fresh copy of itself. Normally this process is tightly controlled. Before a cell divides, it copies all of its DNA. Then it pauses at built-in checkpoints to proofread that copy. If the DNA looks damaged, the cell either repairs it or kills itself on purpose. That tidy self-destruct program is called apoptosis. Cancer begins when this careful system breaks down. The cell then divides on its own schedule, ignores the stop signals, and refuses to die.
So the real question is simple. What damages the DNA and the control genes badly enough to let a cell go rogue? Usually it is a slow buildup of mutations, which are permanent changes in the DNA sequence. They hit the specific genes that run the cell cycle.
Carcinogens: the things that damage DNA
A carcinogen is any agent that causes cancer. Most do it by damaging DNA directly. Others push cells to divide so fast that copy errors pile up. They fall into a few broad groups:
- Chemical: the classic example is tobacco smoke, which carries dozens of DNA-damaging compounds. Others include asbestos, benzene, and certain dyes. Many act right where they touch the body, such as asbestos in the lungs and dyes in the bladder. But some, like benzene, are absorbed and cause blood cancers such as leukemia.
- Radiation: ultraviolet (UV) light from the sun damages skin-cell DNA. It drives melanoma and other skin cancers. Ionizing radiation, such as X-rays and radon, does the same thing inside the body.
- Viral and microbial: some infections insert their own genes, and some cause lasting irritation. Know these: HPV (cervical and oropharyngeal cancers), EBV (some lymphomas), hepatitis B and C (liver cancer), HHV-8 (Kaposi sarcoma), and the bacterium H. pylori (stomach cancer). Herpes simplex is not on the list.
Oncogenes and tumor-suppressor genes
Two families of genes normally keep cell division in check, and cancer usually damages both. Think of driving a car. You need a working gas pedal and working brakes.
Proto-oncogenes are the gas pedal. They tell a cell when it is time to grow and divide. When a proto-oncogene mutates and gets stuck in the "on" position, it becomes an oncogene. That oncogene floors the accelerator and drives nonstop division.
Tumor-suppressor genes are the brakes. They slow division, run the DNA proofreading checkpoints, and trigger apoptosis when a cell is too damaged. The most famous one is p53, nicknamed the guardian of the genome. It halts the cell cycle so repair can happen, and it orders apoptosis when repair fails. When p53 is knocked out, damaged cells sail through the checkpoints and pick up even more mutations. The BRCA1 and BRCA2 genes are tumor suppressors too. They help repair broken DNA. So when they fail, breast and ovarian tissue lose a key safety net.
| Feature | Oncogene | Tumor-suppressor gene |
|---|---|---|
| Normal job | Pushes cell growth (gas pedal) | Holds growth back, repairs DNA, triggers apoptosis (brakes) |
| Effect of mutation | Gain of function, stuck ON | Loss of function, brakes fail |
| Copies needed to cause trouble | Usually one mutated copy is enough | Usually both copies must be lost |
| Examples | Mutated RAS, HER2 | p53, BRCA1/2, RB |
Inherited vs acquired mutations, and why some cancers run in families
Most cancers come from acquired (somatic) mutations. This is damage that builds up in one person’s cells over a lifetime. It comes from carcinogens, random copying errors, and aging. These changes are not passed to children. That is why most cancers are sporadic.
A smaller group involves inherited (germline) mutations. These sit in every cell from birth, because they came from a parent’s egg or sperm. Say someone inherits one broken copy of a tumor-suppressor gene like BRCA1. They only need to lose the second copy for that safety net to fail. They are already halfway there. That head start is why these cancers show up earlier in life. They also often appear in both breasts, or in several family members. This is the mechanism behind family patterns, and the basis for genetic counseling.
Chronic inflammation and failed immune surveillance
Two background factors quietly raise the odds. First, chronic inflammation keeps tissue in a constant cycle of injury and repair. Long-standing hepatitis, H. pylori gastritis, and inflammatory bowel disease all do this. Every extra round of division is another chance for a mutation to slip in. Second, your immune system normally patrols for abnormal cells and destroys them. That process is called immune surveillance. Cancer cells that learn to hide from these patrols, or to wear them out, escape destruction. This is why patients on immune-suppressing drugs often have higher cancer rates.
Stack exposures in the model below and drag the age. Watch the gene board fill as hits add up, and watch the odds curve bend away from the clean one.
- Cancer starts when DNA damage disables the normal controls on cell division. The cell can then divide without limit and dodge apoptosis.
- Carcinogens cause cancer mostly by damaging DNA. They are chemical (tobacco), radiation (UV), and viral or microbial (HPV, EBV, hepatitis B and C, HHV-8, H. pylori). Many are preventable through vaccines and lifestyle.
- Oncogenes are a stuck gas pedal (gain of function). Tumor suppressors like p53 (guardian of the genome) and BRCA1/2 are failed brakes (loss of function).
- Most mutations are acquired over a lifetime. Inherited germline mutations give a head start toward cancer, which explains earlier onset and family clusters.
- Chronic inflammation and failed immune surveillance also play a part. They let mutated cells pile up and escape destruction.
Section 5Grading, staging & living with cancer
Your cells normally follow strict rules. They divide only when told to. They mature into a specific job, such as a skin cell or a colon cell. And they stay in their own neighborhood. Cancer breaks all three rules. The cells divide without permission, they fail to mature, and they invade and travel. Once a tumor exists, the care team asks two early questions. How odd do these cells look under the microscope? And how far has this spread? Those are two different questions. Mixing them up is one of the most common mistakes.
Grading vs staging
Grading is about appearance. A pathologist looks at the tumor cells and asks how much they still look like the normal tissue they came from. Well-differentiated (low-grade) cells still look and act a lot like the parent tissue. They tend to grow slowly. Poorly differentiated or anaplastic (high-grade) cells look wild and disordered. They usually behave more aggressively. Grading is usually reported as G1 through G4.
Staging is about spread. It asks how big the tumor is and how far it has traveled. The most widely used framework is the TNM system. T is the size and reach of the primary tumor. N is how many nearby lymph nodes are involved. M is distant metastasis, which means spread to far-off organs. Higher numbers mean more advanced disease. Staging drives treatment choices and outlook more powerfully than grade does.
| Feature | Grading | Staging |
|---|---|---|
| Question it answers | How abnormal do the cells look? | How far has it spread? |
| How it is measured | Differentiation under the microscope | TNM: Tumor, Nodes, Metastasis |
| Typical scale | G1 (well-differentiated) to G4 (anaplastic) | Stage I to Stage IV |
| Main use | Predicts how aggressive it is | Guides treatment and overall outlook |
The CAUTION warning signs
The American Cancer Society mnemonic CAUTION lists classic early clues. Each one should prompt a checkup. They matter because early detection usually means a lower stage and a better outcome:
- C → Change in bowel or bladder habits
- A → A sore that does not heal
- U → Unusual bleeding or discharge
- T → Thickening or a lump (breast or elsewhere)
- I → Indigestion or trouble swallowing
- O → Obvious change in a wart or mole
- N → Nagging cough or hoarseness
When the tumor causes trouble from a distance
Paraneoplastic syndromes happen when a tumor makes hormones or hormone-like substances. The symptoms then show up far from the tumor itself. Two classic examples: SIADH, where small cell lung cancer makes ADH and drives sodium down, and hypercalcemia, from PTH-related peptide or from bone breakdown.
Tumor lysis syndrome (TLS) is an oncologic emergency. Large numbers of cancer cells can die very fast, often right after chemotherapy starts. They dump their contents into the blood. The result is high potassium (hyperkalemia), high phosphate, high uric acid, and low calcium. That mix can trigger fatal arrhythmias and acute kidney injury. That is why the labs are watched closely and fluids are given.
The four treatment pillars
Most cancer care combines four approaches. Surgery removes the tumor. Radiation damages the DNA of cells in a targeted area. Chemotherapy uses drugs that travel the whole body to kill dividing cells. Immunotherapy retrains or unleashes the patient’s own immune system to find and attack cancer.
Here is the key mechanism behind chemo’s side effects. Most chemotherapy targets rapidly dividing cells, because that is what cancer does. But some healthy tissues divide fast too, so they take collateral damage. That is exactly why chemo predictably causes hair loss (alopecia), since hair follicles divide fast. It causes nausea, vomiting, and mouth sores (mucositis), since the gut lining turns over fast. And it causes bone marrow suppression (myelosuppression), which drops white cells, red cells, and platelets. The low white count (neutropenia) is the scary one. It leaves the patient wide open to infection.
Build a stage yourself below. Set the depth, the nodes, and the distant spread one at a time, and watch the same T land in four different stages.
- Grade describes how abnormal the cells look (differentiation, G1 to G4). Stage describes how far cancer has spread, using TNM (Tumor, Nodes, Metastasis).
- The CAUTION mnemonic flags early warning signs that need a checkup. It can catch cancer at a lower, more treatable stage.
- Paraneoplastic syndromes (such as SIADH and hypercalcemia) cause hormone-driven symptoms far from the tumor. Tumor lysis syndrome is an emergency with hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia.
- The four pillars are surgery, radiation, chemotherapy, and immunotherapy.
- Chemo harms fast-dividing normal cells too. That causes alopecia, mucositis and GI upset, and myelosuppression. Watch for neutropenic fever.
The chapter in one breath
- Carcinogenesis is a stepwise loss of control. A normal cell mutates until it ignores stop signals, dodges apoptosis, and divides on its own. It becomes a clone of rogue cells.
- Cancer arises when proto-oncogenes mutate into oncogenes that are stuck on, the accelerator. At the same time tumor suppressor genes like p53 fail, the brakes. Growth control and DNA-repair checkpoints stop working.
- Benign tumors are usually slow, encapsulated, well-differentiated, and they stay put. Malignant tumors grow fast, lack a capsule, look abnormal, and spread.
- Invasion is local spread. Cancer cells release enzymes to chew through the basement membrane and move into nearby tissue. This is why surgical margins matter.
- Metastasis is distant spread through blood or lymph, forming secondary tumors. Common landing sites are lung, liver, bone, and brain, and it signals advanced disease.
- Causes are many. Carcinogens and risk factors include tobacco, radiation, UV light, certain chemicals, cancer-causing viruses (HPV, hepatitis, EBV), chronic inflammation, and inherited mutations such as BRCA.
- Grading says how abnormal the cells look under the microscope (differentiation). Staging, often TNM for Tumor size, Nodes, and Metastasis, says how far it has spread, and it drives the outlook.
- Treatment follows a few core ideas. Surgery removes local disease, radiation targets one region, and chemotherapy works through the whole body by hitting fast-dividing cells. They are often combined for better cure rates.
- Chemotherapy is not selective, so it also harms fast-turnover normal cells. That explains the classic toxicities: bone marrow suppression, hair loss, nausea, and mucositis.
ReferenceWords worth knowing
A quick reference for the terms in this chapter. Skim it now, or come back whenever a word trips you up.
- Anaplasia
- Anaplasia is the extreme loss of a cell’s normal look and order. The cancer cells look so wild and disordered, with big uneven nuclei and chaotic mitoses, that you often cannot tell what tissue they came from. It marks a highly malignant tumor.
- Angiogenesis
- Angiogenesis is the growing of new blood vessels. A tumor hijacks it by releasing signals like VEGF, so it can build its own blood supply and keep growing past a couple of millimeters.
- Benign
- A benign tumor is a growth that stays put. It grows slowly, is usually well-differentiated and inside a capsule, and does not invade nearby tissue or spread to distant sites. It can still cause harm by pressing on nearby structures.
- Carcinogen
- A carcinogen is any agent that can cause cancer by damaging DNA or pushing abnormal growth. Examples are tobacco smoke, UV and ionizing radiation, certain chemicals, and cancer-causing viruses such as HPV.
- Carcinoma
- A carcinoma is a cancer that starts in epithelial cells. Those are the cells that line and cover body surfaces and glands, such as skin, breast, lung, colon, and prostate. It is the most common group of cancer.
- Carcinoma in situ
- Carcinoma in situ is an early cancer whose malignant cells are still held in their original layer. They have not yet broken through the basement membrane to invade. So it is often curable if it is found and removed at this stage.
- Differentiation
- Differentiation is how closely a cell looks like the mature, specialized tissue it came from. Well-differentiated cells look and act almost normal. Poorly differentiated ones look primitive and tend to be more aggressive.
- Dysplasia
- Dysplasia is disordered cell growth that can still reverse. The cells vary in size, shape, and order. It is a pre-cancerous change that can turn into cancer if the trigger keeps going.
- Malignant
- A malignant tumor is a cancerous growth. It invades nearby tissue, tends to be poorly differentiated, and can spread (metastasize) to distant parts of the body. That makes it life-threatening if it is not treated.
- Metastasis
- Metastasis is the spread of cancer cells from the first (primary) tumor to distant sites through the blood or lymph system. There they seed new (secondary) tumors. It is the main reason cancer becomes deadly.
- Neoplasm
- A neoplasm, literally "new growth," is a mass of cells that keep dividing past normal limits and serve no useful purpose. It may be benign or malignant.
- Oncogene
- An oncogene is a mutated or overactive version of a normal growth-promoting gene called a proto-oncogene. Once switched on, it pushes a cell to divide nonstop, like a gas pedal stuck to the floor.
- Paraneoplastic syndrome
- A paraneoplastic syndrome is a set of symptoms caused by substances a tumor releases, such as hormones or cytokines, rather than by the tumor’s bulk. So a patient may show effects, such as low sodium or high calcium, far from the cancer itself.
- Sarcoma
- A sarcoma is a cancer that starts in connective and supporting tissues, such as bone, cartilage, muscle, fat, or blood vessels. It is far less common than carcinoma.
- TNM staging
- TNM staging is the standard way to describe how far a cancer has gone. It rates three things: T for the size and reach of the primary tumor, N for spread to nearby lymph nodes, and M for distant metastasis.
- Tumor-suppressor gene
- A tumor-suppressor gene, such as p53 or BRCA, normally slows cell division, repairs DNA, or tells a damaged cell to self-destruct. When it is lost or switched off, the cell’s brakes fail and cancer can develop.
DrillFlashcards for this unit
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