PATHO WEEK 3 W/ NOTES

This based off Week 3 PPT + My notes.

Cancer Basics

What is neoplasia?

Uncontrolled “new growth” that continues after the normal stimulus stops.

What is a tumor?

A mass formed by abnormal cell overgrowth.

What 3 processes normally control tissue growth?

Proliferation (division) + differentiation (specialization) + apoptosis (programmed death).

What is cell proliferation?

Cell division used to replace body cells.

What is cell differentiation?

A cell develops the specialized structure + function needed for its tissue.

What is apoptosis?

Programmed cell death that removes damaged or unwanted cells.

How does cancer disrupt normal cell control?

Cells divide continuously + lose differentiation + avoid apoptosis.

Why are cell-cycle checkpoints important?

They detect DNA damage → repair the DNA or stop/remove the cell.

What happens when cell-cycle checkpoints fail?

Damaged DNA is copied → mutations accumulate → cancer may develop.

What happens during G1?

Cell grows + produces RNA and proteins.

What happens during S phase?

DNA is copied for the 2 future daughter cells.

What happens during G2?

Cell continues making RNA/proteins + prepares for mitosis.

What happens during M phase?

Mitosis occurs → 1 cell divides into 2 daughter cells.

What is a stem cell?

A reserve cell that can self-renew + produce specialized cells.

Which cells have a higher cancer risk?

Frequently dividing cells (more DNA copying → more chances for mutations).

Why are epithelial cancers common?

Epithelial cells divide often to replace skin + organ linings.

Does one mutation usually cause cancer?

No → multiple mutations usually accumulate.

What is a driver mutation?

A mutation that helps a cell grow

What is clonal proliferation?

One mutated cell repeatedly divides → many cells with the same mutation.

Benign vs. Malignant

What are the signs of a benign tumor?

Slow + encapsulated + well-differentiated + low mitosis + no metastasis.

What are the signs of a malignant tumor?

Rapid + invasive + poorly differentiated + high mitosis + can metastasize.

What does well-differentiated mean?

Cells closely resemble their tissue of origin → usually less aggressive.

What does poorly differentiated mean?

Cells barely resemble their tissue of origin → usually more aggressive.

What is anaplasia?

Loss of cell differentiation (common in malignant tumors).

What is pleomorphism?

Cancer cells have different sizes + shapes.

How does a benign tumor grow?

Expands and pushes nearby tissue aside.

How does a malignant tumor grow?

Invades + destroys nearby tissue.

Can a benign tumor still be dangerous?

Yes → it can compress organs/vessels

Which finding confirms malignancy?

Metastasis (distant spread).

A tumor is encapsulated and well-differentiated. Benign or malignant?

Benign.

A tumor is invasive with many abnormal mitoses. Benign or malignant?

Malignant.

Why can a fast-growing tumor develop necrosis?

It outgrows its blood supply → ischemia + tissue death.

Which tumor usually has a higher mitotic index?

A malignant tumor; benign tumors usually have a low mitotic index.

What is an adenoma?

Benign tumor of glandular epithelium.

What is an adenocarcinoma?

Malignant tumor of glandular epithelium.

What is a carcinoma?

Malignant tumor of epithelial tissue.

What is a sarcoma?

Malignant tumor of connective/mesenchymal tissue.

What is an osteoma?

Benign bone tumor.

What are lymphoma and leukemia?

Lymphoma = cancer of lymphatic tissue; leukemia = cancer of blood-forming tissue.

Tumor Growth

What is tumor growth fraction?

The percentage of tumor cells actively dividing.

What is tumor doubling time?

The time needed for a tumor mass to double in size.

What suggests faster tumor growth?

Higher growth fraction + shorter doubling time.

Why does tumor growth depend on more than cell division?

Growth also depends on cell-cycle length + how many tumor cells die.

Hallmarks of Cancer

What keeps cancer cells growing?

Continuous growth signals + ignored “stop” signals.

What does evading growth suppressors mean?

Cancer cells ignore the body’s normal “stop dividing” signals.

What does resisting apoptosis mean?

Abnormal cells avoid programmed death → survive + multiply.

What is replicative immortality?

Cancer cells keep dividing beyond the normal limit.

What is genomic instability?

DNA/chromosomes mutate easily → more cancer-promoting changes.

How does cancer avoid immune destruction?

It hides its antigens or suppresses immune cells.

How does chronic inflammation support cancer?

Repeated injury + repair → more mutations + growth signals.

How do cancer cells produce energy?

They use large amounts of glucose and can grow with little oxygen.

Why does cancer cause high energy demand?

Rapidly dividing cells require more glucose + nutrients.

Angiogenesis + Metastasis

What is angiogenesis?

Formation of new blood vessels that supply a growing tumor.

Why is angiogenesis important to cancer?

It supplies oxygen/nutrients + provides a route for spread.

How does a tumor stimulate angiogenesis?

It releases angiogenic factors or decreases inhibitors of blood-vessel growth.

What is invasion?

Cancer directly enters + destroys nearby tissue.

What is metastasis?

Cancer spreads from the primary site → forms a distant tumor.

What are the 3 routes of cancer spread?

Direct invasion + cavity seeding + blood/lymph spread.

How does lymphatic metastasis occur?

Cancer enters lymph vessels → travels to nodes → may spread farther.

How does blood-borne metastasis occur?

Cancer enters blood → travels to distant organs → forms secondary tumors.

What is cavity seeding?

Cancer cells enter a body cavity → implant on another surface (such as the peritoneum).

What steps are needed for metastasis?

Detach → invade → enter blood/lymph → survive transport → exit → grow elsewhere.

A small tumor is found in a distant organ. Is it malignant?

Yes → distant spread means metastasis.

Cell-Surface Changes

What do normal cell-surface proteins control?

Cell recognition

What cell-surface changes occur in cancer?

Changes in receptors

How does loss of cell adhesion promote cancer spread?

Cells detach → invade + metastasize.

What is loss of contact inhibition?

Cells keep dividing after touching neighboring cells → form a mass.

How can altered growth receptors cause cancer?

Receptors stay “ON” → continuous cell division.

How can surface changes hide cancer from immunity?

Cancer changes/hides antigens → immune cells do not recognize it.

Why are tumor surface markers useful?

They help identify cancer + may become treatment targets.

Cancer Genetics

Which 4 gene groups are commonly altered in cancer?

Proto-oncogenes + tumor-suppressor + apoptosis + DNA-repair genes.

What is a proto-oncogene?

A normal gene that promotes controlled cell growth.

What happens when a proto-oncogene becomes an oncogene?

The cell’s growth signal becomes stuck ON.

What is a tumor-suppressor gene?

A gene that slows division

What happens when tumor-suppressor genes fail?

The cell loses its brakes → uncontrolled division.

How do abnormal apoptosis genes promote cancer?

Damaged cells survive when they should die.

How do failed DNA-repair genes promote cancer?

DNA errors remain → mutations accumulate.

Why are multiple mutations needed for cancer?

Several growth-control systems must fail before a cell becomes malignant.

Does an inherited mutation guarantee cancer?

No → it raises risk

What findings suggest inherited cancer?

Young age + bilateral tumors + multiple tumors + strong family history.

Initiation → Promotion → Progression

What happens during cancer initiation?

A carcinogen permanently damages DNA.

What happens during cancer promotion?

Growth signals cause the damaged cell to multiply.

Can cancer promotion be reversible?

It may be reversible early if the promoting stimulus is removed.

What happens during cancer progression?

Cells gain more mutations → become autonomous

How can you remember cancer development?

Initiation = DNA hit; Promotion = multiply; Progression = aggressive spread.

A cell has DNA damage but no tumor. Which stage occurred?

Initiation.

A mutated cell begins rapid growth. Which stage is occurring?

Promotion.

A tumor becomes invasive and metastatic. Which stage is occurring?

Progression.

Cancer Risk Factors

Etiology vs. risk factor?

Etiology = cause; risk factor = increases chance.

How does smoking cause cancer?

Carcinogenic chemicals cause oxidative stress + DNA injury → mutations.

How can pollution cause cancer?

Toxins cause cell injury + inflammation + DNA mutations.