Cell Ab - concept in cell ab Lesson 1

1. controlled cell division

2. regulated apoptosis

3. cell differentiation

4. adherance to contact inhibition

5. cell cycle phase guardedb by strict check point

In normal cell homeostasis, what are it’s characteristics. Enumerate the 5 characteristics.

adherence to contact inhibition

a regulatory process where normal cells stop moving and dividing when they touch neighboring cells

controlled cell division

an orderly process where a cell grows, copies its DNA, and divides into two identical new cells through the cell cycle.

regulated apoptosis

is a genetically controlled, programmed process of cellular self-destruction that maintains tissue balance and eliminates damaged cells without causing inflammation

P53 protein

is a crucial tumor suppressor often called the "guardian of the genome" because it maintains genetic stability and prevents cancer development.

MNEMONIC that is included in nurse’s specialized training (e.g revealing stage 4 cancer)

SPIKES

Enumerate what SPIKES is

S-etting P-erception I-nvitation K-nowledge E-mpathy S-trategy

the cell cycle

ordered series of events where a cell grows, replicates its DNA, and divides into two identical daughter cells.

what is the preparation phase called?

interphase

the 3 stages of interphase

G1, S, G2 and G0

Interphase

the cells are growing, replicating DNA and doing their different cell fucntions

Mitosis (M phase)

this is where cells divide

G1

The cell itself evetually grows

S phase

phase where replication of DNA happens

G2

the cell grows more

Apoptosis

if the cell cannot be fixed or ensures that irreplacable cells will not divide.

In M phase, what are the phases?

prophase, metaphase, anaphase, and telophase

Cell cycle checkpoints, DNA repair systems, Apoptosis, tumor surveillance

protective quality control and surveillance mechanisms

Cell cycle checkpoints

molecular stop signs in the cell

tumor surveillance

Natural Killer (NK) cells and T cells identify abnormal neo-antigens on mutated cells.

Tumor suppresssor genes

are protective segments of DNA that regulate cell growth, repair damaged DNA, and trigger programmed cell death (apoptosis) to prevent cancer.

TP53 genes or proteins

Often called the "guardian of the genome," it is mutated in over 50% of all human cancers.

BRCA1 and BRCA2

Responsible for repairing double-strand DNA breaks; mutations sharply raise breast and ovarian cancer risks.

RB1 gene

human tumor suppressor gene located on chromosome 13 (at position 13q14) that stops cells from growing and dividing too fast.

PTEN GENE

“break” on cell survival and growth pathways. Provides instructions for making an enzyme that acts as a tumor suppressor, regulating cell division and preventing cells from growing too rapidly or uncontrollably

APC (Adenomatous Polyposis Coli)

Controls cellular proliferation signals. Is a crucial tumor suppressor gene that stops cells from growing and dividing too quickly or in an uncontrolled way.

normal cell proliferation

the controlled process where cells grow and divide to increase cell numbers for body growth, tissue repair, and normal maintenance.

contact inhibition

a regulatory process where normal cells stop moving and dividing when they touch other cells.

Proto oncogene

in normal cell proliferation, this is a normal gene that helps regulate cell growth, division, and survival. Act like the accelerator pedal of a car, driving the cell forward through its normal cycle of growth and division.

defective proliferation

an abnormal pattern of cell division where cells either multiply uncontrollably (hyper-proliferation) or fail to divide when needed (hypo-proliferation).

the “pyramid effect”

in defective proliferation, this is the exponential growth pattern of cancer cells, where each round of cell division doubles the population, creating a expanding base like an inverted pyramid.

cell differentiation

the physical and structural specialization of a cell.

defective differentiation

cancer cells, do not mature properly, exhibits anaplasia, lack of cell differentiation and regression to a more disorganize state.

anaplasia

the complete loss of structural and functional differentiation in cells, causing them to revert to an unspecialized, primitive, or embryonic state.

characteristics of defective proliferation

loss of function, morphological chanes, nucleus-to-cytoplasm (N:C) ratio, abnormal mitotic figures

hyperplasia

what is it called when theres an increase in the number of cells in an organ or tissue. Cells divide faster than normal, making the tissue or organ grow larger.

metaplasia

• Meaning: The replacement of one mature cell type with another mature cell type.

• How it works: Cells change into a different type to survive a harsh new environment.

dysplasia

Disordered growth and abnormal changes in cell size, shape, and organization.

Anaplasia

A complete loss of cellular differentiation (primitive, unspecialized features).

neoplasia

is the abnormal and uncontrolled growth of cells that forms a mass of tissue called a neoplasm or tumor.

benign

localized and non cancerous

malignant

invasive and cancerous

initiation, promotion, progression (IPP)

The 3 phases of carcinogenesis

carcinogenesis

a multistep process in which normal cells transform into cancer cells.

initiation

A normal cell is exposed to a carcinogen that causes DNA damage (a mutation) such as tobacco smoke, uv rad, oncagenic virus and chemicals but

• the mutation is permanent

• cell locks ad fucntions normally

• alone, doe not lead to cancer

promotion

The mutated cell is stimulated by promoters to grow and divide more than normal. such as hormones, inflammation, alcohol.

• the mutated cell multiplies, forming a clone

• cells are still abnormal but non-cancerous (reversible)

• removal of the promoter can stop growth

progression

Additional genetic changes occur. Cells become cancerous and invasive.

• irreversible stage

genetic, environmental and lifestyle, viral and bacterial, hormonal and immunologic

etiologic factors of cancer

carcinogenic agents

these are environmental or external agents that directly damage DNA (initiators) or create an

environment that encourages mutated cells to grow

tobacco smoke

The single most lethal, preventable chemical carcinogen.

physical carcinogens

• Ultraviolet (UV) Radiation

• Ionizing Radiation

• Chronic Inflammation and Irritation

biological carcinogens

• Human Papillomavirus (HPV): Types 16 & 18.

• Hepatitis B & C Viruses (HBV/HCV)

• Epstein-Barr Virus (EBV)

• Helicobacter pylori: Bacteria linked to gastric cancers.

chemical carcinogens

Tobacco Smoke: The single most lethal, preventable

chemical carcinogen.

Occupational & Industrial Chemicals: Substances

encountered in workplaces, including:

⁍ Asbestos: Leads to mesothelioma and bronchogenic

carcinoma.

⁍ Benzene: Linked to acute myeloid leukemia (AML).

⁍ Aniline dyes: Linked to bladder cancer.

⁍ Alcohol Consumption: Acts as a solvent and

promoter.

tumor angiogenesis

The formation of new blood vessels from existing ones, which supplies the tumor with oxygen and nutrients,

enabling its growth and survival.

stimulation

The tumor releases signals such as VEGF that stimulate nearby blood vessels to grow toward the

tumor.

activation

The blood vessel cells become activated and prepare to break through the surrounding tissue. 3. Sprouting: New blood vessel branches begin to sprout and grow toward the tumor.

sprouting

New blood vessel branches begin to sprout and grow toward the tumor.

tube formation

The growing blood vessel cells form tube-like structures that can carry blood.

maturation

The new blood vessels become stable and functional, providing oxygen and nutrients to the tumor.

metastasis

The spread of cancer cells from the primary tumor to distant sites where they grow and form new tumors.

local invasion

cancer cells invade nearby normal tissue

intravasion

cancer cells enter blood or lymphatic vessels

survival in circulation

cancer cells survive on bloodstream

extravasion

cancer cells exit the vessel at a distant site

colonization

cancer cells adapt and begin to grow

Common Sites of Metastasis:

lungs, liver, brain, bones

lymphatic, blood, direct

matstasis pathways

angiogenesis

helps tumors grow

metastasis

allows cancer to spread and affect distant organs