Neoplasia Flashcards
1
Q
Metastasis
A
- Cancer spreads to a region other than where it originated
- Commonly develop when cancer cells break away from main tumour and enter bloodstream or lymphatic system
- Can also develop when breaking away from main tumour (in belly, abdominal cavity) and grow in nearby areas (liver, lungs or bones)
2
Q
Dysplasia
A
- Abnormal development of cells within tissues or organs
- Can lead to a wide range of conditions involving enlarged tissue or pre-cancerous cells
- Reversible –> can undergo apoptosis and repair
3
Q
Neoplasia
A
- Uncontrolled, abnormal growth of cells or tissues that is not under physiologic control
o Abnormality = neoplasm or tumour - Irreversible –> can no longer go under apoptosis or cell repair
4
Q
In Situ
A
- Tumour confined to its site of origin and has not invaded neighbouring tissue or gone elsewhere in the body
5
Q
Carcinoma
A
- Abnormal cells that divide without control
- Originates in epithelial cells lining the skin or the tissue lining organs, such as the liver or kidneys
6
Q
8 Behavioural changes that occur in cancer cells
A
- Limitless Replicative Potential
- Evasion of Apoptosis
- Ability to Invade and Metastasise
- Insensitivity to Antigrowth Signals
- Sustained Angiogenesis
- Self-Sufficiency in Growth Signals (Proliferation without external stimuli)
- Warburg Effect
- Defects in DNA Repair
7
Q
Limitless Replicative Potential
A
- Tumour cells can inactivate senescence signals and activate telomerase
- Telomerase replaces telomeres with base pairs and allows unlimited replication
- Three Cell Types that may show unlimited replication
o Germ Cell (normal)
o Stem Cell (normal)
o Tumour Cells (abnormal)
8
Q
Evasion of Apoptosis
A
- P53 (guardian of the genome) is responsible for detecting DNA damage, chromosome abnormalities and arresting the cell cycle to initiate repair
o If not possible, apoptosis is induced - More than half of cancers have mutated or missing gene P53
o Therefore, it is damaged or missing - Cancer cells than either increase the activity of inhibitors of P53 or silence the activators of P53
9
Q
Ability to Invade and Metastasise
A
- Primary tumour masses spawn pioneer cells that invade adjacent tissue
- Allows the tumour to colonise a new region of the body in which nutrients and spacer are not limiting
- Successfulness is dependent on the other hallmarks of cancer
10
Q
Insensitivity to Antigrowth Signals
A
- Antigrowth signals are proteins that inhibit growth
- At a molecular level, nearly all antigrowth signals are funnelled through the Retinoblastoma protein (Tumour Suppressor protein)
o Can be lost through mutation of its gene
o Cancer-promoting proteins (oncoproteins) can block the function of Retinoblastoma - Another antigrowth signal (TGF-Beta) blocks the advancement of cell division when present
o Therefore, cancer cells can reduce the number of TGF-Beta receptors to be irresponsive to its presence
11
Q
Sustained Angiogenesis
A
- Creating leaky and unstable blood vessels
12
Q
Self-Sufficiency in Growth Signals (Proliferation without external stimuli)
A
- Protooncogenes regulate cell proliferation
- Protooncogenes mutate forming oncogenes which promote autonomous growth via the creation of oncoproteins
o Inactivate internal regulator pathways and result in abnormal cell function and transformation - Many cancer cells acquire the ability to synthesise and secrete their own growth factors (creates positive feedback loop)
- Cancer cells can tweak growth factor receptor
o Increases number of receptors on cell surface lower level of growth factor is required to trigger cell division
13
Q
Warburg Effect
A
- Form of modified cellular metabolism found in cancer cell
o Tend to favour a specialised fermentation over the aerobic respiration pathway - Cancer cells predominantly produce energy by a high rate of glycolysis followed by lactic acid fermentation in the cytosol
o Rather than glycolysis, followed by the oxidation of pyruvate - Aerobic glycolysis produces ATP synthesis promotes cell proliferation by reprogramming metabolism to increase glucose uptake and stimulate lactate production
o High proliferating cancer cells use increased fatty acid synthesis to support the rate of cell division
14
Q
Defects in DNA Repair
A
- Enable cancer cells to accumulate genomic alterations that contribute to their aggressive phenotype
- When erroneous DNA repair leads to mutations/chromosomal aberrations affecting oncogenes and tumour suppressor genes
o Cells undergo malignant transformation resulting in cancerous growth
15
Q
Benign tumour characteristics
A
- Never metastasizes
- Well- differentiated
- Encapsulated
- Homogenous
