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
16
Q
Malignant characteristics
A
- Can potentially metastasize
- Well differentiated or undifferentiated
- Heterogenous
- Infiltrative growth
17
Q
Nomenclature: Benign Tumours of Connective Tissue
A
- Connective Tissue + Cell Type = Benign Tumour of Connective Tissue
- Fibrous Tissue + Fibrocyte = Fibroma
- Muscle + Myocyte = Leiomyoma
- Cartilage + Chondrocytes = Chondroma
- Bone + Osteocyte = Osteoma
- Others include:
o Lipoma
o Haemangioma
18
Q
Name of Malignant Tumours of Connective Tissue
A
- Sarcomas
o Name (Sarc = Malignant + CT cells of origin)
Fibrosarcoma
Leiomyosarcoma
19
Q
Epithelial Benign Tumours naming
A
- Papil- (finger like projection)
- Adeno- (relating to glands)
- Cystadena- (cyst like)
- -oma- (denoting tumour and other abnormal growths)
20
Q
Examples of Malignant Epithelial Tumours
A
o Squamous Cell Carcinoma
o Renal Cell Carcinoma
o Adenocarcinoma
21
Q
Name of malignant tumours
A
- Carcinomas
- Sarcomas
- Testicular Tumours
- Mesothelioma
- Melanoma
- Gliomas
- Lymphomas
- Leukaemias
o Blastomas
22
Q
Pathogenesis
A
1) Normal Cell –> Multiple Mutations –> Cancer
2) Normal Cell –> Multiple Mutations –> Benign Tumor OR Normal Cell –> Multiple Mutations –> Benign Tumor –> Further Mutations –> Cancer
3) Normal Cell –> Sustained Stress –> Metaplasia –> Multiple Mutations –> Dysplasia –> Further Mutations –> Cancer
23
Q
3 main routes of metastasis
A
- Blood (haematogenous)
o Bone and Soft Tissue Tumours - Lymphatics (vessels and nodes)
o Melanoma, Breast, Lung and Gastrointestinal Tumours - Direct Seeding (through/within body cavities)
o Certain tumour cells can only successfully colonise selective organs that have suitable growth environments
24
Q
Importance of Early Detection
A
- If it is found early, it may be easier to treat
- If cancer has begun to spread, alternative treatment must be utilised
- If cancer has not spread, tumour may have the ability to be removed without further treatment required
25
3 types of cells
Labile (continuously dividing)
• Epithelial e.g. Skin, GIT, reproductive, urinary
bladder, lining of exocrine ducts
• Haemopoietic stem cells
Stable (quiescent)
• Epithelial e.g. Liver, kidney, lung, pancreas
• Smooth muscle cells, fibroblasts, endothelial
cells
Permanent (non‐dividing)
• Cardiac & skeletal myocytes, neurons
26
What is atrophy
decrease is size of cell or tissue
27
What is hypertrophy
Increase in size of cells
28
What is hyperplasia
increase in the amount of organic tissue that results from cell proliferation.
29
Autophagy
body's way of cleaning out damaged cells, in order to regenerate newer, healthier cell
30
What are mutagens and examples
May act directly to cause damage or may do so
through increasing oxidant production or
reducing anti‐oxidant defences
• Exposure to carcinogens – asbestos, vinyl
chloride, cadmium, chromium and nickel
compounds,
• UV, alcohol, smoking, obesity
• Genetics
• Viruses
31
4 classes of normal regulatory genes are the principle targets of genetic
damage
- Growth promoting proto‐oncogenes
– Growth inhibiting tumour suppressing genes
– Genes that regulate apoptosis
– DNA repair genes
