Module 2.1 (Introduction to Cancer)

Question 1

Define cancer

Answer 1

Abnormal cell growth that divides uncontrollably and invades/spread to other tissue

Question 2

Define Neoplasm

Answer 2

Any abnormal tissue that forms when cells; grow/divide more than they should or don’t die when they should
Can be cancerous or harmless

Question 3

Define Tumours

Answer 3

Non specific term for neoplasm
“Mass” ; any swelling or abnormal enlargement in human body
Either malignant (cancerous) or benign (harmless)

Question 4

What classifies a tumour as benign?

Answer 4

Cannot invade or spread
Can attain +50kg without killing patient
Smooth and round corners

Question 5

What classifies a tumour as malignant?

Answer 5

Can invade other tissues (metastasis)
May kill before 50g
Spiky corners

Question 6

How can you found where the cancer originated?

Answer 6

Full body imaging

Question 7

Describe a carcinoma tumour and where it can be found

Answer 7

Effects epithelial cells
Usually solid tumour
- lung, prostate, breast, colorectal

Question 8

Describe a sarcoma tumour and where it can be found

Answer 8

Begins in tissues that support/connect the body
- fat, muscle, nerves, tendons, joints, blood vessels, lymph vessels, cartilage, bone

Question 9

Describe a lymphoma tumour

Answer 9

Begins in lymphocytes

Question 10

Describe a glioma tumour

Answer 10

Arise from connective tissue in the brain

Question 11

Describe a leukemia tumour

Answer 11

Cancer of the blood and bone marrow cells
Occurs when healthy blood cells change and grow abnormally

Question 12

Etiology of cancer

Answer 12

Genetic mutation

Question 13

Risk factors of cancer and what they are called

Answer 13

Carcinogens
- history of cancer
- tobacco use
- aging
- UV radiation

Question 14

How tobacco use leads to cancer

Answer 14

Smoke kills epithelial cells that line airway and lungs
Stem cells must undergo rapid division to replace damaged cells
(usually cells restored, division stops returning to resting state)
Chronic activation caused by consistent need to mutate to keep producing cells
CANCER

Question 15

Explain the evolution and clonality of cancer

Answer 15

Cell undergoes change to genetic code
Accumulations of mutations of daughter cells lead to variants/clones
Additional mutations provide further growth advantages
Each cell may obtain different set of advantageous mutations (leading to HETEROGENOUS TUMOUR)

Question 16

What are the challenges to understanding and treating cancer

Answer 16

Various tissue types respond differently to treatments
Continuous mutation means each subclone differs in ability to spread and respond to drugs
Diversity thousands of tumours from 1 cell and none are alike

Question 17

Describe oncogenes

Answer 17

Once mutated they produce proteins with new/altered function
Typically involved in growth factor receptor pathways
Mutation in 1 gene is strong enough to initiate cancerous effects

Question 18

What are the 2 cancer associated genes?

Answer 18

Oncogenes
Tumour suppressor genes

Question 19

What are proto-oncogenes?

Answer 19

Un-mutated oncogenes

Question 20

Which cancer associated gene is associated with sporadic cancers?

Answer 20

Oncogenes

Question 21

Describe tumour suppressor genes

Answer 21

Mutations disable normal functions that prevent uncontrolled growth
Both alleles must be mutated

Question 22

Which cancer associated gene is associated with familial cancers?

Answer 22

Tumour suppressor genes

Question 23

Describe TP53

Answer 23

Tumour suppressor
Produces p53 protein

Question 24

Describe p53 and its role

Answer 24

Protein product that regulates cell division
On chromosome 17
Responds to genomic damage by activating repair/death programs
“Brakes” for cells
Component of G1/S checkpoint checking for DNA damage

Question 25

What happens in p53 deficient cells?

Answer 25

Tolerate and even thrive with oncogenic mutations
There is no cell cycle arrest or DNA repair

Question 26

Mechanisms of p53 activity

Answer 26

DNA damage
p53 binds to DNA
Cell cycle arrest at G1
DNA repair by transcriptional upregulation of repair genes
–if fails - cell death

Question 27

Describe ERBB-1

Answer 27

Oncogene
Codes for Epidermal Growth Factor Receptor (EGFR)

Question 28

Describe EGFR’s role

Answer 28

Detects extracellular signals/ligands
Forms dimers to transmit signal into cell
Signal is tightly regulated in normal cells avoiding unwanted proliferation

Question 29

What kind of receptor is EGFR?

Answer 29

Tyrosine kinase

Question 30

Explain the process of gene expression through EGFR

Answer 30

Ligand bonding leads to structural change that activates
Secondary messengers phosphorylated by active
Transmits signal to nucleus
Increase transcription of genes in cell survival/multiplication
Drives mechanisms outside of cell (cell migration and angiogenesis)
Ligand is released/receptor is broken down by lysosomes to terminate

Question 31

Hyperactivation of EGFR

Answer 31

More secondary messengers
Increase of cancerous processes (angiogenesis, adhesion, cell proliferation, invasion, inhibition of apoptosis, migration)

Question 32

Constitutive Activation of EGFR

Answer 32

No stimulus to initiate signal = cannot be terminated
Cancerous process always on

Question 33

EGFR as therapeutic target

Answer 33

CHEMOTHERAPY: doesn’t target directly, kills any rapidly dividing cell in body
ANTIBODIES: inactivation/destruction of target protein, works because ligand binding domain is extracellular
KINASE INHIBITORS: both EGFR and secondary messengers, small molecules disrupt signalling cascade

Question 34

How does cancer impact the ideal patient journey?

Answer 34

WELL: Identifying carcinogens and changing routine
DIAGNOSIS: Screening catches before it is severe
TREATMENT: Cancer cells gain ability to resist treatment drugs