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Stage 4 Oncology > Pathogenesis of Cancer > Flashcards

Pathogenesis of Cancer Flashcards

1
Q

What are the 5 basic steps to cancer development?

A
  1. Cell has genetic mutation
  2. Hyperplasia (inc. reproductive rate of cells causing enlarged tissue/organ size)
  3. Dysplasia (abnormal cell within tissue/organ)
  4. In-situ cancer
  5. Invasive cancer
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2
Q

Why do people get cancer?

A

Genetics cause the birth and death of cells

If the genetic mutation creates a variant that proliferates quicker, that mutant takes over the organism

(natural selection)

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3
Q

Who developed the theory of evolution by NATURAL SELECTION?

A

Charles Darwin

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4
Q

Define: Benign Tumour

A

A mass of cells (tumour) that currently LACKS the ability to:

  • invade surrounding tissues
  • spread to other areas of the body
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5
Q

Define: Malignant Tumour

A

A mass of cells (tumour) that HAS the ability to:

  • invade surrounding tissues
  • spread to other areas of the body (metastasis)
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6
Q

Benign vs Malignant

  • edges
  • metastasis
  • growth rate
  • nuclei
  • life-threatening ?
A 
BENIGN vs MALIGNANT
Edges: Encapsulated vs Irregular
Metastasis: No vs Yes
Growth rate: Low vs High 
Nuclei: Normal vs Irregular 
Life-threatening: No vs Yes
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7
Q

Leimyo-

A

smooth muscle

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8
Q

Rhabdomyo-

A

striated muscle

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9
Q

(Structure of Tumours)

Define: Neoplastic cell

A

Rapid division of cells (reproduce) to variable growth patterns and/or functions to parent cell
Abnormal growth of cells that leads to a tumour (can be malignant or benign)

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10
Q

(Structure of Tumours)

Define: Stroma

A

Connective tissue framework that provides mechanical support (contains fibroblasts) and nutrition to the tumour cells

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11
Q

Growth of tumours depend on what?

A

Angiogenesis: The ability of the stroma to induce blood vessels into the tumour

Tumours are clonal. Multiple genetic changes are required

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12
Q

Define: Tumour Differentiation

A

The extent to which neoplastic cells resemble comparable normal cells which they have arisen from (morphologically and functionally)

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13
Q

Define: Well differentiated tumour/cancer

A

Neoplastic cells also composed of normal cells from the original parent cell

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14
Q

Where do well differentiated cancers/tumours arise from?

A

Mature stem cells

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15
Q

Where do undifferentiated cancers/tumours arise from?

A

Immature stem cells

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16
Q

How do you classify tumours/neoplasms?

Secondly, describe each stage (HINT: There are 3)

A

Using the TNM staging system (3 stages)

  1. T = Tumour. Size of primary (original) tumour and the extent of invasion
  2. N = Nodes. Describes the presence and number of lymph nodes if involved
  3. M = Metastasis. Distance of metastasis (distance it spread from one part of body to another)
17
Q

What are the factors to consider during prognosis?

Or the factors prognosis is based on ?

A

3 factors

  1. Tumour type
  2. Grade (degree) of differentiation
  3. Stage or Extent of metastasis (spread)
    - Assess resected (cut-out) tumour AND
    - MRI imaging of patient)
18
Q

Terminology! Explain the difference between sarcoma and carcinoma.

A

Sarcoma is a tumour originated from connective tissue

Carcinoma is a tumour originated from epithelial tissue

19
Q

Terminology!

Grade vs Stage ?

A 
Grade = degree of histological resemblance to parent tissue
Stage = extent of spread

(histology = structures)

20
Q

What can cause cancer? (list up to 6)

A 
The Sun
Ionising radiation 
Asbestos
Viruses
Genetics
Parasites
Hormones
Red meat
Cigarettes
21
Q

What can increase cancer incidence? Lifestyle factors

A

Diet e.g. Fatty foods (colonal cancer)

Bacterial e.g. H pylori (stomach)

Lifestyle e.g. Smoking, Alcohol

Viral e.g. HPV (cervical)

Hormonal e.g. oestrogens (breas and ovarian)

Environmental e.g. radiation, UV

Occupational e.g. asbestos (mesothelioma - cancer develops from the thin layer of tissue that covers many internal organs. Most commonly: lungs and chest wall)

22
Q

What is the difference between:
Somatic mutations
Germline mutations?

A

Somatic mutations occur in non-germline cells hence are non-inheritable
Germline cells are inherited because they are present in the sperm or egg. If there is a mutation in the egg or sperm then all cells affected in the offspring.

23
Q

Define: Proto-oncogene

A

Normal gene that when altered by a mutation becomes an oncogene which contributed to cancer.
KEY: (Internal) oncogene signalling drives cell proliferation (cell division) via transcription

24
Q

What are the differences in function between

Normal Cell vs Cancer Cell

A

Normal genes prevent cancer by removing or inactivating tumour suppressor genes (TSG)

In a cancer cell, there is damage to the genes in the nucleus due to mutated/inactivated tumour suppressor genes **QUESTION THIS

25
Q

Activation of oncogenes and inactivation of TSGs

A

Normal genes regulate cell growth

1st mutation leads to a susceptible carrier

2nd mutation leads to cancer

26
Q

What are the steps of Tumourigenesis?

A

Normal cell –> INITIATION –> Initiated cell –> PROMOTION–> Pre-neoplastic cells –> PROGRESSION

INITIATION: Irreversible genetic change to the cell (genetic or due to carcinogen e.g. tobacco smoke)

PROMOTION: Further genetic changes due to further mutation (e.g. increased exposure to smoke).
Associated with genomic instability and PERTURBATION of oncogenes and TSGs (p53, retinoblastoma etc.)

PROGRESSION: Errors in genes involved with cell division, cell death and DNA repair
Cells now have metastatic potential to move to diff body areas

Problem: ** No cancers have same genetic changes**

27
Q

CANCER PATHOGENESIS

What are the effects of a mutation in the genome of somatic cells?

A
  • Alters genes that promote apoptosis
  • Inactives tumour suppressing genes (TSGs)
  • Activates tumour growth promoting genes :(
28
Q

CANCER PATHOGENESIS

Steps?

A
  1. Normal cell can undergo DNA damage
  2. If DNA repair is successful continues as normal cell, if unsuccessful –> mutations in genome of somatic cells occur (3 effects of this stated in another flashcard Q)
  3. Altered gene products expressed and regulatory gene products lost
  4. Clonal expansion –> Further mutation –> Heterogeneity –> NEOPLASM
29
Q

What is Gene vs Genome ?

A

A gene is made of DNA. Genes (have enough DNA to) code one protein.
A genome is the total DNA in one organism

30
Q

Colorectal tumorigenesis (overall accumulation rather than sequence is important)

A
  1. Loss OR somatic mutation of adenomatous polyposis coli (APC) gene
  2. DNA hypomethylation (genomic instability) - loss of the methyl group (-CH3) in the 5-methylCYTOSINE
  3. Mutation of K-ras
  4. Loss or Mutation of SMAD4
  5. Loss or Mutation of p53
31
Q

Which of the genes listed (all tumour suppressor genes, TSG) is NOT a TSG?

APC
K-ras
SMAD4
p54 
MSH2
MLH1
A

K-ras

Because it is in fact an ONCOGENE (the only one in the tumourigenesis process) hence this is GAINED whereas the TSGs are LOST in the formation of a tumor.

FUNCTION: Signal transduction for cell proliferation.

32
Q

What genetic changes do oncogenes (gene amplifiers) make?

A
  • Genetic translocation
  • Activate mutations
  • Activate gene promotors
33
Q

What genetic changes do TSGs (gene inactivators) make?

A
  • Silence mutations
  • Haploinsufficiency (a model of dominant gene action in diploid organisms)

Epigenetic Mechanisms
 Promoter Methylation
 Promoter Phosphorylation
 Histone Deacetylation

34
Q

What is the hereditary marker for breast cancer?

A

BRAC1

35
Q

Define: Epigenetics

A

Hereditary modification of genetic activity that does NOT involve DNA sequence changes

FUNCTION: alters DNA conformation (structure/shape) within chromatin resulting in an altered gene expression

E.g. DNA methylation and histone modifications can lead to silencing of gene (TSGs). Suppressing transcription of TSGs means cancer cells proliferate

36
Q

List hallmarkers of cancer?

A

Replicative potential (limitless)
Sustain angiogenesis (stroma induce blood vessles)
Evasion of apoptosis (programmed cell death)
Ability to invade and metastasis
Evade TSGs (growth suppressors)
Self-sufficiency in growth signals

Stage 4 Oncology (10 decks)

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