Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Biology > Molecular Biology of Cancer > Flashcards

Molecular Biology of Cancer Flashcards

You may prefer our related Brainscape-certified flashcards:
AP® Biology flashcards Biology 101 flashcards
1
Q

Definition: Cancer

A
  • disorder of cell growth that results in the invasion and destruction of healthy tissues by abnormal cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Definition: Checkpoint

A
  • critical control point where stop and go-ahead signals can regulate the cell cycle
  • cell monitors internal equilibrium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Checkpoints in the Cell Cycle

A
  1. G1-S
  2. G2-M
  3. M
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

G1 Checkpoint; what is assessed?

A

Assessment of CELL GROWTH

  1. Presence of growth factors; proteins required to stimulate cell division
  2. Adequate cell size; initiate DNA replication in S phase
  3. Nutrients availability
  4. Conditions are favourable for DNA replication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

G2 Checkpoint; what is assessed?

A

Assessment of DNA REPLICATION

  1. Results of DNA replication (by DNA repair enzymes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

M Checkpoint; what is assessed?

A

Assessment of MITOSIS

  1. Formation of spindle fibre apparatus
  2. Proper attachment of spindle fibres to all kinetochores assiciated with centromeres of chromosomes
    - enzyme, separase, cleaves cohesin molecules, allowing sister chromatids to separate; ensures daughter cells do not have extra or missing chromosomes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens if DNA/chromosome damage is too severe to repair?

A

Cell initiates apoptosis (programmed cell death)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Action of Growth Factors (Stimulatory pathway)

A
  1. Bind to cell surface receptor on plasma membrane
  2. Signal transduced into cell and relayed to nucleus
  3. Transcription and translation; production of protein that promotes cell division
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Action of Growth-inhibiting Factors (Inhibitory pathway

A
  1. Bind to cell surface receptor on plasma membrane
  2. Signal transduced into cell and relayed to nucleus
  3. Transcription and translation; production of protein that inihibits cell division
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cell Cycle Regulators

A
  1. Proto-oncogenes
  2. Tumour Suppressor Genes
  3. Contact-dependent / density-dependent inhibition
  4. Platelet-derived growth factor
  5. Environmental factors (e.g change in pH, nutrients, temperature)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Function of Proto-oncogenes

A
  • promote cell division
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Examples of Proto-oncogenes

A
  • Ras gene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Function of Tumour Suppressor Genes

A
  • inhibit cell division to prevent inappropriate cell growth

- initiate apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Examples of Tumour Suppressor Genes

A
  • p53 gene

- retinoblastoma (RB) gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Contact-dependent / Density-dependent Inhibition

A
  • most cells require adhesion to a substratum to divide

Stop dividing when:

  1. Lose anchorage
  2. Close proximity to one another

NOT APPLICABLE TO CANCER CELLS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Platelet-derived Growth Factor (PDGF)

A
  • released when platelets come into contact with damaged blood vessels
  • fibroblasts, the main cells of commective tissues, have receptors for PDGF
  • binding of PDGF triggers fibroblasts in the area of the wound to divide repeatedly, causing it to heal
17
Q

Definition: Carcinogen

A
  • any agent that can lead to cancer formation due to ability to cause DNA damage or disrupt cellular metabolic processes
18
Q

CAUSES OF CANCER

• 1A) Lifestyle and diet - SMOKING

A
  • tobacco smoke contains carcinogens; polycyclic aromatic hydrocarbons (PAHs)
  • PAHs can bind to DNA and form adducts
  • formation of adducts can cause mistakes in DNA synthesis, introducing mutations to DNA
19
Q

CAUSES OF CANCER

• 1B) Lifestyle and diet - UNHEALTHY DIET

A
  • diet rich in salted, pickled and smoked foods (e.g smoked fish, meats treated with nitrates)
20
Q

CAUSES OF CANCER

• 1C) Lifestyle and diet - FREE RADICALS

A
  • are dangerous, highly reactive chemical compounds that can damage DNA and lead to cancer
  • build-up in person’s body happens when one’s own biochemical mechanisms to reduce them are unable to keep up with their production; abundance of free radicals in system
21
Q

CAUSES OF CANCER

• 2A) Radiation exposure - IONISING RADIATION

A
  • overexposure can cause DNA mutations, leading to cancer

- potential sources include medical diagnostic and therapeutic procedures

22
Q

CAUSES OF CANCER

• 2B) Radiation exposure - ULTRAVIOLET RADIATION

A
  • radiation from the sun that reaches earth
  • damages DNA by forming pyrimidine dimers through formation of covalent bonds between adjacent pyrimidine bases
  • if damage remains unprepared, this distortion of the double helix results in improper base pairing during DNA replication; distinctive mutation patterns
23
Q

CAUSES OF CANCER

• 3) VIRAL INFECTIONS

A
  • some cancers involve certain RNA and DNA viruses
  • termed transforming viruses; can integrate their genomes into host DNA and transform normal cells into tumourigenic cells by activating proto-oncogenes or inactivating TSGs
  • DONE BY:
    1. directing expression of viral proteins that can inactivate TS proteins like p53
    2. Introducing oncogenes
24
Q

CAUSES OF CANCER

• 4) GENETIC PREDISPOSITION

A

E.g breast cancer

  • PREDISPOSITION is inherited, NOT the CANCER itself
25
Q

Mutations that can bring about uncontrolled cell division

A
  1. Over-expression of proto-oncogenes
  2. Under-expression of tumour suppressor genes
  3. Mutations in genes responsible for apoptosis
  4. Exposure to mutagens
26
Q

Definition: Proto-oncogene

A
  • stimulatory gene; can be made overactive or active at inappropriate times
  • mutations usually dominant as mutation in a single copy of the gene is sufficient to produce a stimulatory effect
27
Q

Proto-oncogenes encode for gene products that promote cell growth such as:

A
  • growth factors
  • growth factor receptors
  • transcription factors
  • protein kinases
  • inhibitors of apoptosis
28
Q

Definition: Tumour Suppressor Gene

A
  • inhibitory gene that can mutate to become less active
  • mutation usually recessive as both copies of the gene must be mutated to produce inhibitory effect
  • inhibit inappropriate cell growth and proliferation
29
Q

Action of gene products encoded by TSGs:

A
  • halt cell division when DNA is damaged
  • trigger DNA repair to prevent accumulation of DNA damage
  • maintain cell anchorage to substratum
  • involved in cell signalling pathways that inhibit cell cycle
30
Q

Loss of function mutation in p53

A
  • p53 encodes for a transcription factor (p53 protein) that inhibits the cell cycle when cell incurs DNA damage or abnormalities in chromosome attachment are detected
  • prevents proliferation of cells that have incurred DNA damage
  • loss of function mutations in p53; cell growth and division continues and DNA damage is retained, increasing risk of cancer
31
Q

Gain of function mutation in Ras gene

A
  • Ras gene encodes for the Ras protein that relays signal for a growth factor from a receptor to a protein kinase cascade, giving rise to a protein that stimulates cell division
  • pathway will not normally operate unless triggered by appropriate growth factor
  • gain of function mutation in Ras gene; hyperactive Ras protein that triggers the protein kinase cascade even in absence of appropriate growth factor; results in increased cell division, increasing risk of cancer
32
Q

Point-mutations / base-pair substitutions in PROTO-ONCOGENES

A
  1. In CONTROL SEQUENCES (PROMOTER, REGULATORY SEQUENCES & ENHANCERS)
    - increase in expression of gene
    - increase in amount of gene product
  2. In CODING REGIONS
    - alter protein structure
    - changes activity of gene product; more active and more resistant to degradation
33
Q

Gene amplification in PROTO-ONCOGENES

A
  • extra copies result from random over-replication of small segments of DNA
  • increase in amount of gene product; uncontrolled cell division
34
Q

Chromosomal translocation in PROTO-ONCOGENES

A

A) chromosomes that break and rejoin incorrectly are translocated from one chromosome to another

  • proto-oncogene may end up next to an especially active promoter or control sequence
  • increased transcription; increase in gene product

B) reciprocal translocation

  • results in chromosome being shorter than normal
35
Q

Multi-step process

A
  • cells in malignant tumours no longer respond to cellular control mechanisms
  • invasion; spread into neighbouring tissues from the primary tumour
  • may travel to distant tissues and organs and establish secondary tumours via metastasis
  • may also be carried to other body parts through blood/lymphatic system
  • angiogenesis occurs (formation of blood vessels) to supply adequate O2 and nutrients, removal of waste products

Biology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions