Brainscape's Knowledge GenomeTM

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


See full index

BDS1 Pathology > Neoplasia 2 > Flashcards

Neoplasia 2 Flashcards

1
Q

What are some important genes in carcinogenesis?

A
  • Oncogenes (accelerators)
  • Tumour suppressor genes (brakes)
  • DNA repair genes
  • miRNA’s (non-coding, controlling factor over the rest of genes
  • many others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are proto-oncogenes?

A

Normal genes which regulate cell division

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

Give some examples of proto-oncogenes?

A
  • Growth factors
  • Growth factor receptors
  • Signal transducers
  • Control of gene expression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are abnormal variants of proto-oncogenes?

A
  • Oncogenes

- They produce oncoproteins

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

How many genes need to be mutated for oncogenes to cause malignancy?

A

1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does mutated growth factor cause?

A

Increasing the amount of growth factor encourages cells to divide at a greater rate than they normally would do

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is enhanced transcription?

A
  • Translocation
  • Chromosome rearrangement
  • During cell division parts of the chromosomes break off and attach themselves to the same chromosome or a different chromosome - when this happens sometimes genes become fused with each other ‘hybrid’ gene - product of their expression is different genes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How many genes need to be mutated for tumour suppressor genes to cause malignancy?

A

2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens if tumour suppressor genes are mutated?

A

The brakes mechanism is lost so there is nothing stopping cells from growing and proliferating at a faster rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What do tumour suppressor genes do?

A
  • Act to inhibit cell division and suppress growth

- Act as ‘anti-oncogenes’ and act by a variety of mechanisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are inherited cancer syndromes (Inherited factors)?

A
  • Single mutant genes, often tumour suppressor genes

- Retinoblastoma, some colon cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is familia cancer (inherited factor)?

A
  • Family clusters
  • genes and patterns of inheritance not clear
  • breast, ovary, colon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is defective DNA repair (inherited factors)?

A
  • Increased sensitivity to carcinogens and general increased cancer risk
  • Xeroderma pigmentosum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is P53’s function and where does it act?

A
  • Acts just before the restriction point (at the restriction point the cell cycle stops)
  • 2 main functions in response to DNA damage:
  • Stops the cell cycle to allow DNA repair
  • Apoptosis (if repair not possible)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What systems are affected by cancer?

A
  • other cell division controls
  • DNA repair mechanisms
  • Apoptosis inhibited
  • Stimulation of blood vessel formation
  • Destructive enzymes activated
  • Cell motility increased
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the characteristics of cancer?

A
  • Growth rate - must divide quickly
  • Growth potential - must be able to detach from surrounding abnormal cells
  • Differentiation
  • Invasion/destruction
  • Avoid apoptosis
  • Angiogenesis (formation of new blood vessels)
  • Evasion of host defences
  • Cell surface change (tumour antigens)
  • many others…
17
Q

What are the 6 main hallmarks for cancer?

A
  • Self-sufficiency in growth signals
  • Insensitivity to anti-growth signals
  • Tissue invasion and metastasis
  • Limitless replicative potential
  • Sustained angiogenesis
  • Evading apoptosis
18
Q

What are the malignant tumour modes of spread?

A
  • Local spread
  • Lymphatic spread
  • Blood spread
  • Transcoelomic spread
  • Intraepithelial spread
19
Q

What is metastasis?

A

Spread of the malignant cells to distant organs forming secondary tumours

20
Q

What is metastases?

A

Patterns of spread of cancer cells

21
Q

How are carcinomas spread?

A
  • Lymphatic

- Blood

22
Q

How are sarcomas spread?

A
  • blood (lymphatic spread rare)
23
Q

What are some examples of predictable patterns of spread?

A
  • Lung to local nodes, liver, bone and brain

- Tongue to neck nodes, later lung and spine

24
Q

What is involved in the ‘metastatic cascade’?

A
  • All steps brought about by all different factors that help tumour cells in invasion
  • Tumour cells interact with cells and molecules in the local environment
  • Motility is often enhanced
  • Tumour cells may:
  • Alter adhesion molecules
  • Make poor basement membrane
  • Increase protease production or reduce inhibitors
  • Alter extracellular matrix
25
Q

What is tumour grading?

A

Biological nature of the tumour (histopathology)

  • Dependent on the changes of the tissue
  • The more like the original tissue the better it will respond to treatment
26
Q

What is tumour staging?

A

Extent of spread - clinical

- By observation or by imaging

27
Q

In tumour grading what is assessed?

A
  • Invasion into the underlying tissue
  • Cellular atypia (do the cells look like the original cells?)

Various methods to do this:

  • Numerical grades e.g. 1, 2, 3
  • Low, intermediate, high
  • Degree of differentiation e.g. well differentiated, moderate and poor
28
Q

What does cancer staging describe?

A

The EXTENT or SEVERITY of a person’s cancer. Knowing the stage of the disease helps planning treatment and estimating the person’s prognosis

29
Q

What tests are used to determine cancer staging?

A
  • Physical exams
  • Imaging procedures
  • Lab tests
  • Pathology and surgical reports
30
Q

What is the TNM system?

A
  • Used for staging oral cancer
  • Tumour size (T)
  • Lymph node involvement (N)
  • Presence of metastases (M)
31
Q

What are the clinical effects of lung cancer?

A
  • Cough
  • Haemoptysis
  • Chest pain
  • Pneumonia
32
Q

What are systemic effects often caused by cytokines or hormones released by tumour cells or dysfunction of the organ?

A
  • Fever
  • Anorexia
  • Extreme weight loss
  • Neurological problems
  • Endocrine syndromes
  • Metabolic effects
33
Q

What is the treatment of malignant tumours?

A
  • Depends on type, grade and stage
  • Surgery
  • Chemotherapy
  • Radiotherapy
  • All 3 approaches may be used at different stages
34
Q

What is tumour immunology?

A

Using a patients own immune system to attack malignancies

35
Q

How does the immune system recognise tumour cells?

A

Tumour associated antigens

  • Products of mutated genes
  • Overexpressed proteins
  • Viral proteins
  • Oncofoetal antigens
  • Others
36
Q

What is elimination in the body’s immune response to tumour antigens?

A
  • Cytotoxic T-lymphocytes (CD8+)
  • NKC - first line defence against tumour cells
  • Macrophages - mechanisms similar to anti-microbial killing
37
Q

Escape: How do tumour cells evade the immune response?

A
  • Alter tumour antigen expression. Lack of T cell recognition
  • Activation of immunoregulatory pathways leading to T cell unresponsiveness and apoptosis
  • Immunosuppressive factors e.g. cytokines. Inhibit T cell response
38
Q

What are the possible methods of immunotherapy?

A
  • Active immunization
  • Reversal of immunosuppression
  • Adopted cell transfer
  • Strengthening natural immune responses
39
Q

When is immunotherapy generally used?

A
  • In advanced stages of the disease

- However more research is needed

BDS1 Pathology (14 decks)

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