Brainscape's Knowledge GenomeTM

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


See full index

Pathological Processes > Session 9 > Flashcards

Session 9 Flashcards

1
Q

How many cases of cancer are preventable?

A

38%

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

What are the intrinsic causes of cancer?

A
  • Heredity
  • Age and prolonged lifespan (constant accumulation of mutation and lower immunodefences of people)
  • Sex (hormones)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the extrinsic causes of cancer?

A
  • Environment (chemicals, radiation, infection)

- Behaviour

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

How can cancer be prevented?

A
  • Smoking (biggest factor!)
  • Maintaining a healthy weight
  • Sun safety
  • Balanced diet
  • Less alcohol
  • Activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What cancers can be prevented by smoking?

A

Mouth, pharynx, noes, oesophagus
Liver, stomach, kidney,
Some leukaemia

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

What are the EXTRINSIC factors of carcinogenesis?*

A
  • Chemicals
  • Viruses
  • Radiation
  • Infection

Will cause initiation and promotion

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

What are INTRINSIC factors of carcinogenesis?*

A
  • Inherited mutation (initiation and promotion)

- Chronic inflammation (promotion)

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

What factors of carcinogenesis are mutations?*

A

Can be both extrinsic and intrinsic:

  • Monoclonal population
  • Gaining additional mutation to progress
  • Deregulated cell signalling pathways results in hallmarks of cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What percentage of cancer risk do environmental/extrinsic factors count for?*

A

85% (reduction past generations of migrants so environmental factors)

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

What can be the hereditary causes of cancer?

A
  • Autosomal dominant genes: ‘guaranteed’ cancer

- Less frequent genes (eg. having a first degree relative) = more neoplastic phenotype

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

What chemical used in dye manufacturing causes cancer and how does it do that?

A

2-NAPTHYLAMINE

  • Long delay (decades) between carcinogen exposure and malignant neoplasm onset
  • Risk depends on total carcinogen dosage
  • Sometimes organ specificity (bladder)
  • Present in cigarettes and so smokers at increased risks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does chemical carcinogenesis occur?*

A
  • Initiation and promotion
  • Initiators come first and then are followed by promoters
  • Promoters take many years (growth, growth factor pathways, proliferation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What chemicals can cause cancer?

A
  • Alkylating agents (vinyl chloride)
  • Benzopyrene (cigarette smoke)
  • Asbestos
  • Aflatoxin
  • 2-naphthylamine (aromatic amine)
  • Aromating agents
  • N-nitroso compounds (created in stomach on nitrite exposure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is radiation and what are some examples of radiation?

A

Any type of energy travelling through space, some forms being mutagenic by causing direct DNA damage or generating free radicals (hydroxyl radicals)

  • Alpha, beta particles, gamma rays, X rays, UV rays
    (25% of malignant neoplasms)

Beware of medical testing (CT, X rays)

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

How can infections cause cancer?

A
  • Directly affecting genes that control cell growth (eg. HPV)
  • Indirectly by causing chronic tissue injury and regeneration acting as a promoter for pre-existing mutation or causing new mutation (eg. Hepatitis B by chronic inflammation )
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What can cause cancer by reduced immunity?

A

HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does HPV cause cancer and what cancers is it associated with?

A
  • Makes E6 and E7 proteins
  • Virus infects cells and ensures they don’t die
  • Then hijacks DNA to make more virus
  • E6 inhibits p53 (tumour suppressor) so preventing apoptosis
  • Hijacks cell cycle by interfering with retinoblastoma protein which is a cell cycle checkpoint
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do you test if something is a carcinogen?*

A

Use media with minimal histidine and a high number of revertants (his- to his+) suggests that it causes mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is an initiator?

A

Anything that can cause a mutation

20
Q

What is a promotor?

A

Anything that causes the expansion of initiator population

21
Q

What is a pro-carcinogen?

A

Pro-carcinogen is converted into a carcinogen by cytochrome P450 in the liver

22
Q

What is a complete carcinogen?

A

A carcinogen capable of being an initiator and promoter

23
Q

What is familial retinoblastoma?

A

Cancer of the eye that is inherited (family) - about 40% of retinoblastomas

24
Q

What are the 2 types of retinoblastoma?

A
  • Bilateral - earlier (greater increase due to gene inheritance, 40%)
  • One eye - later (sporadic due to mutation, needs 2 sporadic hits and is happening later in one eye, 60%)
25
Q

How does familial inheritance cause retinoblastoma?

A
  • First hit at germline as one abnormal cell
  • Hit 2 occurs as going through life
    = Retinoblastoma
26
Q

How does sporadic mutation cause retinoblastoma? (2-hit hypothesis)

A
  • 2 normal cells into germline
  • Over time get one hit
  • Time passes, get second hit
    = Retinoblastoma
27
Q

What is the retinoblastoma gene?

A

2 forms: active hypophosphorylated and inactive hyperphosphorylated

  • Negative regulator of G1/S checkpoint
  • Allows continuous proliferation
28
Q

What is the RAS gene?

A

The most common type of abnormality involving human tumours and proto-oncogenes

  • Mutated in 15-20% of all malignant neoplasms
  • Higher (90%) in some cancers, eg. pancreatic adenocarcinomas
29
Q

How does the RAS gene work normally?*

A
  • RAS encodes a small G protein binding to GTP
  • Conformational changes
  • Enters cell, makes cyclin D
  • Activates CDK
  • Retinoblastoma gets hyperphosphorylated and allows cell to progress to the next point of the cell cycle
30
Q

What happens when RAS gets a mutation?

A

eg. point mutation allows RAS to be permanently switched on
- Permanently activates RB gene
- Constant proliferation
= Cancer

31
Q

How do proto-oncogenes and tumour suppressor genes work?*

A

Together but opposing function

RAS = proto-oncogene, tumour suppressor gene is trying to stop it from happening

32
Q

Where must abnormalities occur to create cell cycle restriction?

A

ACCUMULATION

  • Proto-oncogene: one abnormality
  • Tumour suppressor: two abnormalities
33
Q

What can proto-oncogenes encode?*

A

SLIDE 26

34
Q

What genes prevent accumulation of DNA damage?

A

Caretaker genes (some neoplasms caused by indirectly affecting DNA repair)

35
Q

What is hereditary non-polyposis colon cancer? (HNPCC)

A

An autosomal dominant syndrome that is associated with colon cancer, where the germline mutation affects one of several DNA mismatch repair genes

36
Q

What is xeroderma pigmentosa (XP)?

A

An autosomal recessive disease due to mutation affecting DNA nucleotide excision repair

37
Q

What are the effects of xeroderma pigmentosa?

A
  • Skin that is very sensitive to UV damage

- Developing skin cancer at a very young age

38
Q

What genes cause familial breast carcinoma?*

A

BRCA1/BRCA2 genes which are normally unrelated to each other and are expressed in the breast

39
Q

What are BRCA genes involved in?

A

Repairing double strand DNA breaks

40
Q

What are the signs that the breast carcinoma is a BRCA mutation?

A
  • DNA damage cannot be repaired and mutations accumulate

- Breast cancer development at a younger age

41
Q

What do chromosome aggregations contribute to in malignancies?

A

Accelerated mutation rate (genetic instability)

42
Q

What genes maintain stability?

A

Caretaker genes (tumour suppressor genes)

43
Q

How does 80% of colorectal cancer develop?*

A

Gradual accumulation of gene abnormalities

dysplasia - intermediate then late adenoma - carcinoma - metastases

44
Q

How many mutations do malignant neoplasms usually consist of?

A

Around 10 but variable by tumour type and individual

45
Q

What are the hallmarks of cancer?

A
  1. Self-sufficient growth signals (proliferate with no need for stimuli)
  2. Resistance to growth stop (tumour suppressor faulty)
  3. Limitless cell division number (telomerase activation)
  4. Sustained angiogenesis (VEGF)
  5. Resistance to apoptosis
  6. Ability to invade and produce mets (EXCLUSIVE TO MALIGNANT NEOPLASMS)

Pathological Processes (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions