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Pathological Processes > Session 9: Neoplasia 3 > Flashcards

Session 9: Neoplasia 3 Flashcards

1
Q

Define carcinogenesis.

A

Basically causes of cancer.

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2
Q

Give common intrinsic host factor of carcinogenesis.

A

Hereditary
Age
Sex (mainly hormonal)

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3
Q

Give common extrinsic factors of carcinogenesis.

A

Environment

Lifestyle/behavioural

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4
Q

About 30% of cancer deaths are due to what five leading behavioural factors?

A 
High BMI
Low fruit and vegetable intake
Lack of physical activity
Tobacco
Alcohol
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5
Q

Which of the five leading behavioural factors is associated with approx. 25% of all cancer deaths?

A

Tobacco smoke

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6
Q

Extrinsic carcinogens fall into three main categories.

Which?

A

Chemicals
Radiation
Infection

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7
Q

Explain exposure to onset of extrinsic carcinogens.

A

There can be a long delay between carcinogen exposure and the malignant neoplasm onset.

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8
Q

Which factors of extrinsic carcinogens affect the likelihood of developing malignant neoplasms?

A

The carcinogenic dosage.

The exposure in terms of time.

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9
Q

Explain organ specificity for carcinogens.

A

Different chemicals usually cause different types of cancers.

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10
Q

Give common industrial carcinogens.

A

Asbestos
Coal tars
Vinyl chloride

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11
Q

In which people would you most commonly find cancers associated with industrial carcinogens?

A

People who work in such industries.

This emphasises how important dosage and time exposure is.

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12
Q

How can chemical carcinogens be subdivided?

A

Into initiators which are and promoters.

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13
Q

Briefly explain initiators.

A

Mutagens -> causing mutations

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14
Q

Briefly explain promoters.

A

Cause prolonged proliferation in target tissues.

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15
Q

Give classifications of mutagenic chemical carcinogens. (Initiators)

A 
Polycyclic aromatic hydrocarbons
Aromatic amines (like 2-naphthylamine)
N-nitroso compounds
Alkylating agents (Vinyl chloride)
Natural products (aflatoxin and asbestos)
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16
Q

Explain what pro-carcinogens are.

A

Inactive carcinogens which needs activation to be carcinogenic.

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17
Q

How are pro-carcinogens activated?

A

By P450 enzyme in the liver.

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18
Q

What are complete carcinogens?

A

Carcinogens which are both initiators and promoters.

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19
Q

How can radiation cause mutation?

A

By direct DNA damage -> altering bases or single/double strand break

By indirect DNA damage by generation of free radicals

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20
Q

Most common radiation exposures.

A

UV leading to increased skin cancer risk
Ionising radiation from radon from earth’s crust.
Medical tests such as x-ray, CT etc.

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21
Q

How are infections carcinogenic?

A

Some directly affect genes that control cell growth.

Some indirectly affect growth by causing chronic tissue injury.

22
Q

How can chronic tissue injury from infection be carcinogenic?

A

The resulting regeneration can act as a promoter for any pre-existing mutations.
Others can cause new mutations from DNA replication errors.

23
Q

Give common infections which are carcinogenic.

A 
HPV
Hep B and C
Helicobacter pylori
Parasitic flukes
HIV
24
Q

Explain how HPV (Human Papilloma virus) is carcinogenic.

What kind of cancer does HPV usually cause?

A

Strongly linked with cervical carcinoma.
A direct carcinogen which expresses E6 and E7 proteins which inhibit p53 and pRB protein function respectively.

Both p53 and pRB are both important for cell proliferation.

25
Q

Explain how Hep B and Hep C are carcinogenic.

A

Cause chronic liver cell injury. The chronic inflammation and the regeneration in the liver which ensues can act as either promoters or initiators.

This means that Hep B and Hep C are indirect carcinogens.

26
Q

What kind of cancer is associated with Helicobacter pylori and why?

A

Gastric cancer due to chronic gastric inflammation.

27
Q

What kind of cancers are associated with parasitic flukes, and why?

A

Cholangiocarcinoma and bladder carcinomas due to inflammation in bile ducts and bladder mucosa.

28
Q

Explain how HIV is carcinogenic.

A

It is not carcinogenic in itself but indirectly. HIV lowers immunity making host more susceptible to other infections which can be carcinogenic.

29
Q

Briefly explain retinoblastoma.

A

Malignant retina tumour which is autosomal dominant.. Mutation in RB gene which is a tumour suppressant gene.

30
Q

What is the two hit hypothesis?

A

Two hit hypothesis refers to cancers caused by inactivation of tumour suppressant genes. It explains the differences between tumours occurring in families and those in general population.
Two hit mutations involves the mutation of one allele of a tumour suppressant which can either be through germline and then somatic mutation.

Or two somatic mutations of the same gene of the same cell.

31
Q

What is familial retinoblastoma?

A

Hereditary cancer where the first hit was delivered through the germline, in familial retinoblastoma it is due to mutation in RB which is passed on from mother or father. Another (second hit) somatic mutation then occurs causing retinoblastoma, this is during the development of the retina.

32
Q

What is sporadic retinoblastoma?

A

Non-hereditary cancer. This is caused by the first hit being a somatic mutation and not germ line. The second hit is also somatic and in the same cell. Also during the development of the retina.

33
Q

What are tumour suppressor genes?

A

Genes that inhibit neoplastic growth.

34
Q

What are oncogenes?

A

Genes that enhance neoplastic growth.

35
Q

What are proto-oncogenes?

A

Inactivated oncogenes.

36
Q

What is the main difference in activation of proto-oncogenes and deactivation of tumour suppressor genes?

A

TSG needs inactivation of both alleles

POG only needs activation of one allele to be activated

37
Q

What is RAS? Explain what it does.

A

It is an oncogene which is mutated in approx. a third of all malignant neoplasms.
The RAS proto-oncogen encodes a small G protein that relays signals into the cell. These signals will push the cell past cell cycle restriction point (RP is a point where the cell becomes committed to the cell cycle, acts as a threshold).

A mutant RAS encodes a protein which is instead always active and will produce a constant stimulus to pass through the cell cycle’s restriction point so the cell just keeps dividing.

38
Q

Explain what RB does.

A

RB is a TSG. It restrains cell proliferation by inhibiting passage through restriction point. This means that it inhibits further mitotic divisions.

If both alleles are inactivated mitosis can keep occurring.

39
Q

Give examples of what proto-oncogenes can encode.

A 
Growth factors
Growth factor receptors
Plasma membrane signal transducers
Intracellular kinases
Transcription factors
Cell cycle regulators
Apoptosis regulators
40
Q

Give examples of what TSGs can encode.

A

The same as proto-oncogenes but in the opposite way.

41
Q

What are caretaker genes?

A

Prevent accumulation of DNA damage. They are a class of TSGs which promote genetic stability.

42
Q

What is Xeroderma pigmentosum?

A

Autosomal recessive disease du to mutation in one of 7 genes that affect DNA nucleotide excision repair.
Patients are sensitive to UV radiation at young age and can therefore develop skin cancer.

43
Q

Give examples of DNA damage which caretaker genes prevent accumulation of.

A

Nucleotide excision
Mismatch
Double-strand breaks
Single-strand breaks etc…

44
Q

What happens if you have a mutation in a caretaker gene?

A

It means that the repair of DNA is not functioning correctly.

45
Q

What is hereditary non-polyposis colon cancer syndrome?

A

HNPCC is an autosomal dominant syndrome associated with colon carcinoma. There is a germline mutation in this condition which affects several caretaker genes responsible for DNA mismatch repair.

46
Q

What caretaker genes are familial breast carcinoma associated with?

A

BRCA1 or BRCA2 which are important for the repair of double strand DNA breaks.

BRCA1 and BRCA2 mutations can be found in many sporadic malignant neoplasms as well.

47
Q

What is genetic instability? What does it lead to?

A

Any mutation in caretaker genes which leads to less repair of damage.
This can be nucleotide instability, microsatellite instability or chromosomal instability.

It leads to increased mutation rate.

48
Q

Can a single mutation lead to malignant neoplasm?

What is the usual course of malignancy?

A

No, multiple mutations are needed.

It usually starts as an adenoma. Early adenoma -> later adenoma -> primary carcinoma -> metastatic carcinoma.

There is an accumulation of mutations throughout what usually is years of change.

The steady accumulation of these mutations is called cancer progression.

49
Q

How many mutations are usually needed for the evolution of a malignant neoplasm?

A

Ten or less.

50
Q

What are hallsmarks of neoplasms.

A

Features which cancer exhibits in order to classify it as cancer.

51
Q

Give the six hallmarks of neoplasms

A
  1. Self-sufficiency in growth signals (autonomy)
  2. Resistance to growth stop signals
  3. No limitation in how many times the cell can divide also called cell immortalisation.
  4. Angiogenesis
  5. Resistance to apoptosis
  6. Ability to invade and produce metastases.
52
Q

Which hallmarks are seen in benign vs malignant neoplasms?

A

1-5 found in benign.

1-6 found in malignant.

Pathological Processes (14 decks)

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