Neoplasia 3 Flashcards

1
Q

What is carcinogenesis

A

The causes of cancer

For example intrinsic causes : hereditary ( autosomal genes more likely to give cancer , for example BRACA1 Gene is autosomal dominant), age ( as we get older , our immune system gets naturally compromised) , sex ( this is particularly hormone driven)

Extrinsic factors : chemicals , radiation , infection , behaviour

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2
Q

How can cancer be prevented ?

A

4 in 10 cases of cancer can be prevented

  • smoking
  • maintain a healthy weight
  • healthy balanced diet
  • sun safety
  • cut back on alcohol
  • being active ( this is independent on BMI , your BMI could be good but you need to exercise )
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3
Q

What is the second biggest cause of cancer ?

A

Overweight and obesity

Keeping a healthy weight reduces the risk of 13 different types of cancer

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4
Q

What is the biggest cause of cancer ?

A

Smoking

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5
Q

Name a few chemicals that can cause mutations

A
  • benzopyrene( found in cigarettes )
  • N-nitroso compounds : contained in foods that are high in nitrites for example pickled foods.
  • vinyl chloride ( alkylating agents ) - found in plastics
  • Aflatoxin B1 - common factor that contributes to liver cancer
  • Asbestos : this acts as a promoter because it promotes the mutation , but also an initiator.
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6
Q

What is a pro-carcinogens

A

They are activated by cytochrome P450 in the liver which converts them into carcinogen.

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7
Q

What is a complete carcinogen ?

A

Something that is able to act as a initiator and promoter for example Asbestos

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8
Q

How does radiation contribute to cancer - acti g as an initiator

A

They can either damage DNA directly or they can damage DNA indirectly by generating free radicals. Examples would be alpha particles , beta particles , gamma rays , X-rays and UV rays,

25% of all malignant neoplasms are skin neoplasms for example UV ionising radiation.

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9
Q

How can infections contribute to cancer ?

A

Infections can act as initiators and promoters. Some can directly affect genes that control cell growth. ( HPV)

But some can act indirectly : as a promoter to pre existing mutations OR can cause new mutations from DNA replication errors. Or causing chronic tissue injury. ( Hep B) ( HIV )

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10
Q

What is human papilloma virus. ( HPV ) ? And how does it overtake our cervical cells

A

Associated with cervical carcinoma

  • it makes two proteins E7 and E6. The virus infects the cell , ensures it doesn’t die and then hijacks the DNA replication machinery to make more virus particles. E6 inhibits p53 which prevents cell from undergoing apoptosis. Hijacks cell cycle by interfering with Retinoblastoma protein which is important as a cell cycle checkpoint.
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11
Q

What is a retinoblastoma gene

A

A key negative regulator of G1/S cell cycle checkpoint

It also controls cellular differentiation.

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12
Q

What are protonated onco genes

A

They are involved in signalling pathways that drive proliferation’s. Mutation skin these genes means that there were will be an increase in proliferation.

The RAS gene is the first human oncogene that was discovered. This is the most common type of abnormality invoking proto onco genes in human tumours. They are mutated in approx 15-20% of all malignant neoplasms.

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13
Q

Outline the process of RAS gene working in a normal cell vs abnormal

A

X

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14
Q

What is xeroderma pigmentosa

A

Autosomal recessive disease

Due to mutations in one of 7 genes that affect DNA nucleotide excision repair.

Very sensitive to UV damage and develop skin cancer at a young age.

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15
Q

What is the most common cause of familial breast carcinoma ?

A

BRCA1 /BRCA2 genes mutations

Involved in repairing double strand DNA breaks

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16
Q

What does a cancer have to be able to do in order to survive ? ( Hallmarks of Cancer )

A

Self sufficiency in growth signals

Resistance to growth stop signals

Cell immortalisation ( no limitation of the number of times a cell can divide)

Sustained ability to induce new blood vessels ( the bigger the tumour gets , the more blood vessels it requires because it needs oxygen and own nutrient supply)

Resistance to apoptosis

Ability to invade and produce metastases