Smoking Cancer And The Environment Flashcards

1
Q

Neoplasia

A

Autonomous or independent growth of an abnormal cell or tissue
Growth of which is more rapid than normal tissues and continues after the stimulus that initiated new growth is removed

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2
Q

Lifetime cancer risk

A

1 in 2
1 in 3 in developed world

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3
Q

What factors contribute to individuals cancer risk

A

Hereditary genetic factors
Environment/ lifestyle
Age

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4
Q

What is the development of tumours dictated by

A

Interaction between exogenous environmental factors endogenous process and host genetics

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5
Q

Environmental factors contributing to individuals cancer risk

A

Exposure to carcinogenic substances
Radiation
Oncogenic viruses

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6
Q

Lifestyle factors contributing to individuals cancer risk

A

Diet
Smoking
Weight
Exercise

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7
Q

Exogenous agents as sources of dna damage

A

Chemical
Radiation

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8
Q

Endogenous processes as sources of dna damage

A

Cellular metabolism
Replication stress
Spontaneous

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9
Q

Mutation drivers

A

Endogenous spontaneous
Exogenous induced

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10
Q

Endogenous spontaneous mutations

A

Errors in dna replication (dna polymerase)
Deaminatiom (cytosine to uracil)

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11
Q

Exogenous induced mutations

A

Exposure to endogenous carcinogens
Exposure to environmental carcinogens

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12
Q

Carcinogens reacting with dna to cause mutations

A
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13
Q

What is found in cigarette smoke and burnt toasts

A

Polycyclic aromatic hydrocarbons
Benzo a pyrene
Is a pro carcinogen
Activated by cytochrome p450

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14
Q

Mechanism of action of polycyclic aromatic hydrocarbons

A

Intercalates in DNA (forms bulky adducts)

-Covalently binds to Adenine and Guanine bases

-Leads to base pair changes in DNA

-Purine to pyrimidine transversion (Adenine to Thymine)

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15
Q

What do mutations in polycyclic aromatic hydrocarbons cause

A

Activation of proto oncogenes
Inactivate tsp

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16
Q

Uv mediated dna damage

A

Direct and indirect dna damage
Cross linking adjacent thymine bases
Prevents dna polymerase function

17
Q

Ionising radiation definition

A

Radiation that Carries enough energy to free electrons from atoms or molecules thereby ionising them

18
Q

Source of ionising radiation

A

X rays
Used in radiotherapy
Kill cancer cells

19
Q

Exposure to ionising radiation

A

Leukaemia
Breast
Thyroid

20
Q

Exposure to uv radiation

A

Basal cell carcinoma
Squamous cell carcinoma
Melanoma

21
Q

Polycyclic hydrocarbons as an agent

A

Exposes in building fuel and dye industries
Skin lung and bladder cancer

22
Q

Aromatic amines 2-napthylamine

A

Rubber and plastic industries
Bladder cancer

23
Q

Benzene

A

Drugs plastic rubber and dye industries
Leukaemia

24
Q

Asbestos

A

Construction of buildings and ships
Mesothelioma cancer

25
Q

Mesothelioma

A

Malignant cells in the mesothelium linings around lungs abdomen and heart
Pleura peritoneum and pericardium respectively

26
Q

Environment and lung cancer

A
27
Q

Genetic predisposition to cancer

A

Xeroderma pigmentosum
Autosomal recessive inherited condition
Mutations inxeroderma pigmentosum genes, defect in NER
sensitivity to sunlight so 1000 fold significance incidence of skin cancers

28
Q

HPV

A

Human papilloma virus
Benign warts
Cervical cancefx

29
Q

Hepatitis b and c

A

Liver cancer.

30
Q

EBV

A

Epstein Barr virus
Burkitt lymphoma

31
Q

HIV

A

Kaposi sarcoma

32
Q

HPV16

A

One of most common stds in young people
Higher in women
Biggest causative agent of cervical cancer and genital warts
Causes cancers by deregulating p53 and rb

33
Q

HPV16 mechanism

A
34
Q

Activating mutations to proto oncogenes

A

Ras
Raf
Myc

35
Q

Inactivating mutations to tumour suppressor genes

A

APC (colorectal cancers)
CDK inhibitors e.g. wee1
P53 (master regulator)

36
Q

Base excision repair BER

A

Removal of modified bases in the DNA

37
Q

Nucleotide excision repair NER

A

Repairs bulky distortions in DNA

  • Repairs polycyclic aromatic hydrocarbon adducts and UV cross links
  • Key protein in repair pathway is xeroderma pigmentosum (XP)
38
Q

DNA double stranded breaks

A

Most dangerous type of DNA damage

  • Pathway 1: rapid Non-Homologous End Joining (NHEJ) and
  • Pathway 2: slower Homologous Recombination Repair (HRR) involving BRCA