Brainscape's Knowledge GenomeTM

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


See full index

Neoplasia > Causes of cancer > Flashcards

Causes of cancer Flashcards

1
Q

What is another phrase for cancer progression?

A

Darwinian clonal evolution

Each mutation gives a survival or fitness advantage to the neoplastic cell in that particular environment

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

What are the three major sources of risk factors?

A

Populations/ occupational risk/ direct accidental exposure

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

How is cigarette smoking linked to cancer?

A

Smoking 10 a day increases risk by x10

Cause 30% cancer UK (higher with passive smoking)

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

What are the environmental factors?

A

Chemicals/ radiation/ Infectious agents

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

What are the occupational risks?

A
  • Historically= scrotal cancer chimney sweeps/ bladder cancer in dye industry workers
  • Contemporary= Cervix and anal sex workers/ mesothelioma building and construction (asbestos)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Examples of direct exposure radiation

A

Hiroshima
iatrogenic contrast medium in diagnostic radiology radiation for thyroid disease in childhood X-rays during pregnancy- leukaemia

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

What are chemical carcinogens?

A

Mutagens, most are metabolically inactive pro-carcinogens, need to be activated to an active form= ultimate carcinogen, highly reactive electrophilic molecules, directly damages DNA

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

What specificity do chemical carcinogens show?

A

Tissue/ stage/ species

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

Examples of synthetic chemical carcinogens

A

Require in vivo activation

  • polycyclic hydrocarbons (tar and cigarette)
  • aromatic amines and azo dyes (removal of glucuronyl groups= cancer)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Examples of naturally occurring chemical carcinogens

A
  • Nitrosamines (amines+nitrates stomach acid)

- Aflatoxin (peanut contaminant)

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

What are the types of radiation?

A

-Ionising (alpha, beta, gamma, x-rays, neutrons)
Radiation exposure measured as energy absorbed per unit of tissue, 1 gray= 100 rads
Damages DNA by making tracks of free radicals
-UV light (photo-activates adjacent pyrimidines- dimers)
Nucleotide excision repair pathway

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

Describe the epidemiology of retrospective human carcinogens

A
  • Bladder cancer (dye workers)
  • Pleural Malignant Mesothelioma= asbestos
  • Bronchus Squamous Cell Carcinoma= cigarette smoke
  • Tongue Squamous Cell Carcinoma= pipe smoke
  • Head and Neck Squamous Cell Carcinoma= tobacco chewers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the infectious agents?

A
  • Parasites (Schistosoma haematobium= bladder wall, chronic inflammation)
  • Bacteria (Helicobacter pylori- gastric carcinoma and lymphoma)
  • Viruses (prevented by prophylactic immunisation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What human viral infections are associated with cancers?

A
  • Carcinoma cervix= HPV 16,18
  • Hepatocellular carcinoma= hepatitis B and C
  • Kaposi’s sarcoma= human herpesvirus type 8
  • Adult T cell leukaemia= human T cell lymphotropic virus type 1
  • Nasopharyngeal carcinoma/ Burkitt’s lymphoma/ Post-transplant lymphoproliferative disorder/ Hodgkin’s lymphoma= EBV (Epstein- Barr virus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Koch’s postulates?

A

Classical demonstration that infection causes disease
Agent isolated from each case of disease/ isolate grown in culture as clone isolate/ disease induced in animals by inoculation of cultured isolate
Difficult/ impossible for putative human tumour viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the alternative to Koch’s postulates?

A
  • Detect viral genomes in each cancer biopsy
  • Clone the viral genome from a cancer biopsy
  • Transfect cloned viral genomes into normal cells and show biological effect (immortalisation)
17
Q

What is promoter activity?

A

Multiple proliferative events will increase the risk of mutation and fix (make permanent) these mutations
Probability of mutation increases with cell division

18
Q

What oncogenes are activated in Burkitt’s lymphoma?

A

c-myc due to t(8;14)

Rare cancer in children in African Malarial Zone

19
Q

How do retroviruses activate oncogenes?

A
  • Transduction
  • Insertional mutagenesis (proviruses integrated close to oncogenes)
  • Transactivation (virus protein acts as transcription factor)
20
Q

How is HTLV-1 thought to act by?

A

Transactivation of genes encoding cell cycle competence factors in T cells (IL-2)
Tax protein of HTLV-1 may also activate genes important in the spindle assembly checkpoint
All rare events but if viral gene expression persists then rare events become more probable

21
Q

How does HPV (16/18) inactivate tumour suppressor genes?

A

Two viral oncogenes in viral genome E7 and E6
E7 binds unphosphorylated pRB (releasing E2F), deregulating pathway
E6 binds and targets p53 for degradation

22
Q

How does HHV-8 inactivate tumour suppressor genes?

A

Encodes a homologue of cyclin D that phosphorylates Rb

Encodes a homologue of bcl-2 that inhibits apoptosis

23
Q

What is the link between HPV and cervical carcinomas?

A

99.7%

Mucosal HPV infection can cause vulval/ vaginal, anal, penile and oral/ throat pre-cancerous lesions and genital warts

24
Q

What is the history of HPV?

A 
1976= koilocytes found in low grade CIN= characteristic cells of wart virus HPV so link 
1983/4= HPV DNA detected and cloned in cervical cancer- 16/18 not 1 (skin) or 6/11 (genital warts)
25
Q

How is HPV common?

A

Transmitted by intimate contact
80% sexually active women will be exposed to the virus by age 50
Most infections regress spontaneously 6-12 months after
Persistent infection= cancer/ other dieases

26
Q

How is HPV associated with cervical cancer?

A

HPV DNA sequences from 15 HPV types are detected in over 99% of cancers
HPV 16 most prevalent (50-60%)
HPV 18 10-30% in Europe, more prevalent in Africa
Same HPV DNA sequences detected in 90% high grade CIN (CIN 2/3)

27
Q

Describe a HPV particle

A 
Non-enveloped, double stranded DNA viruses
8kb circular genome 
At least 100 genotypes
Epitheliotropic
Associated with warts and neoplasia
28
Q

What is high risk HPV?

A

Cause high grade CIN- 40% progress to cancer

DNA sequences detected in both squamous cell carcinoma and adenocarcinoma of cervix

29
Q

What are the three main areas for HPV testing application?

A
  • Triage of patients with low-grade abnormalities
  • Primary screening
  • Follow-up after treatment
30
Q

What are the key features of HPV testing application?

A
  • The effect of age
  • The role of type-specific persistence
  • The high negative predictive value
31
Q

Why are HPV 16 and 18 transforming viruses?

A

Immortalise primary genital keratinocytes in culture

E6 activates telomerase

32
Q

How are neutralising antibodies involved in HPV prevention?

A

Directed against the L1 capsid protein but generation of such L1 protein requires the tertiary or native structure of the protein- can’t grow in tissue culture

33
Q

How are HPV vaccines made?

A

Virus-like particles (VLP)
-Cut L1 gene from virus DNA
-Paste DNA into DNA of another microbe (yeast/baculovirus)
-Grow recombinant microbe in large amounts
Chemistry of protein self-assembles into VLP

Neoplasia (13 decks)

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