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MoD > Lesson 8 > Flashcards

Lesson 8 Flashcards

1
Q

What is neoplasm?

A

Newly- formed collection of cells resulting from abnormal cellular proliferation - persists after initial stimulus is removed.

neo = new
plasm = formed material
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2
Q

Describe a benign lipoma

A

Well circumscribed, slow growing, non-invasive, closely resembled the tissue of origin (fat)

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3
Q

Explain uterine fibroids

A
  • Most common benign tumours in women of childbearing age
  • Development of fibroids increases with age
  • Present in 80-90% of all women by age 50 years.
  • Cause pain, excessive menstrual bleeding or infertility
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4
Q

Describe meningioma

A

Most frequently reported primary CNS tumours (approx. 36% of all CNS tumours)

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5
Q

The etiology of cancer is _____________ (i.e. it is caused by _____ and ______ factors)

A

Multi factorial
Intrinsic
Extrinsic

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6
Q

Give examples of intrinsic factors?

A 
Genetic mutations
Age
Ethnicity 
Gender
Family disease history
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7
Q

Give examples extrinsic factors?

A

Environment influences/lifestyle choices:

- physical exercise
- diet
- weight management 
- tobacco intake 
- exposure to environmental pollutants 
- infections 
- exposure to chemical carcinogens 
- exposure to radiation 
- alcohol intake
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8
Q

What are some examples of carcinogenic agents?

A

Polycyclic aromatic hydrocarbons (PAHs) - benzopyrene -> lung/skin cancer
Aromatic amines - 2 naphthylamine -> urinary bladder disease
Nitrosamines - sodium nitrate -> gut cancers
Asbestos -> malignant mesothelioma, lung carcinoma

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9
Q

Most _________ enter the body as __________, which are then converted to _________ by cellular machinery

A

Carcinogens
Procarcinogens
Carcinogens

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10
Q

Describe benzopyrene

A

Is a procarcinogen - one of the main carcinogenic agents in cigarette smoke
Must first be oxidized by cytochrome P4501A1 -> modified by other enzymes -> benzopyrene diol epoxide -> binds covalently to DNA -> form an adduct where it causes mutations

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11
Q

What is the effect of ionising radiation on the body?

A

strips electrons from atoms and includes X-rays

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12
Q

Describe nuclear radiation

A

Arising from radioactive elements. Nuclear radiation comprises alpha particles, beta particles and gamma rays

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13
Q

What can UV light not penetrate?

A

Cannot penetrate deeper than the skin

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14
Q

How does radiation cause cancer?

A
  • Radiation can damage DNA directly
  • Misrepairs by DNA repair proteins allow the mutation/chromosomal rearrangement to persist
  • Radiation can damage DNA indirectly by:
    • Generating free radicals.
    • Producing secretable soluble factors that can affect distal non- irradiated cells
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15
Q

What are some occupations that are associated with the development of tumours?

A

Construction - asbestos -> lung, stomach, larynx
Painters - solvents -> childhood brain tumours
Aircrew, nuclear worked - ionising radiation -> bone, liver, lung
Farming, agriculture - pesticides -> soft tissue sarcoma, lung

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16
Q

What are the stages of carcinogenesis?

A

Initiation - carcinogen/UV:
- irreversible genetic mutation in stem cell/progenitor cell
Pronation - tumour promoter/UV:
- clonal expansion of initiated cells within generalised hyperplasia
- outgrowth of pre-malignant tumours = papillomas
Progression:
- malignant conversion to invasive carcinoma

-> metastasis

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17
Q

What is the latency period in carcinogenesis?

A

Long interval between exposure to a carcinogen and clinically-detectable neoplasia

18
Q

What are papillomas?

A

Papillomas are pre-malignant (benign) tumours that can ultimately progress (following the acquisition of additional mutations) to an invasive, malignant carcinoma.

19
Q

Animal tests have shown that chemical carcinogens, called ______, must be given first, followed by a ______ class of carcinogens called _______

A

Initiators
Second
Promoters

20
Q

Describe retinoblastoma

A

• A type of eye cancer that usually develops in early childhood <6
• Affects ~1 in every 15,000 children)
• Approximately 60% of cases are sporadic (no family history of
disease).
• Approximately 40% = family history (inherited)
• Mechanism involves loss of the retinoblastoma protein RB the
prototypic tumour suppressor gene

21
Q

Loss of _____ __________ gene function explains the susceptibility of developing _____________

A

Tumour
Suppressor
Retinoblastoma

22
Q

Describe the inheritance pattern for high risk bilateral retinoblastoma

A

Inherited mutation or absence of one of the paired RB1 genes

Mutation or loss of RB1 gene in any retinal cell

23
Q

Describe the inheritance pattern for sporadic retinoblastoma

A

Normally paired RB1 genes
Mutation or loss of one RB1 gene
Mutation or loss of the other RB1 gene in same cell or its daughter cells

24
Q

Describe familial breast cancer (BC)

A
  • BC is the primary cause of cancer- related deaths in women globally.
  • Familial BC - accounts for ~12% of all BC cases
  • Mutations in either BRCA1 or BRCA2 genes, encode BRCA1/BRCA2 tumour suppressor proteins, involved in repairing DNA double-strand breaks feature in ~20-50% of familial BC cases

Mutations in BRCA1/2 are also associated with ovarian cancer, prostate cancer and pancreatic cancer

25
Q

Describe xeroderma pigmentosum (XP)

A

Autosomal recessive due to mutations in one of 7 genes that affect DNA nucleotide excision repair (NER). These patients are very sensitive to UV damage + develop skin cancer at a young age

26
Q

What are the process Ames Test? ( (Exposure of strains of Salmonella typhimurium to potential mutagens)

A

Rat liver extract

  1. Possible mutagen -> plate (media with minimal histidine) -> incubate (high number of revertants suggests the mutagen causes mutations)
  2. Plate (media with minimal histidine) -> incubate (control plate - natural revertants)
27
Q

What are some conditions that can increase the risk of cancer?

A

Ulcerative colitis -> colorectal cancer
Liver cirrhosis -> liver cancer
Hashimoto’s thyroiditis -> thyroid cancer
Chronic strophic gastritis -> stomach cancer

28
Q

Explain indirect carcinogenesis?

A

Chronic tissue injury, where the resulting regeneration acts either as a promoter for any pre-existing mutations or else causes new mutations from DNA replication errors

29
Q

What cancer does the human papillomaviruses (HPVs)?

A

Cervical cancer (also penile cancer, vaginal cancer and others)

30
Q

What cancer does Hepatitis B virus (HBV) and Hepatitis C virus (HCV)?

A

HBV and HCV can cause the long-term (chronic) infections that increase a person’s chance of liver cancer.

31
Q

What cancer can Human Immunodeficiency Virus (HIV)?

A

Kaposi sarcoma

32
Q

What cancer can Helicobacter pylori (bacterium)?

A

Gastric adenocarcinoma

33
Q

HPV-__ and HPV-__ are direct carcinogens that act by ________ cell proliferation and resistance to ________ in infected host cells

A

16
18
Sustaining
Apoptosis

34
Q

Explain HPV-16 and HPV-18?

A

HPV-16 and HPV-18 (DNA viruses) are strongly associated with cervical carcinoma (95- 100% of cases) they express the viral oncogenes E6/E7.

Integration of HPV DNA into the host (human) genome allows the transcription of two oncoproteins (E6 and E7).
E6 inhibits human TP53 function
E7 inhibits human RB1 (pRB) protein function.

35
Q

Explain Epstein-Barr virus (EBV)?

A

Epstein Barr virus (EBV) association frequencies of nasopharyngeal carcinomas (NPC) and Burkitt lymphomas in different geographic areas

36
Q

What are some proto-oncogenes and proteins do they code for?

A 
growth factors (e.g. PDGF),
growth factor receptors (e.g. HER2),
plasma membrane signal transducers (e.g. RAS)
intracellular kinases (e.g. BRAF),
transcription factors (e.g. MYC),
Cell-cycle regulators (e.g. CYCLIN D1)
apoptosis regulators (e.g. BCL2)
37
Q

Explain tumour suppressor proteins (TSPs) ‘the breaks’

A

(e.g. the tumour suppressor transcription factor tumour protein 53 TP53)
regulate the expression of downstream proteins that act to stop the cell-cycle to facilitate DNA repair and/or to induce apoptosis.

38
Q

Explain the difference between proto-oncogenes and TSPs

A

When they have a function-altering mutation, proto- oncogenes can become oncoproteins (i.e. ‘jammed accelerator pedals’)
Conversely, when TSPs don’t work, they effectively become ‘broken break pedals’

39
Q

Explain the implication of a mutation on the RAS proto-oncogene?

A

one component of growth control, the restriction point, can be deregulated either by oncogenic mutations in the RAS protoncogene to yield the RAS oncoprotein or by an the inactivated TSP (tumour suppressor protein) RB.

40
Q

Explain ‘gatekeeper’ proteins

A
  • The tumour-suppressor proteins RB and TP53 are ‘Gatekeeper proteins’
  • TP53 protein (‘The Guardian of the Genome’) is a transcription factor that is involved in regulating expression of several pro-apoptotic proteins
  • TP53 is mutated in >50% of cancers

MoD (11 decks)

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