8- Cancer Biology Flashcards

1
Q

Why do cancerous cells stain yellow with FDG (flourdeoxyglucose)?

A

Cancerous cells exhibit increased glucose uptake. Usually get energy from glycolysis because they are in anaerobic conditions

Tumors will be yellow in the scan

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2
Q

What is the carcinogen Vinyl Chloride associated?

A

liver angiosarcoma

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3
Q

What is the carcinogen Benzene associated with?

A

leukemia

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4
Q

What is the carcinogen Arsenic associated with?

A

Skin and bladder cancer

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5
Q

What is the carcinogen Asbestos associated with?

A

mesotheliema

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6
Q

What is the carcinogen radium associated with?

A

osteosarcoma

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7
Q

What does cytochrome P 450s role in cancer?

A

Can activate some carcinogens (indirect acting agents)

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8
Q

What is the doubling time for breast cancer?

A

100 days

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9
Q

the Philadelphia chromosome is related to chronic myelogenous leukemia (CML) , what is this mutation?

A

Philadelphia chromosome (the small abnormally paired chromosome) is translocation between chromosomes 9 and 22.

Forms oncogene, BCRADL –> associated with proliferation.

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10
Q

What is the ‘proof’ that all cancer arrives from one cell?

A

The inactive X is the same inactive X in all of the tumor.

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11
Q

Cancer progresses through different stages. Example of uteran cancer. What defines low grade intraepithelial neoplasia, high grade intraepithelial neoplasia, and invasive carcinoma?

A

low grade: dividing cells invade lower 1/3 of epithelium.

High grade: cells in all of epithelium are proliferating

Invasive (malignant): cells move through or destroy basal lamina.

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12
Q

Clonal evolution *****

A

cells around each other have the initial mutation. One might get new mutation (cell prolif or decrease cell death) and will try to out compete surrounding cells for malignancy.

Harbor different mix of mutations and competing to be dominant clone in the tumor.

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13
Q

What can cancer stem cells do that is bad?

A

Give rise to all types of cells within the microenvironment of the tumor.

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14
Q

Two ways that tumors can break off and spread to others.

A
  1. cross into blood stream

2. cross into lymphatic system.

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15
Q

Why is it important to know that a tumor is a microenvironment?

A

It might be beneficial to target all the types of cells in the tumor. Example fight off angiogenesis.

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16
Q

How are cancers and viruses related to cancer?

Simple broad explanation

A

They damage the cell and can induce mutations.

17
Q

What cancer is related to the Hrpsevirus family and Epstein- Barr virus

A

Burkitt’s lymphoma ( B lymphocyte cancer)

Nasopharyngeal carcinoma

18
Q

What cancer is HIV related to?

HTLV1?

A

HIV= Kaposi’s sarcoma

HTLV1= Adult T-cell leukemia/ lymphoma
– (Human Tcell Leukemia Virus-1)

19
Q

How can viruses produce cancer?

What two proteins work in HPV?

A
  1. SRC integrate oncogene into DNA
  2. E6 and E7- Cell proliferation AND lose of suppressant function
    - - E6 inhibits p53
    - - E7 bind Rb and prevents binding to EIIF
  3. Also HPV- plasmid chromosome entered into cell, accidentally incorporated into the human chromosome. Upregulation of certain viral proteins interferes with the control of cell division in basal cells
20
Q

Proto oncogene

A

Normal gene that could become an oncogene by over expression

21
Q

Overactivity (proliferation, oncogene) and tummor suppressants are needed to, what types of mutations are they?

A

oncogene (gain of function) = dominant

tummor suppresant (loss of function) = recessive

22
Q

Mechanism of retinoblastoma?

A

p16 (Cdk inhibitor) > cyclin DCdk complex > Rb > E2F > transcription of target genes to control s phase entry

23
Q

Non hereditary vs hereditary retinoblastoma

A

Non-hereditary= mutates both alleles (recessive) then goes on to tumors

Hereditary= acquire copy of bad allele, second allele mutation acquired. Leads to multiple tumors in both eyes

24
Q

how to convert proto oncogene into an oncogene?

A

Point mutation or deletion- leads to overactive gene

Mutation in regulatory gene= overactive gene

Gene amplification= too much normal protein

Chromosomal rearrangement

25
Q

How does microarray help with cancers?

A

You can analyze gene expression to see what has changed from the normal cell. Binds PROTEINS

26
Q

p16s role in cancer?

A

Mutated/inactive form does not bind to Cdk4 and can’t inhibit it.

27
Q

How are growth factors related to cancer?

How about metabolism and what does mTOR do?

A

Growth factor is unregulated.

Glucose inport will increase to meet the demand of the higher metabolic activity.

mTOR leads to increased protein synthesis, increased glycolysis and glucose uptake.

28
Q

Colon cancer pathway

A

normal epithelium > loss of Apc > early adenoma > activation of K-ras (protooncogene) > intermediate adenoma > loss of Smad4 and other tumor suppressors > late adenoma > loss of p53 > carcinoma > other unknown alterations > invasions and metastasis

  1. lose Apc
  2. activate K-ras
  3. loss of Smad4 and other tumor suppressors
  4. loss of p53