Term #1. Flashcards

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1
Q

What two features make a cell “cancerous”?

A

“divide without control” and “able to invade other tissues”.

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2
Q

Define carcinoma.

A

Malignancies of epithelial cells and tissues.

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3
Q

Explain cell differentiation using the example of skin epithelial cells.

A

Basal layer = cells divide and replicate.
Cells die and shed from skin surface and cells from the basal layer move upwards to replace them.
As they do, they undergo keratinisation and become denucleated.
Different layers = varying levels of differentiation = functionally different.

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4
Q

List 3 features of intestinal epithelium.

A

Mucus-secreting, high turnover rate, exposed to potential carcinogens from diet.

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5
Q

How does cancer target intestinal epithelium?

A

Because these cells already proliferate rapidly, cancer must prevent apoptosis to develop a tumour.

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6
Q

List 3 features of urothelium (bladder epithelium).

A

Urinary barrier, low turnover rate, exposed to carcinogens secreted in urine.

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7
Q

How does cancer target urothelium (bladder epithelium)?

A

Because these cells do not undergo apoptosis regularly, cancer must induce higher division rates to develop a tumour.

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8
Q
What are the following cancers of?
Sarcoma
Leukemia
Lymphoma / Myelomas 
CNS
A

Bone, cartilage, muscle or connective tissue.
Bone marrow.
Lymphoid cells.
Brain and spinal cord.

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9
Q

What changes do mutations cause in cells, and what does this cause?

A

Start dividing more and growing faster.

Causes a growth advantage and cells become antisocial and selfish.

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10
Q

What 2 things must happen for a mutation of a cell to become a cancer?

A

Mutation accumulation and natural selection.

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11
Q

Why can most cancers be traced back to the original source?

A

They arise from a single abnormal cell.

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12
Q

What are the 2 main classes of cancer-critical genes (and give an example of each)?

A

Proto-oncogenes e.g. Ras.

Tumour-suppressor genes e.g. p53.

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13
Q

What 3 advantages must cell mutations provide to lead to cancer?

A

Overcome growth/division constraints.
Allow accumulation of mutations.
Activate intracellular signalling pathways which can a) support increased proliferation or b) inhibit apoptosis.

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14
Q

Name the six hallmarks of cancer.

A
Self sufficiency in growth signals.
Insensitivity to anti-growth signals.
Evasion of apoptosis.
Limitless replicative potential.
Sustained angiogenesis.
Metastasis.
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15
Q

Give an example of an extracellular signalling factor used for cell communication.

A

Growth factors.`

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16
Q

Why will epithelial cells only proliferate if serum is provided?

A

Contains growth factors required for cells to multiply.

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17
Q

What is PDGF and what does it stand for?

A

Platelet-derived growth factor is a potent stimulator of fibroblast growth.

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18
Q

What happens when PDGF is a) absent and b) present when a monolayer of cultured cells is scratched?

A

a) the scratch is left untreated.

b) cells divide and migrate to fill in the gap and heal the wound.

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19
Q

What is the word for a cell that has left the cell cycle, and what is the cell cycle stage called?

A

Quiesence, and the cell cycle stage is G0.

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20
Q

What is EGF and what is its job?

A

Epidermal growth factor causes changes in cell shape and induces proliferation and migration of several cell types.

21
Q

What is the word for growth stimulating factors?

A

Mitogens.

22
Q

What do mitogens do and how?

A

Trigger growth related signal transduction pathways by binding to receptors on target cells.

23
Q

What is a kinase?

A

Enzymes that transfer phosphate groups to specific AA residues on other proteins.

24
Q

What is a signal transduction pathway?

A

Cascades of phosphorylation.

25
Q

How are transduction pathways turned on and off?

A

Phosphorylation of proteins with specific activities.

26
Q

What system is used to make simple YES/NO or ON/OFF cellular decisions?

A

Binary.

27
Q

If a cell is receiving _________ signals, it cannot divide.

A

Apoptosis.

28
Q

List the 6 features of the cell cycle.

A

Clock/timer.
Mechanism for initiating events in the right order.
Mechanism to ensure each phase is only triggered once per cycle.
Binary checkpoints.
Robustness.
Adaptability and responsiveness.

29
Q

What is the fundamental task of the cell cycle?

A

To produce 2 genetically identical daughter cells.

30
Q

What are the 2 major phases of the cell cycle?

A

DNA replicated to produce 2 identical copies.

Replicated chromosomes are accurately segregated to 2 daughter cells.

31
Q

What is the difference between normal cell lines and immortalised cell lines?

A

Normal cell lines have finite replicative potential.

Immortalised cell lines have infinite replicative potential.

32
Q

What is the term for a permanent cease in cell division?

A

Replicative senescence.

33
Q

What are immortalised cells?

A

Cells that have either undergone mutations or are tumour cells.
Overcome contact inhibition of growth and form piles of cells (foci).
Grow indefinitely in culture.

34
Q

What 3 things do checkpoints (ckpts) ensure?

A

Each phase is successful and complete.
Errors are repaired, or if they are irreparable the cell dies.
No step is repeated.

35
Q

Why do checkpoint (ckpt) defects promote cancer?

A

Often accumulate mutations.

36
Q

What is the function of the restriction point checkpoint (ckpt)?

A

Cell commits to cell cycle entry and chromosome duplication.

37
Q

Name the 5 major checkpoints (ckpts)?

A
Restriction point
G2/M
Metaphase-to-anaphase 
DNA damage #1
DNA damage #2
38
Q

What is the function of G2/M checkpoint (ckpt)?

A

Early mitotic events triggered, leading to chromosome alignment.

39
Q

What is the function of metaphase-to-anaphase checkpoint (ckpt)?

A

Sister chromatid separation and cytokinesis.

40
Q

What is the function of DNA damage checkpoint 1?

A

Ensures a cell cannot advance to S phase if genome needs repairs (G1 phase).

41
Q

What is the function of DNA damage checkpoint 2?

A

Ensures a cell cannot advance to M phase if genome needs repairs (G2 phase).

42
Q

Why do checkpoints (ckpts) operate through negative control?

A

Receiving many positive signals is confusing, but one negative signal is much clearer.

43
Q

What AA kinase is a cdk?

A

Ser/Thr.

44
Q

What regulatory protein does a cdk depend on?

A

Cyclin.

45
Q

What is the function of a cyclin?

A

Activate the catalytic activity of their cdk partners and guide them towards their substrates.

46
Q

What do EGF and EGFR stand for?

A

Epidermal growth factor, and epidermal growth factor receptor.

47
Q

What AA kinase is epidermal growth factor receptor (EGFR)?

A

Tyrosine.

48
Q

How does epidermal growth factor receptor lead to expression of growth factors? (14 stages.)

A

EGF ligand binds EGFR tyrosine kinase (RTK).
Dimerisation of RTK.
Phosphorylation of RTK and its paired subunit.
GRB2 binds to phosphorylated RTK.
Protein SOS binds membrane bound protein Ras.
SOS catalyses Ras + GDP to Ras + GTP.
Ras is activated.
Ras binds effector protein Kinase B-Raf.
B-Raf phosphorylates and activates kinases MEK 1 and 2.
MEK 1 and 2 phosphorylate and activate kinases ERK 1 and 2.
Activation of AP-1 transcription factors jun and fos.
jun and fos move to cell nucleus and form a heterodimer.
Heterodimer binds to AP-1 motif of DNA.
Expression of genes for growth factors.