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Anatomy > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

What are four DNA viruses associated with cancer?

A
  1. papillomavirus-HPV
  2. Hep B
  3. Hep C
  4. Epstein-Barr
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2
Q

What are two RNA viruses that can cause cancers?

A
  1. Human T-cell leukemia type 1 can cause leukemia/lymphoma

2. HIV can cause Burkitt’s lymphoma

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3
Q

What is the Warburg Phenomenon?

A

Most cancer relies on glycolysis for energy rather than Ox Phos.

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4
Q

Why use PET scanning for cancer detection?

A

It has to do with the cancer’s preferred method of glycolysis for energy; it preferentially takes up 18-Fluorodeoxyglucose.

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5
Q

Why would the cancer prefer to use glycolysis?

A

It allows the cancer to rapidly increase mass.

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6
Q

What is mitogen?

A

activation needed to drive cell cycle.

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7
Q

What is growth factor?

A

activation needed for nutrient uptake and utilization.

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8
Q

What does a mutation to PI3 Kinase pathway do?

A

Increases glucose uptake and utilization.

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9
Q

What is maybe the most mutated gene in human cancers

A

PIK3

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10
Q

What are some activators and inhibitors for angiogenesis?

A

Activators: VEGF, aFGF, bFGF, Anionpoietin-1

Inhibitors: Thrombospondin-1, Interferon (alpha and beta), Angiostatin, Endostatin

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11
Q

What is the significance of p53 mutations in cancer?

A

Destabilizes the genome and enables cancer. Loss of p53 can prevent DNA damage repair.

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12
Q

What do PI3 mutations do?

A

They affect metabolism and encourage the cell not to use the OxPhos pathway.

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13
Q

What is APC?

A

APC is a negative regulator of the Wnt pathway.

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14
Q

What does GTP do to Ras?

A

activates it.

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15
Q

What happens in the more common Ras mutation that affects cancer?

A

Ras has a single point mutation which makes it lose its hydrolyzing abilities, so it is always attached to GTP and always active.

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16
Q

What is the Philadelphia chromosome? What happens, and how is it treated?

A

Philadelphia chromosome is a translocation between chromosome 22 and 9. It leads to a c-able gene that is unregulated. Gleevec (Imatinib) inhibits Bcr-Abl, is a kinase inhibitor.

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17
Q

What is the relationship of Rb and E2F?

A

When Rb is active (unphosph) it sequesters E2F which prevents the cell from entering S. If Rb has a mutation and cannot sequester E2F, then the cell proliferates without regulation.

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18
Q

What happens with an amplification of Cyclin D1?

A

Excess G1 cyclin, abbreviated G1

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19
Q

What happens with an activating mutation in Ras?

A

It mimics growth factor signals which leads to abbreviated G1.

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20
Q

What happens with a loss of function mutation in RB?

A

loss of restraint for “start”, abbreviated G1.

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21
Q

What happens with a deletion of p16ink?

A

Loss of Cdk inhibition, abbreviated G1.

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22
Q

Are BAX and BCL-2 pro- or anti-apoptotic?

A 
BAX = pro
BCL-2 = anti (it inhibits BAX)
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23
Q

Why can BCL-2 make cancer worse?

A

It helps to inhibit the apoptotic signal. Therefore, if it is round tumorgenic cells, it will inhibit their programmed cell death.

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24
Q

What are the three functions of p53?

A
  1. It hits the pause button on transcription by activating p21 which inhibits CDK.
  2. It initiates DNA repair so that damaged DNA is not replicated.
  3. In extreme cases it can also initiate apoptosis.
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25
Q

Is p53 a common mutation in many cancers? Why is it important?

A

Yes. Because it does two things: 1) repairs damaged DNA, and 2) can trigger apoptosis.

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26
Q

HPV and Adenovirus can inactivate what?

A

p53 and Rb.

Rb- sequesters E2F

p53- pauses the transcription of bad DNA, fixes DNA and can lead to apoptosis.

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27
Q

What is hTERT? Why does it matter?

A

It’s the gene for telomerase. It is important for the cell to be able to maintain it’s telomere length. 70-90% of cancers are hTERT+. Transfecting hTERT into normal human cells makes the human cells proliferate indefinitely in culture.

28
Q

What does PK-M2 and PK-M1 do to tumors?

A

M2: tumors get bigger bc more pyruvate is sent down lactic acid pathway. These ones have a more emphasized glycolysis pathway.

M1: tumors don’t really grow bc more pyruvate is sent to OxPhos

29
Q

Which may be the most frequently mutated gene in human cancers (especially women)?

A

PI3 Kinase (PIK3)

30
Q

What are angiogenesis activators?

A

VEGF, aFGF, bFGF, Angiopoietin-1

31
Q

What are angiogenesis inhibitors?

A

Angiostatin, Endostatin, Angiopoietin-2, Thrombospondin-1, Interferon alpha/beta.

32
Q

What is APC?

A

Adenomatous polyposis coli. It is a gene that when truncated and double hit will lead to lots and lots of polyps, ~100% chance of getting colon cancer.

33
Q

What is FAP?

A

One can inherit a truncated APC gene, which means that only a single mutation can lead to colon cancer.

34
Q

What is the Wnt/Beta-Catenin pathway?

A
  1. Wnt binds to receptor
  2. Receptors inhibit the beta-Catenin ‘destruction complex’ (of which APC is part)
  3. beta-Catenin goes into nucleus and turns on target genes.
35
Q

How does a mutant APC upregulate proliferation?

A

APC degrade beta-Catenin. But if APC is mutated and cannot degrade beta-Catenin, then the cell proliferates in an unregulated manner.

36
Q

What is a common way for cancer cells to cross the BM?

A

using matrix metaloproteinases (MMPs).

37
Q

What is a premetastatic niche?

A

Somehow the tumor cells send signals to neighboring cells that will send the bone marrow derived cells (BMDC) to the future tissue of metastasis. If they are brain tumor cells, they will send BMDC to brain to prepare the tissue for the arrival of the tumors.

38
Q

What receptor is necessary for the formation of the niche?

A

VEGF receptor.

39
Q

Are metastatic and primary tumors very different genetically?

A

no.

40
Q

What is EMT?

A

Epithelial to Mesenchymal Transition. An alternative to the gene mutation and selection model to explain metastasis. In classical embryology, cells delaminate and migrate. This makes the epithelial cells more like mesenchymal cells with increased motility and invasive ability.

41
Q

EMT brings loss of what?

A

intermediate filament, E-cadherin, epithelial cell polarity

42
Q

EMT bring acquisition of what?

A

motility, invasiveness, mesenchymal adherens, protesase secretion.

43
Q

Is EMT reversible?

A

Yes. Mesenchymal to Epithelial Transition (MET).

44
Q

What is ATM, and can ATM deficient patients receive radiation?

A

ATM is a cell repair enzyme/molecule. Patients who are ATM deficient in their healthy cells cannot receive radiation.

45
Q

What is electron radiation good for?

A

Skin lesions. Electrons don’t go too deep.

46
Q

What’s the difference between protons and photons?

A

Protons can have a very specific depth set so that the radiation will not permeate the entire body. Photons have much less depth accuracy and will be more diffusive.

47
Q

What is Brachytherapy?

A

High dose radiation to specific areas. Can either be used via a needle and the radiation comes in and returns to its safety bin. Or seeds can be sown into an area.

48
Q

What is the max dose for the spinal cord in terms of radiation?

A

50 Gy

49
Q

What is one of the largest concerns regarding repeated radiation therapy?

A

spinal cord damage. Re-irradiation can always cause damage bc the tissue never “forgets” that it was irradiated the first time.

50
Q

What are some non-specific, active immunotherapies?

A

microbial products
BCG
cytokines
immunostimulatory molecules

51
Q

What is BCG?

A

protein derivative of TB, it causes an intense granulomatous inflammation that helps to fight the cancer. It is an active, non-specific immunotherapy. Used in bladder cancer treatments.

52
Q

How are cytokines used in immunotherapy?

A

They can recruit T cells to the microenvironment, and that can stimulate an immune response to the cancer cells.

53
Q

How are IL-2 and IFN-alpha used? How is IL-12 and GM-CSF used?

A

IL-2 and INF-alpha are used as standard therapy. IL-12 and GM-CSF (granulocyte macrophage colony stimulating factor) can (maybe in the future) be used as adjuvant with cancer vaccines.

54
Q

How was IL-2 used? Why is it no longer used?

A

It would recruit tumor fighting cells. However, it also increased a lot of vascular permeability and had lots of toxicity issues.

55
Q

What is the relationship between CD28/B7 and CTLA4/B7? How has it been used therapeutically?

A

CD28 and CTLA4 are on T cells. B7 is on APCs.

CD28 is the gas pedal for starting an immune response. CTLA4 is the brake pedal. By inhibiting the inhibitor (brake pedal), you can create a larger immune response.

56
Q

What are Tremelimumab and Ipilimumab?

A

Anti-CTLA4 blockade drugs.

57
Q

How does an anti-PD1 drug work?

A

It is similar to anti-CDLA4. It blocks the receptors that lead to an inhibitory response of the immune system. It removes the brake pedal.

58
Q

What are some means to deliver specific response immune vaccines? What does this guy think will work the best and why?

A

Peptides, proteins, DNA (viral delivery) and RNA are all potential ways to deliver a vaccine. He thinks proteins will be the best bc they promote both MHCI and II responses and are more durable.

59
Q

How does a Chimeric Antigen Receptor (CAR) work?

A

Find an Ab to a tumor. Then put the receptor on a synthesized T-cell stimulating transmembrane protein. Current models have 3 synthesized co-stimulatory regions.

60
Q

What type of cancer is carcinoma? Sarcoma? Leukemia? Lymphoma? Myeloma?

A

Carcinoma: epithelial tissue
Sarcoma: connective tissue
Leukemia: blood
Lymphoma: lymph system

61
Q

How do antimetabolites work? And how does the cancer defend against them? What is an example?

A

Folic acid analogs, like MTX, work as folic acid antagonists and interfere with formation of DNA/RNA.

Cancers fight them by decreasing influx of the drug. Transporters become more specific.

Methotrexate is an example.

62
Q

How do DNA alkylating drugs work? How do cancers fight them? What is an example?

A

They cause intra- and inter-strand DNA links. Interferes with cell division. Given as prodrug and activated by P450.

Cancers fight this by decreasing drug permeability and sequestering the drug.

Cyclophosphamide is an example.

63
Q

How do Non-Covalent DNA Binding Drugs work? How do cancers fight them? What is an example?

A

Drugs bind to DNA and inhibit topoisomerase 2 causing strand breaking.

ABC transporters pump the drug out as a form of resistance.

Anthracycline is an example.

64
Q

how do microtubule targeting drugs work? How do cancers fight them? What is an example?

A

They inhibit microtubule function leading to cell arrest.

Mutations lead to microtubule stability, also efflux of the drug.

Taxol, and other taxanes, are an example.

65
Q

What are ABC transporters?

A

They are ATP dependent pumps that remove drugs from cells. They are common in cancer cells.

66
Q

What are the dark black pebbles in the slides?

A

mitotic figures

Anatomy (12 decks)

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