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IHO Week 4 > Fitz- Antineoplastics VI > Flashcards

Fitz- Antineoplastics VI Flashcards

1
Q

Must angiogenesis inhibitors work by decreasing substances that promote angiogenesis like:

A

VEGF

mTOR

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2
Q

What are the 3 things that mTOR does?

A

reduces cell growth/proliferation
prevent angiogenesis
increase the cytotoxicity of drugs that damage DNA

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3
Q

Thalomide is used to treat what two diseases?

A

Hansen’s disease

multiple myeloma

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4
Q

What is the significant teratogenic effect of thalidomide?

A

phocomelia

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5
Q

What is the role of naturally occurring angiogenesis inhibitors in the growth of secondary tumors following surgery?

A

Some tumors secrete substances that inhibit angiogenesis at other tumor sites, so when a primary tumor is removed, some weeks later, metastases of the tumor can appear throughout the body.

*this indicates they were present all along but too small to be detected

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6
Q

What is rebound angiogenesis?

A

Rapid growth of cancer when an angiogenesis inhibitor is stopped

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7
Q

What drug acts on VEGF?

A

Bevacizumab

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8
Q

STIs (pazopanib, sorafenib, sunitinib) inhibit what two proteins?

A

VEGF-R

PDGF-R

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9
Q

What drugs inhibit FGF?

A

Thalidomide

Interferon

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10
Q

What drugs are mTOR inhibitors?

A

Everolimus

Temsirolilumus

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11
Q

What drug induces INFy?

A

IL-12–> increases inducible protein 10–> angiogenesis inhibtion

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12
Q

What drug decreases FGF production?

A

INF alpha

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13
Q

What is the role of VEGF-R in cancer?

A

VEGF-R is a tyrosine kinase receptor that activates mTOR in order to promote angiogenesis

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14
Q

What is mTOR and what does it do?

A

An intracellular serine/theronine kinase

Plays a central role in the control of cell growth and proliferation

Senses changes the availability of GFs/E sources and induces synthesis of proteins necessary for angiogenesis, cell growth/survival and nutriet uptake.

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15
Q

What proteins are regulated by mTOR?

A

Cell cycle regulators (cyclin D1)
AA and glucose transporters
proangiogenic factors
enzymes required for DNA repair

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16
Q

When is the mTOR pathway activated in cancer cells?

A

Uncontrolled proliferation

Increased mTOR in cancer cells–> secretion of VEGF and PDGF—> promote angiogenesis by increasing mTOR in vascular cells

17
Q

What happens when you decrease the activity of VEGF-R and mTOR?

A

Synergistic kill of cancer cells

18
Q

What is the MOA of bevacizumab?

A

Blocks VEGF

19
Q

What are the SE of bevacizumab?

A

GI perforation
woud dehiscence
hemoptysis (spitting up blood)–> fatal

20
Q

What drugs inhibit VEGF-R and PDGF-R?

A

Pazo and Suni- ckit

Sora- raf

21
Q

What STI is associated with:

hepatotoxicity, hemorrhage, GI perforation and hypertension

A

Pazo

22
Q

What STI is associated with:

hemorrhage, hypertension?

A

Sora

23
Q

What STI is associated with:

hand-foot syndrome, skin discoloration?

A

Suni

24
Q

What is the MOA of mTOR inhibitors?

A
  1. Decrease cell growth and proliferation by blocking mTOR (decreasing bioenergetics)
  2. Decrease VEGF and PDGF release from cancer cells
  3. Increase cytotoxicity w/ drugs that damage DNA (damage w/ alkylating agent then mTOR force to continue cell cycle)
25
Q

What are some of the toxicities associated w/ mTOR inhibitors?

A 
hypersensitivity
immunosuppression
angioedema
kidney thrombosis
delays in wound healing
nephrotoxicity
male infertility
hyperlipidemia
26
Q

What drug shifts the immune system from Th1–> Th2 and is a potent TNFalpha agent?

A

Thalidomide?

27
Q

What are the SE of thalidomide?

A

Few in adult M and non-pregnant F

N/V, rashes, peripheral neuopathy, increased risk of DVT

28
Q

What are the severe teratogenic effects of thalidomide if women take it 3-4 weeks post conception?

A

miscarriage
birth defects: malforned intestines, hearing defects, ocular/renal defects, phocomelia

  • children and grand children affected
  • single dose
29
Q

What are the advantages of combination chemotherapy?

A
  1. Synergistic effect: allowing you to decrease dose and therefore decrease toxicity to the pt
  2. Decrease development of resistance–> decreased likelihood of clonal selection
  3. Broader cell kill in cancers that consist of heterogenous tumor cell population
30
Q

What strategies are used to select drugs for combination therapy?

A
  1. effective alone
  2. diff mechanism of action and diff mechanism of resistance
  3. CCNS/CCS
  4. Diff toxicities
31
Q

What is pulse therapy? and why is it used?

A

Intermittent treatment w/ high doses of a drug, followed by free drug periods

Allows hematologic and immunologic recovery between treatment cycles

32
Q

What is an example of pulse treatment?

A

MTX for the tx of choriocarcinoma

33
Q

What is recruitment?

A

Use a CCNS drug to achieve a significant log kill

This causes cancer cells in Go to be recruited back into the cell cycle

THEN

You administer a CCS drug to kill dividing cells.

HUZZAH

34
Q

What are examples of drugs used for recruitment?

A

CMF in breast cancer

DAUNOrubicin and cytarabine in AML

35
Q

What is synchrony?

A

Use CCS drugs to synchronize cells into simultaneous cell division so that they’re more sensitive to drugs/radiation.

36
Q

What are examples of drugs used for synchrony?

A

Hydroxyurea followed by radiation

Vinca alkaloids followed by etoposide

MTX follwed by L asparaginase for ALL

37
Q

What is rescue therapy?

A

Following the administration of toxic doses of a drug, normal cells are rescued by “antidotes” that ONLY they can use

38
Q

What is an example of rescue therapy?

A

leucovorin following high dose of MTX

IHO Week 4 (15 decks)

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