Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Disease and Defense: Unit 2 > Anti-Tumor Agents > Flashcards

Anti-Tumor Agents Flashcards

1
Q

What is primary induction chemotherapy?

A

ONLY chemotherapy
It is a chemotherapy used for patients with cancer that can be cured with chemotherapy

Also used for patients with no other options

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is neoadjuvant chemotherapy?

A

Chemotherapy used to treat tumors that are LOCALIZED but surgery/radiation may not be completely effected

BEFORE surgery

Used to treat micrometastatic disease

Increase surgical or radiation therapy success

Decrease damage to other organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is adjuvant chemotherapy?

A

Chemotherapy used in treatment of local tumors AFTER surgery or radiation

Decrease incidence of local and systemic recurrence

Increase effectiveness of surgery or radiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the therapeutic window of chemotherapy.

A

Small therapeutic window

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Mutation rate can correlate to what physical feature of the tumor.

A

Size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

True or false:

Multiple drugs are needed to treat and cure one cancer

A

True.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Tumor death occurs though which process?

A

Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Apoptosis is cause by signaling pathways usually focused on what organelle?
What is produced?

A

Mitochondria

Caspases- cysteine protease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the function of BH3?

A

Measures how close to apoptosis the cancer cell is

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What cells are particularity sensitive to chemotherapy…besides cancer cells?

A

Bone Marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are some common mechanisms of chemoresistance?

A 
Increasing efflux
Decreasing apoptosis
Alter target
Increase repair 
Resistant tumor stem cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What enzyme inactivates cyclophosphamide?

A

Aldehyde dehydrogenase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cells with high levels of ALDH are resistant to what chemotherapeutic drug?

A

Cyclophosphamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Name three resistance mechanisms for alkylating agents.

A
  1. Glutathione-tripeptide with free cysteine sulphydryl
  2. Repair DNA by removing alkyl group on guanine
  3. Repair cross-link
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the toxic effects of alkylating agents?

A
  • Hematopoietic toxicity
  • Gastrointestinal toxicity, nausea, vomiting
  • Gonadal toxicity
  • Alopecia
  • Carcinogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What organ is commonly damaged by cisplatin?

A

Kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the anti-tumor mechanism of cisplantin?

A

Cross-linking DNA&raquo_space;>Apoptosis

18
Q

What are three types of DNA damaging agents?

A

Alkylating agents
Cisplantin
5-fluoruracil

19
Q

What is the mechanism of action of cyclophasphamide?

A

Forms covalent chemical adduct and interstrand crosslinks in DNA. If not repaired, prevents DNA relication-recognized as DNA damage activating apoptosis

20
Q

What is the mechanism of action of cisplantin?

A

Crosslink DNA making relication impossible and triggering apoptotic response

21
Q

What is the mechanism of action of 5-fluoruracil?

A

Pyrimidine analog that inhibits thymidylate synthase to cause dTTP depletion and inhibit DNA synthesis. Activates apoptosis because of DNA breakage

22
Q

What is the major toxicity for cyclophosphamide?

A

Hematopoietic toxicity

Gastrointestinal toxicitym nausea, vomiting

Gonadal toxicity

Alopecia

Carcinogenesis

23
Q

What is the major toxicity for cisplantin?

A

Highly nephrotoxic

24
Q

What is the major toxicity for 5-fluoruracil?

A

Alopecia

Dermatological problems

Myelosuppression

Gastrointestinal toxicity

25
Q

What is the mechanism of resistance to cyclophosphamide?

A

Increased glutathione (GSH)-tripeptide + free cysteine sulphydryl

DNA repair through remove alkyl group from guanine

DNA repair through nucleotide excision repair to remove crosslink

26
Q

What is the mechanism of resistance to cisplantin?

A
  1. Reduce accumulation
  2. Inactivation
  3. Increase DNA reapair
  4. Increased tolerance for DNA damage
27
Q

What is the mechanism of resistance to 5-fluoruracil?

A
  1. Alteration in target enzymes

2. Increase levels of thymidylate synthase

28
Q

What is the mechanism of action of topoisomerase interacting agents?

A

Inhibits religation of double stranded DNA

29
Q

What is the major toxicity for topoisomerase interacting agents?

A

Myelosuppression

Cardiotoxicity associated with chelating ability

Secondary malignancies

30
Q

What is the mechanism of resistance of topoisomerase interacting agents?

A

Increased drug efflux

Mutations in topoisomerases

31
Q

What is the mechanism of action of microtubule interacting agents?

  • Vinca alkaloids
  • Taxanes
A

Bind to tubulin at microtubule ends. Stabilization or destabilization of microtubule dynamics activates apoptosis and kills cells

  • Destabilization
  • Stabilization
32
Q

What is the major toxicity for antimicrotubule agents?

  • Vinca Alkaloids
  • Taxanes
A

-Neurotoxicity
Myelosuppression
Neutropenia

-Myelosuppression-neutropenia
Peripheral neuropathy
Alopecia

33
Q

What is the mechanism of resistance of antimicrotuble agents?

  • Vinca alkaloids
  • Taxanes
A

-Increased drug efflux
Mutations in tubulin

-Increased drug efflux
Mutations in tubulin
Inhibition of apoptosis

34
Q

What is the mechanism of action of hormonal agents?

A

Either inhibit the receptors (tamoxifen or antiandrogens) or they inhibit the hormone

35
Q

What is the major toxicity for hormonal agents?

A

Side effects associated with altered steroid hormone signaling

36
Q

What is the major resistance for hormonal agent?

A

Mutation in receptor

Mutation in enzyme that activates receptor without presence of hormone

37
Q

What is the mechanism of action of antibodies?

A

Binding to target and decreasing function

Antibody conjugated to toxin binds to cancer cell killing it

38
Q

What is the mechanism of kinase inhibitors?

A

Inhibits kinases good for treatment in CML which have an increase in BCR-abl kinase

39
Q

What is the major difference between “targeted therapies” and conventional cytotoxics?

A

Conventional agents damage normal cells as well as tumor cells- therapeutic window is largely based on tumor cells being closer to their apoptotic threshold, MTD relevant for conventional agents less so for targeted agents, which are usually less toxic, resistance mechanisms different.

Remember: conventional cytotoxic hit specific targets just like “targeted” agents do-difference is that with the newer “targeted” agents we aim to hit a target that is different/faulty in tumor cells but not normal cells.

40
Q

Why do we combine anti tumor agents?

A

Combine agents that work to at least some extent on their own, avoid overlapping toxicities, use drugs at optimal doses, keep treatment-free schedules as short as possible. Works because of the heterogeneity in the tumor cells population- some tumor cells respond to drug A some to drug B

Disease and Defense: Unit 2 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions