Brainscape's Knowledge GenomeTM

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


See full index

BMR 607 Test 1 > Antineoplastic 1 > Flashcards

Antineoplastic 1 Flashcards

1
Q

When cancer cannot be cured what are the goals of treatment?

A
  • Shifts to palliation
  • Amelioration of symptoms
  • Preservation of quality of life
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Types of Systemic Cancer Treatments?

A
  • Conventional “cytotoxic” chemotherapy agents
  • Targeted agents: Biologics (antibodies or cytokines)
  • Hormonal therapies
  • Biologic therapies: manipulate the host-tumor interaction in favor of the host.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define Gompertzian tumor growth:

A

The growth fraction of a tumor declines exponentially over time.

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

Total Kill Hypothesis:

A
  • Single cancer cell can multiply and kill the host
  • For microbial infections a “3-log kill” by antibiotics may be sufficient to allow host defense mechanisms to eradicate the infection.
  • For successful cancer treatment: All of the cancer cells must be killed.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Log-Kill Model by Skipper states what for a given dose of a drug?

A

It kills a constant fraction of cells, not a constant number, regardless of the cell numbers present.

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

Describe adjuvant chemotherapy?

A

Assumes the presence of undetectable cell masses after the initial surgical therapy that are capable of producing tumor relapse.

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

Clinically sequential use of drugs that works per Gompertzian growth.

A
  • Cell-cycle nonspecific agents (cyclophosphamide) to bring down the mass.
    • When tumor shrinks, proliferation begins.
  • Cell-cycle specific agent (methotrexate)
    • Kills the cell as it tries to proliferate.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Vinca Alkaloids work by what mechanism?

A
  • Inhibition of tubulin polymerization, which disrupts assembly of microtubules, an important part of the mitotic spindle.
    • Causes mitotic arrest at Metaphase, cell division stops, cell dies.
  • Bind to B-tubulin and prevents interaction with a-tubulin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the principal mechanism of resistance to Vinca Alkaloids?

A

Increased P-Glycoprotein

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

What are the three vinca alkaloids mentioned and what is said of them?

A
  • Vincristine
    • Neurotoxic
      • Prednisone is useful in childhood leukemias.
  • Vinblastine:
    • Myelosuppressive (bone marrow suppression)
    • Metastatic testicular cancer and Hodgkin’s lymphoma.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the mechanism and outcome of Taxanes?

A
  • Hyper-stabilizes microtubule structure (freezes them)
  • Taxanes bind to the B-subunit of tubulin, the resulting microtubule/taxane complex does not have the ability to disassemble.
  • This adversely affects cell function and leads to apoptosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What Taxane is especially known for stocking and glove neuropathy?

A

Paclitaxel

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

What cancers have Taxanes become central treatments of?

A

Metastatic ovarian, breast, lung, GI, genitourinary, head and neck cancers.

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

What is the prototype of Epothilones and what is it approved for?

A

Ixabepilone

Metastatic Breast Cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the mechanism for Epothilones?

A
  • They bind to B-tubulin and trigger microtubule nucleation at multiple sites away from centriole.
  • Chaotic stabilization triggers cell cycle arrest at G2-M interface and apoptosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What step in the cell cycle do Topoisomerase inhibitors target?

A

S-phase Specfic

17
Q

When are Topoisomerase I inhibitors used?

A

Ovarian and small cell lung carcinoma.

18
Q

What is the mechanism for Topoisomerase I inhibitors?

A
  • Initial cleavage action of topoisomerase I is not affected, but re-ligation step is.
    • Leading to an accumulation of single-stranded breaks in DNA.
  • Collision of a DNA replication fork with this cleaved strand causes an irreversible double-strand DNA break, leading to cell death.
19
Q

What is the mechanism of Anthracyclines?

A
  • Inhibition of Topoisomerase II
  • Binding to DNA through intercalation
    • Blocks synthesis of DNA and RNA, and DNA strand scission
    • Generation of oxygen free radicals through an iron-dependent process.
20
Q

What are the three Anthracyclines described in the lecture?

A

Doxorubicin

Daunorubicin

Mitoxantrone

21
Q

Doxorubicin details

A
  • Important anticancer drug
  • Cons:
    • Produces severe alopecia
    • Potent vesicant (irritant)
    • Toxicity: Cardiotoxic
      • Acute: Arrhythmias
      • Chronic: Digitalis-resistant congestive heart failure.
22
Q

Role and Mechanism of Dexrazoxane

A
  • Protects against doxorubicin-induced congestive heart failure.
  • Prodrug that is hydrolyzed in heart cells to a metal chelating metabolite.
  • Its likely function in preventing doxorubicin-induced damage to heart cells involves binding of ferric ions (Fe3+) by its chelating action.
23
Q

Describe the Mechanism of Dactinomycin (Actinomycin-D)

A
  • First Antibiotic shown to have anti-cancer activity
  • Binds to ds-DNA through intercalation between adjacent guanine-cytosine base pairs.
  • Inhibits transcription by binding to initiation complex and prevents elongation by RNA polymerase.
24
Q

When is Dactinomycin used in cancer treatment?

A
  • Treatment of rhabdomyosarcoma and Wilms tumor in children.
    • In combo with primary surgery, radiotherapy, and other drugs.
25
Q

Epipodophyllotoxins: Etoposide

inhibits?

Used for?

A
  • Topoisomerase II
  • Testicular tumors, when used with bleomycin and cisplatin.
  • Small cell carcinoma of the lung when used with cisplatin and ifosfamide.
26
Q

Downside of Epipodophyllotoxins: Etoposide

A
  • Leukemogenic and may cause acute nonlymphocytic leukemia in children.
  • Myelosuppression is the most common toxicity.
27
Q

Downsides with Bleomycin?

A
  • Toxicity to skin and lungs
    • Pulmonary toxicity
      • Pulmonary fibrosis (irreversible)
28
Q

Mechanism of action for Bleomycin?

A
  • Cleaves DNA
  • Causes oxidative damage to deoxyribose of thymidylate and other nucleotides, leading to single- and ds breaks in DNA. Damaged cells accumulate in G2 phase.
29
Q

Forms of cancer that Bleomycin is good against?

A

Germ cell testicular cancer

Hodgkin’s lymphoma

30
Q

90% of patients with CML have what?

A
  • Philadelphia Chromosome t(9:22)
  • Encodes BCR-ABL non-receptor tyrosine kinase (w/ increased enzyme activity)
31
Q

What are the results of BCR-ABL-dependent signaling?

A
  • Enhanced Survival
  • Inhibition of apoptosis
  • Perturbation of cell adhesion and migration.
32
Q

>90% of patients with CML were cured with?

A

Gleevec (imatinib)

33
Q

Protein tyrosine kinase inhibitors have efficacy in diseases with what factors?

Common cancers?

A
  • ABL, kit, PDGFR are dominant roles in driving the proliferation of the tumor.
  • CML, gastrointestinal stromal tumors (GIST), chronic myelomonocytic leukemia.
34
Q

Principle toxicity of BCR-ABL kinase inhibitors?

A

GI distress and fluid retention.

35
Q

The IGF-1 receptor corresponds to what pathway?

A

PI3K

BMR 607 Test 1 (7 decks)

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