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Foundations of Disease and Therapy > Chemotherapy > Flashcards

Chemotherapy Flashcards

1
Q

Cell-Cycle Specific Drug Classes

A
  1. Antimetabolites
  2. Topoisomerase Inhibitors
  3. Microtubule Inhibitors
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2
Q

Methotrexate

A

Antimetabolite that inhibits dihydrofolate reductase

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3
Q

Pazopanib, Levantinib, Cabozantinib

A

Small molecule inhibitors of the VEGF Receptor

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4
Q

Microtubule Inhibitors

A

Block microtubule polymerization and inhibit mitosis

Can cause neurotoxicity and peripheral neuropathy because microtubules are important for transport of cargo along neurons

Induce resistance via MDR1

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5
Q

Imatinib, Dasatinib, Ponatinib

A

Small molecule inhibitors of BCR-Abl tyrosine kinase that causes CML

Effective single-agent therapy that causes long-lasting remission

Resistance is driven by mutations in BCR-Abl that prevent binding of the drug, but the drug can be modified to combat these mutations

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6
Q

Strategies to maximize efficacy of treatment and minimize side effects

A
  1. Combination Therapy
  2. Rationaly Designed Therapies
  3. Prophylaxis
  4. Intermittent therapy
  5. Optimization of dosing and route
  6. Support of bone marrow function
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7
Q

Cell Cycle Nonspecific Drug Classes

A
  1. DNA Intercalating/Damaging Agents
  2. Alkylating Agents
  3. Protein Synthesis Inhibitors
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8
Q

Inhibit mutant B-Raf kinase

A

Vemurafenib, Dabrafenib

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9
Q

MDR1

A

Multi-Drug Resistance 1 gene

Recognizes toxic compounds and pumps them out of the cell

Expression of MDR1 increases dramatically over course of treatment

Allows cell to develop resistance to chemotherapeutics such as Microtubule Inhibitors and Topoisomerase Inhibitors

MDR1 is non-selective, so resistance to one drug gives resistance to many other drugs

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10
Q

Trastuzumab

(What is it, and what are the side effects?)

A

Monoclonal antibody against HER2 receptor

Can cause heart toxicity when used with Doxorubicin

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11
Q

Anti-Angiogenesis Drugs

(Mechanism)

A

Target VEGF

Theoretically stop cancer by preventing blood supply to cancer

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12
Q

Purpose of combination therapy

A

Using multiple mechanisms makes cells less likely to develop resistance

Therapy is more effective because you are targeting multiple pathways

Fewer side effects because you can use less of each drug

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13
Q

Topoisomerase Inhibitors

A

Topoisomerase is required for DNA replication and mitosis

These drugs induce resistance via upregulation of MDR1

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14
Q

Panitumumab

A

Monoclonal antibody against Epidermal Growth Factor Receptor

Treats EGFr-expressing metastatic colorectal carcinoma

High dermatologic toxicity

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15
Q

Examples of Alkylating Agents

A
  1. Nitrogen Mustards
  2. Nitrosoureas
  3. Hydrazines
  4. Platinum Compounds
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16
Q

Drug that can cause cardiomyopathy due to free radical generation as well as red urine

A

Doxorubicin

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17
Q

Tamoxifen

A

Hormonal therapy that acts as an antagonist to estrogen receptor

Used to prevent estrogen-receptor positive breast cancers

Less effective in pre-menopausal women cause they have more estrogen

18
Q

Estrogen Receptor Antagonist

A

Tamoxifen

19
Q

Tumor lysis syndrome

A

Occurs when a chemotherapeutic drug is so effective that proteins from lysed tumor cells can cause kidney failure

20
Q

If RAS is mutated, would targeting a growth factor receptor be effective?

A

NO; RAS is downstream of growth factor receptors and is operating independently if mutated

21
Q

Vemurafenib, Dabrafenib

A

small molecule inhibitors of mutant B-Raf kinase

This mutation is present in most melanomas

Resistance may develop months later with elevated ERK signaling

22
Q

Longest parts of cell cycle? Shortest?

A

G1 and S phase take up around 40% of the cell cycle each

M phase takes up only 2% of the cell cycle

23
Q

Rationally Designed Therapy

A

Drugs that target causitive molecular abnormality of fundamental, universal cellular processes

Require precise knowledge of cause of disease

Include:

  1. Small molecule inhibitors
  2. Antibodies
24
Q

Antibiotics

A

Intercalate into DNA, cause single strand DNA breaks, and prevent transcription

Toxicity associated with longterm use

Minimally myelosupressive and immunosuppressive

25
Q

Alkylating Agents

A

Highly reactive compounds that crosslink DNA and proteins

Prevent DNA replication and transcription of RNA

High toxicity to bone marrow and intestinal mucosa

All are mutagenic/carcinogenic and can induce secondary leukemia

Cells mutant for p53 have intrinsic resistance

26
Q

5-fluorouracil

A

Antimetabolite that inhibits synthesis of thyidine from uracil

Potent radiosensitizer ; useful for locally advanced and accessible tumors

27
Q

Venetoclax

A

Used to treat CLL where there’s an overexpression of Bcl-2

It acts as a Bcl-2 antagonist in order to allow apoptosis

May lead to Tumor Lysis Syndrome

28
Q

Antimetabolites

A

Analogs of molecules required for DNA Synthesis (amino acids and vitamins)

S Phase Specific

Most effective for rapidly proliferating tumors - all cause myelosuppression (decreased bone marrow)

29
Q

Aromatase Inhibitors

A

Exemestane and Anastrozole

Block Aromatase, which is responsible for synthesis of estrogen

30
Q

Cells with a p53 mutation have intrinsic resistance to what class of drugs?

A

Alkylating Agents

31
Q

Rituximab

A

Monoclonal antibody that binds CD 20

Found on 90% of non-Hodgkin’s lymphomas

Can cause Tumor Lysis Syndrome

32
Q

GnRH Analogs

A

Leuprolide, Goserelin

Block sex hormone synthesis in testes and ovaries

33
Q

Bevacizumab

A

Humanized antibody to VEGF that prevents it from binding to receptors

34
Q

PD-1

A

Receptor on T cell that reduces cytotoxic activity when stimulated

35
Q

Support Therapy

A

Drugs designed to support bone marrow function, etc

These drugs enable patients to tolerate chemotherapy, but do not play any role in killing cancer

36
Q

Nivolumab, Pembrolizumab

A

Binds PD-1 on T cell and prevent inhibitory signal, thus allowing T Cells to kill cancer cells via production of IL-2 and Interferon

37
Q

Trametenib

A

Inhibit MEK1 and MEK2 (downstream substrates of B-Raf)

Used in combination with B-Raf inhibitors

38
Q

Inhibits MEK1 and MEK2

A

Trametenib

39
Q

Progestins

A

Megestrol

Inhibit pituitary release of gonadotropins and can stimulate apetite in patients with cachexia

40
Q

Antiandrogens

A

Used to treat prostate cancer

Steroidal Antiandrogens - inhibit androgen binding to receptor (cyproterone)

Non-steroidal Antiandrogens - inhibit nuclear translocation of receptor (bicalutamide)

Basically they inhibit Androgen Receptor-dependent gene transcription

41
Q

Doxorubicin and Daunorubicin

A

Members of Antibiotic class (DNA Damaging drugs)

Doxorubicin causes unusual cardiomyopathy due to free radical generation

Also causes Red Urine

Induces upregulation of MDR1 and has resistance

Foundations of Disease and Therapy (12 decks)

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