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Heme/ Lymph > Antineoplastic Agents Part I: Chemotherapy in general > Flashcards

Antineoplastic Agents Part I: Chemotherapy in general Flashcards

1
Q

Top 4 cancer sites

A
  1. Breast cancer (female)
  2. Lung and bronchus
  3. Prostate
  4. Colon and Rectum
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2
Q

Alkylating Agents (list)

A

Nitrogen mustards:

  • cyclophosphamide
  • ifosfamide

Alkyl sulfonate:
- Busulfan

Platinum coordination complexes:
- Cisplatin

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3
Q

Natural Products (originally isolated from plants or bacteria, etc.)

A

Vinca alkaloids:
Vinblastine
Vincristine

Taxanes: Paclitaxel

Tpipodophyllotoxins: Etoposide

Antibiotics: Bleomycin, Doxorubicin

Enzymes: L-Asparaginase

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4
Q

Antimetabolites

A

Folic acid analogs: Methotrexate (MTX)

Pyramidine analogs: Fluorouracil

Purine analogs: mercaptopurine

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5
Q

Differentiating agents

A

Tretinoin

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6
Q

Biological response modifiers

A

Interferon-alfa

Interleukin-2

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7
Q

Immunomodulators

A

Thalidomide

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8
Q

Rescue agents

A

Leucovorin

Mesna

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9
Q

Protein tyrosine kinase inhibitors

A

Dasatinib
Erlotinib
Imatinib
Lapatinib

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10
Q

Proteasome inhibitor

A

Bortezomib

Remember it by “Borteasome”

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11
Q

Monoclonal Antibodies

A

Bevacizumab
Cetuximab
Rituximab
Trastuzumab

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12
Q

Agents used to minimize adverse effects

A

Filgrastim
Ondansetron
Ondansetron

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13
Q

Cancer Treatment Modalities

A

Chemotherapy

  • Immunotherapy
  • Targeted Therapies
  • Vaccines

Radiation Therapy
Surgery
Transplantation

Combinations are the norm

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14
Q

Primary Induction Therapy

A

The main treatment that provides the best possible outcome

Also called first-line therapy

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15
Q

Neoadjuvant Therapy

A

Treatment given BEFORE primary induction therapy in order to improve outcome
E.g., Chemo or radiation to shrink a tumor before surgery

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16
Q

Adjuvant Therapy

A

Additional therapy given CONCOMITANTLY or AFTER primary induction therapy in order to reduce the probability of relapse

17
Q

Biology of Cancer: The Cell Cycle

A

Cell cycle checkpoints control transitions between cell cycle stages

DNA damage?
Spindle assembly?
Favorable conditions?
Completed replication?

Failure to pass checkpoint: cell cycle is delayed or cells apoptose

18
Q

Cycling Out of Control

A

In many forms of cancer, proteins or pathways involved in regulating the checkpoints between the phases of the cell cycle may be absent or mutated
For example: p53, CDKs

Aberrations in checkpoint regulation result in uncontrolled and unregulated cell proliferation

Cell cycle specific (dividing) vs. cell cycle nonspecific (regardless of whether they are dividing or not)

19
Q

Cell cycle specific agents

A 
Antimetabolites
antitumor antibiotic-bleomycin
Taxanes
Vinca alkaloids
Toppoisomerase inhibitors
20
Q

Cell cycle nonspecific agents

A

Alkylating agents
anthracyclines
platinum analogs

21
Q

Growth fraction

A

the ratio of proliferating cells to resting cells (G0)

Growth fraction is a determinant of responsiveness to chemotherapy
Cells with high growth fraction:
- Bone marrow
- GI tract
- Hair follicles
- Sperm-forming cells
22
Q

Growth Fraction and Therapeutic Response

A

The initial growth rate of most solid tumors is rapid but decreases over time

Burkitt lymphoma (high growth fraction; curable by chemotherapy) vs. colorectal carcinoma (low growth fraction; chemotherapy has minor activity)

Some disseminated tumors can be cured by single-agent chemotherapy

The growth fraction of solid tumors can be increased by reducing the tumor burden (i.e., surgery or radiation)

23
Q

Log Cell Kill Hypothesis

A

A fraction (not an absolute number) of cells are killed
A three-log cell kill eliminates 99.9% of cells:
10^12 to 10^9 cells
10^6 to 10^3 cells

24
Q

Therapeutic Balance: Efficacy vs. Toxicity

A

Challenge: provide dose that is therapeutic without being (too) toxic

Antineoplastic drugs harm both cancerous tissues and healthy tissues

Not all drug regimens are appropriate for all patients

Factors to consider:
Renal and hepatic function
Bone marrow reserve
General performance status
Concurrent medical problems
Patient willingness
25
Q

Primary resistance

A

An absence of response on the first drug exposure

Thought to be due to genomic instability

26
Q

Acquired resistance

A 
Develops in response to exposure to a given antineoplastic agent
Often highly specific to a single drug, or class of drugs, and is usually due to an increased expression of one or more genes
27
Q

Examples of single agent resistance pathways include:

A

decreased drug transport into cells
reduced drug affinity due to mutations or alterations of the drug target
increased expression of an enzyme that causes drug inactivation
increased expression of DNA repair enzymes for drugs that damage DNA

28
Q

Multidrug resistance and ATP-dependent Transporters

A

ATP-dependent transporter gene amplification in neoplasms confers resistance to a broad range of agents used in cancer treatments

The P-glycoprotein is an ATP-dependent efflux pump that actively pumps antineoplastic agents out of cells (MDR1 gene)

Anthracyclines, vinca alkaloids, etoposide, paclitaxel, and dactinomycin

29
Q

Toxicity of Antineoplastic Agents

A

The lack of neoplastic specificity for chemotherapeutic drugs is a major limiting factor in the treatment of cancer

Rapidly proliferating normal tissues (tissues with high growth fractions) are the major sites of toxicity
bone marrow, gastrointestinal tract, hair follicles, buccal mucosa, sperm forming cells

Many antineoplastic agents are mutagens themselves and can give rise to neoplasms years after treatment (e.g., alkylating agents have caused AML and ALL)

30
Q

Common Adverse Effects of Chemotherapy

A

Occur during therapy with nearly all classic antineoplastic agents:

Nausea
Vomiting
Fatigue
Stomatitis
Alopecia

Myelosuppression – can lead to impaired wound healing and predisposition to infection
Low sperm counts and azoospermia
Depressed development of children exposed to antineoplastic agents

31
Q

Minimizing Adverse Effects of Chemotherapy

A

Choose the route of administration that minimizes systemic toxicity as much as possible

Pharmacologic agents that help decrease adverse effects:

  • Hematopoietic agents for neutropenia, thrombocytopenia, and anemia (will discuss later in the course)
  • Serotonin receptor antagonist (ondansetron) and other drugs for emetogenic effects
  • Bisphosphonates to delay skeletal complications

Rest and recovery

Heme/ Lymph (15 decks)

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