Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/46

Click to flip

46 Cards in this Set

  • Front
  • Back
Replace hydrogen atoms with an alkyl radical causing covalent bonds with electron rich nucleic acids, proteins, amino acids, and glutathione leading to misreading of DNA code, cross-linking of DNA, single or double strand breaks, and inhibition of DNA, RNA, and protein synthesis
Alkylating Agents
Subgroup of Alkylating agents with additional MOA of inhibiting DNA replication
Nitrosureas
Disrupt nucleic acid synthesis (work only on dividing cells in S phase) by either:
1. interfering with normal synthesis of nucleic acid by falsely substituting for purines or pyrimidines in the metabolic pathway
2. competitively binding for enzymes which process the purines and pyrimidines into DNA and therefore inhibit the synthesis of DNA
Antimetabolites
Bind to dihydrofolate reductase, resulting in depletion of reduced folates (tetrahydrofolate), which is necessary for thymidine and purine synthesis (thus inhibiting DNA synthesis) cell cycle specific
Folate antagonists
Metabolized to fluorodeoxyuridine monophosphate, (FdUMP), which, in the prescence of folates, binds tightly and interferes with thymidylate synthetase (enzyme required for synthesis of thymidine)
Fluorinated Pyrimidines
Phosphorylated to the active triphosphate form which competes with deoxycytidine for DNA polymerase, inhibiting DNA synthesis
Cytidine Analogues
Inhibits de novo nucleotide production
Gemcitabine ribonucleotide reductase
Covalent bond with topoisomerase I; binding allows uncoiling of double strand DNA which results in single-stranded DNA breaks
Topoisomerase I inhibitors
Intercalation of an area of the DNA double helix thus preventing DNA transcription and replication
Topoisomerase II inhibitors
Anthracylines-Intercalators
Semi-synthetic podophyllotoxins that bind to tubulin; cell damage caused by DNA strand breaks through topoisomerase inhibition
Topoisomerase II inhibitors
Epipodophyllotoxins-Non Intercalators
Bind to microtubular proteins, which are essential contractile proteins of the mitotic spindle; arrest mitosis at the metaphase (cell-cycle specific)
Vinca Alkaloids

Tubulin Interactive Agents
Bind to tubulin, inducing the formation of aberrant, stabilized microtubules
Taxanes

Tubulin Interactive Agents
Analogue of epitholene B, inhibits microtubules, arresting cell division in mitotic phase, causing cell death
Epitholenes

Non-taxane microtubule stabilizing agent
Active metal complex causes single and double strand breaks via intercalation folowed by production of free radicals from oxygen (inhibits DNA replication)
Antitumor Antibiotics (DNA strand breakage agent)
Hydrolyzes the circultating aminoacid L-asparagine into aspartic acid, thus indirectly inhibiting protein synthesis.
Asparaginase

Misc.
Blocks DNA synthesis by inhibiting the enzyme ribonucleotide reductase
Hydroxyurea
Initially stimulate release of gonadotropins, followed downregulation of pituitary receptors for LHRH (resulting in downregulation due to excessive stimulation). Pituitary stops producing FSH adn LH and eventually testes stop production of testoterone and ovaries stop production of estrogen.
LHRH agonists (gonadotropin-releasing hormone analogs)

Antiestrogens and antiandrogens
Blocks estrogen receptors in most hormonal tissues. Stimulates production of transforming growth factor beta (inhibitory growth factor)
Estrogen receptor modulators (antiestrogens, mixed estrogen agonist/antagonist)
Non-steroidal inhibitors of corticosteroid synthesis; inhibits conversion of circulating androgens into estrogens
Aromatase inhibitors
May slow DNA synthesis through inhibition of glucose transport or phosphorylation, leading to a decrease of cellular energy
Corticosteroids
Induces the enzyme, 17-hydrooxysteroid dehydrogenase, which oxidizes estradiol to the less potent form, estrone. Also activates estrogen sulfatransferase, which catalyzes the sulfation of estrogen to less active forms, thus antagonizing growth
Progestins
Inhibits BCR-ABL tyrosine kinase (abnormal gene of the Ph chromosome in CML) specific inhibitor of the translocation-created enzyme, works by blocking the rapid growth of white blood cells
Imatinib mesylate

Signal Transduction inhibitor
Inhibits the intracellular phophorylation of numerous tyrosine kinases associated with transmembrane cell surface receptors, including the tyrosine kinases associated with the epidermals growth factor (EGFR-TK), (blocks growth stimulatory signals in cancer cells)
Gefitinib

Signal Transduction inhibitor
Human epidermal growth factor receptor Type 1/epidermal growth factor receptor (HER1/EGFR) tyrosine kinase inhibitor
Erlotinib

Signal Transduction inhbitor
Targets the tyrosine kinase domains of HER-2 and EGFR-1, inhibiting growth of tumor cells and causing apoptosis.
Lapatinib

Signal Transduction inhibitor
Inhibits TK domains of VEGFR and other factors associated with metastasis and cell proliferation
Sorafenib and Sunitinib

Signal Transduction inhibitor
Target receptors that are unique to or overexpressed in tumors
Monoclonal Antibodies
Reacts with CD20 (a B lymphocyte surface antigen) and depletes normal and malignant B cells; it also binds complement and increases antibody-dependent cell-mediated cytotoxicity
Rituximab
Antibody directed against HER/2 receptors on some breast cancer cells
Transtuzumab
Antibody to CD33 (expressed on leukemic blasts on > 80% in AML)

MOA: After binding, ozogamicin is released inside the myeloid cell, binding to DNA and causing double-stranded breaks
Gemtuzamab ozogamicin
Binds to CD20, resulting in apoptosis
Alemtuzumab
Radiolabeled monoclonal antibody for refractory non-Hodgkin's lymphoma
Tositumomab
targets the EGFR and blocks the ability of EGF to initiate receptor activation and signaling to the tumor. Blockade results in an inhibition of tumor growth by interfering with the effects of EGFR activation including tumor invasion and metastases, cell repair and angiogenesis
Cetuximab
binds to EGFR, resulting in interference of EGFR signaling, producing an anti-tumor effect.
Panitumimab
Radiopharmaceutical for one type of non-Hodgkin's lymphoma, used with Rituxan
Ibritumomab
Diagnostic imagining agent
Nofetbumomab
Anitiviral and antitumor effects of interferons are thought to be due to induction of enzymes that inhibit the synthesis of protein and DNA (block viral replication, suppress cell proliferation, enhances phagocytosis by macrophages)
Interferons

Type I - interferon alpha and interferon beta

Type II - interferon gamma
Immunoregulatory protein produced by lymphocytes that exhibits a wide range of immunologic effects. It has no direct antitumor activity, but mediates its cytotoxicity through activation of effector cells including T-cells, natural killer cells, and lymphokine-activated killer cells
Interleukins-Interleukin 2
Fusion protein designed to direct the cytocidal action of diptheria toxin to cells which express the IL-2 receptor
Denileukin difitox
Recombinant humanized monoclonal IgG1 antibody that binds to and inhibits a natural protein called human vascular endothelial growth factor (VEGF) which plays a role in the formation and maintenance of tumor blood vessels; works by targeting and inhibiting the function of a natural protein called "vascular endothelial growth factor" that stimulates new blood vessel formation.
Bevacizumamb

Antiangiogensis agents
Inhibits TNF-alpha, reduces phagocytosis by neutrophils, increases production of interleukin-10, alters adhesion molecule expression, and enhances cell-mediated immunity via interactions with T-cells

Angiogensis inhibitor
Thalidomide
Proteasome inhibitors
Bortezomib
Interacts with retinoic acid receptor to terminally differentiate leukemic promyeloblasts
Tretinoin
Other MOA
Arsenic trioxide
Synthetic retinoid analogue that selectively activates a subclass of retinoid receptors called retinoid X receptors (RXR); once activated, they regulate cell differentiation, proliferation, and apoptosis
Bexarotene
Chemoprotectants
Mesna (sodium-2-mercapto-ethanesulfonate)
Dexrazoxane (Zinecard)
Amifostine (Ethyol)