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FPP MSS > Anti-Neoplastics > Flashcards

Anti-Neoplastics Flashcards

1
Q

Cell cycle-nonspecific

A
  • Exerts cytotoxicity in a nonspecific manner - kills cells in any stage of cell cycle (even G0) - kills normal and neoplastic cells to the same extent Examples: alkylating agents
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2
Q

Cell cycle-specific, phase-specific

A
  • More active at specific phase of cell cycle
  • Some selectivity of action ( more cytotoxic for neoplastic cells)
  • given by continuous infusion of in frequent small doses
  • *G1**: Predisone
  • *S**: Cytarabine, 5FU, MTX, 6MP, Hydroxyurea
  • *G2**: Bleomycin, etoposide, Paclitaxel
  • *M**: Vinbastine, vincristine
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3
Q

Cell cycle-specific, phase-nonspecific

A
  • Preferential killing of proliferating neoplastic cells BUT without regard for phase of cell cycle - administered in large doses to take advantage of their sparing effect on normal cells in G0 Ex: cyclophosphamide, cisplatin, Doxorubicin
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4
Q

sequential blockade

A

Simultaneous action of two inhibitors acting on different steps of a linear metabolic pathway

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5
Q

concurrent inhibition

A

inhibitors block two separate pathways that lead to same end product

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6
Q

rescue

A

High doses of MTX necessary to bind DHFR. Rescue normal cells with leucovarin ( folate coenzyme that does not require reduction by DHFR). Normal cells have increased capacity to bring in leucovorin

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7
Q

complementary inhibition

A

One drug affects the function of an end product, the other drug affects the synthesis of that end product

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8
Q

Synchronization

A

Synchronize cells so that they are in one phase and then use drug that is specific for that phase

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9
Q

recruitment

A

Mobilizing slowly proliferating or non-proliferating cells to more rapid proliferation ( bring cells out of G0 into cell cycle)

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10
Q

Mechlorethamine

A

Mechanism: Bi-functional alkylating agent that produces DNA crosslinks

Cell Cycle: phase non-specific

Use: Hodgkin’s and non-Hodgkin’s lymphoma

Toxicity: Hematopoiesis suppression, damage to intestinal mucosa, N/V, alopecia

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11
Q

Cyclophosphamide

A

Mechanism: Activated by cyt. P450 Cell Cycle: phase non-specific

Use: very broad spectrum, Hodgkin’s and non-Hodgkin’s lymphoma, mutiple myeloma, neuroblastoma, leukemias. Carcinoma of the endometrium, breast, lung

Toxicity: May cause sterile hemorrhagic cystitis ( Prevented with Mesna)

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12
Q

Carmustine

A

Mechanism: Introduce alkyl groups into DNA. Highly lipophilic– rapidly crosses blood-brain barrier

Cell Cycle: Non-specific

Use: brain tumors, multiple myeloma, melanoma

Toxicity: Hematopoiesis suppression, N/V, alopecia

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13
Q

Methotrexate

A

Mechanism: metabolite binds to dihydrofolate reductase (DHFR) and prevent formation of tetrahydrofolate (THF) - use is followed with rescue with Leucovorin

Cell Cycle: S phase specific

Use: ALL; choriocarcinoma

Toxicity: Binds serum albumin so avoid use with other drugs that will displace it from albumin. Intestinal epithelium, bone marrow suppression, renal tubular necrosis

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14
Q

5 fluorouracil

A

Mechanism: Activated in cells to FUTP ( inhibits RNA synthesis) and FdUMP ( interferes with thymidylate synthetase –> DNA synthesis)

Cell Cycle: S- phase specific

Use: Carcinoma of the stomach, colon, pancreas, ovary, head, neck, breast, bladder. Basal Cell carcinoma

Toxicity: nausea, anorexia, diarrhea, delayed myelosuppression

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15
Q

Cytarabine

A

Mechanism: cytidine analog that competes with cytidine for all 3 phosphorylation steps to dCTP. competes with dCTP for incorporation into DNA

Cell Cycle: S-phase specific

Use: Acute leukemia (AML)

Toxicity: Myelosuppression and neurotoxicity

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16
Q

Mercaptopurine

A

Mechanism: Purine analog that is converted in cells to ribonucleotide that inhibits RNA and DNA synthesis

Cell Cycle: S-phase

Use: acute leukemia

Toxicity: bone marrow depression, N/V, anorexia, jaudice

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17
Q

Hydroxyurea

A

Mechanism: inhibits ribonucleotide reductase ( blocks DNA synthesis)

Cell Cycle: S-Phase (G1/S interface)

Use: Chronic granulocytic leukemia, head and neck cancer. Useful w/ radiation

Toxicity: Hematopoietic depression, GI disturbances

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18
Q

Vinblastine

A

Mechanism: Binds to tubulin, inhibits formation of microtubules and mitotic spindle

Cell Cycle: M-phase

Use: Hodgkin’s and non-Hodgkin’s lymphoma, breast cancer

Toxicity: Strongly myelosuppressive, epithelial ulcerations

19
Q

Vincristine

A

Mechanism: binds to tubulin, inhibits formation of microtubules and mitotic spindle

Cell Cycle: M- phase

Use: ALL, lymphomas, Wilm’s tumor, nueroblastoma

Toxicity: alopecia, neuromuscular abnormalities (peripheral neuropathies), less bone marrow suppression

20
Q

Paclitaxel

A

Mechanism: enhances assembly and stability of microtubules by binding to Beta subunit of tubulin

Cell Cycle: G2 phase (G2/M interface)

Use: refractory ovarian cancer; breast

Toxicity: Dose limiting leukopenia, peripheral neuropathy, myalgia/ Arthralgia

21
Q

Doxorubicine

A

Mechanism: 1) Prevents DNA/RNA synthesis by intercalating between DNA bp–> distorts helix. 2) causes lipid peroxidation and free radical generation. 3) binds to DNA and topoisomerase II

Cell Cycle: phase non-specific

Use: Hodgkin’s and non-Hodgkin’s lymphoma, breast, ovary, small-cell lung

Toxicity: Cardiomyopathy, bone marrow depression, alopecia, GI disturbances - antiangiogenic properties

22
Q

Bleomycin

A

Mechanism: glycopeptides that bind DNA–> causes oxidative like damage to DNA that leads to strand breaks

Cell Cycle: specific for M phase

Use: germ cell tumors of testes and ovaries, head, neck, lung, lymphomas

Toxicity: dose-related pulmonary toxicity, vesiculation of the skin, skin hyperpigmentation, minimal myelosuppression and immunosuppression Lung and skin have lowest levels of Bleomycin hydrolase

23
Q

Etoposide

A

Mechanism: Stabilizes DNA topoisomerase II complexes–> ds DNA breaks

Cell Cycle: late G2 phase (late S)

Use: lymphomas, acute nonlymphocytic leukemia, small cell carcinoma of lung, testicular tumors

Toxicity: Leukopenia, N/V, diarrhea

24
Q

Filgrastim

A

Mechanism: stimulates granulocytes (neutrophils) production by marrow

Cell Cycle:

Use: give after myelosuppression to speed neutrophil recovery (used to limit neutropenia) Toxicity: bone pain

25
Q

Trastuzumab

A

Mechanism: Monoclonal antibody that binds to HER2 receptor

Use: Breast cancers that overexpress HER2

Toxicity: Cardiomyopathy, hypersensitivity, infusion reactions

26
Q

Cisplatin

A

Mechanism: Platinum coordination complex. Hydrolysis leads to activated species that causes DNA crosslinks

Cell Cycle: Cycle-specific Phase non-specific

Use: Wide spectrum– cancer of testis, ovary, head, neck, bladder, colon, esophagus, small cell lung

Toxicity: Nephrotoxicity, otoxicity, peripheral neuropathy, electrolyte disturbance, N/V, myelosuppression

27
Q

Procarbazine

A

Mechanism: activated in-vivo to a methylating agent that causes chromosomal damage

Cell Cycle: Most effective in G1 and S

Use: Hodgkin’s lymphoma

Toxicity: myelosuppression, N/V

28
Q

Prednisone

A

Mechanism: binds to steroid receptors that regulate cell growth (may arrest cells in G1). Depresses RNA synthesis of many growth genes. Induces nucleases that may modulate cell lysis

Use: Acute and chronic lymphocytic leukemia, Hodgkin’s disease, non-Hodgkins lymphoma, breast cancer

Toxicity: Immunosuppression, limited myelosuppression Palliative: anti-emetic, stimulates appetite, anti-inflammatory

29
Q

Tamoxifen

A

Mechanism: anti-estrogen that competitively blocks estrogen receptors. Activated by CYP2D6

Use: Adjuvant therapy in post-menopausal breast cancer. Prophylaxis in women at high risk for breast cancer

Toxicity: hot flashes, fatigue, nausea, bone and other MSK pain Tumor regrows when Tamoxifen is stopped. Stop growth, but does not kill

30
Q

Letrozole

A

Mechanism: Aromatase inhibitor (inhibits conversion of androgens to estrogens)

Use: 1st line tx of R+ breast carcinoma in post- menopausal women

Toxicity: bone pain and other MSK pain, hot flashes, nausea, fatigue

31
Q

Leuprolide

A

Mechanism: analog of GnRH. Initially causes surge in testosterone but after 2 -4 weeks, it desensitizes GnRH signaling (inhibits LH/FSH secretion) and decreases testosterone synthesis

Use: Advanced hormonally responsive prostate cancer

Toxicity: hot flashes, impotence

32
Q

Flutamide

A

Mechanism: Potent non-steroidal anti-androgen that blocks androgen receptor

Use: Metastatic prostate cancer

Toxicity: gynecomastia, diarrhea, hepatotoxicity

33
Q

When is a tumor mass first detected?

A

When there are 10^9 cells

34
Q

When are tumor cells most sensitive to chemotherapeutic agents?

A

During active (early) growth periods

35
Q

What is the principle of the Log Kill hypothesis

A

Killing of tumor cells follows first order kinetics– a constant dose of drug kills a constant fraction of tumor cells Tx that kills 90% of cells produces one-log kill.

36
Q

To be curative, what efficiency must the chemo regimen have?

A

2-4 log kill efficiency ( repeated for 4-12 cycles of therapy)

37
Q

What is the total kill concept?

A

One surviving cell can regenerate the tumor The lifespan of the host is inversely related to the number of cells that survive the therapeutic measures

38
Q

What is the optimal dosing frequency for one cycle of treatment?

A
  • Class I and III: given as a single dose for each cycle - Class II: given by continuous infusion or in frequent small doses - Optimal intervals are those that deliver the next cycle of tx when there is the greatest difference between recovery of normal tissues and of the tumor
39
Q

Imatinibmesylate (Gleevect)

A

Kinase inhibitor

40
Q

Mesna

A

Cyclophasphamide induced sterile hemorrhagic cystitis can be partially prevented with Mesna

41
Q

Leucovorin

A

Used in “rescue” after high dose MTX

42
Q

Nitrosoureas

A

Alkylating agent– Carmustine

43
Q

Acrolein

A

FPP MSS (13 decks)

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