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Fundamentals 3- Heme > Anticancer Drugs > Flashcards

Anticancer Drugs Flashcards

1
Q

What are the five subcategories of cytotoxic agents?

A
  1. Antimetabolites
  2. alkylating agents
  3. other DNA binders
  4. Anti-topoisomerase
  5. Anti-microtubule agents
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2
Q

What are the 3 anti-metabolite drugs we are responsible for?

A
  1. 5-Fluorouracil
  2. Cytarabine
  3. Methotextrate (+leucovorin)
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3
Q

What are the three alkylating agents we are responsible for?

A
  1. Mechlorethamine
  2. Cyclophosphamide
  3. cisplatin
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4
Q

What cytotoxic chemotherapy drugs bind to DNA?

A
  1. Doxorubicin

2. Bleomycin

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5
Q

What are the two anti-topoisomerase drugs? Which inhibits topo1? topo2?

A
  1. Irinotecan (topo1)

2. Etoposide (topo2)

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6
Q

What drugs inhibit the formation of microtubules?

What drugs inhibit the disassembly of microtubules?

A

Assembly:
Vincristine, Vinblastine

Dis-assembly:
1. Paclitaxel

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7
Q

What chemotherapy drugs operate as hormone agonists or antagonists?

A 
Prednisone
Tamoxifen 
Anastrozole
Flutamide
leuprolide (AGONIST)
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8
Q

What chemotherapy drugs inhibit tyrosine kinase?

A
  1. Imatinib (inhibits BCR-ABL)

2. bevacizumab (inhibits VEGF)

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9
Q

What are the three tissues in the body that divide through adulthood?

A
  1. Bone marrow
  2. Intestinal crypts
  3. Hair follicles
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10
Q

What stage of the cell cycle are most cells of the body in?

A

G0 - non-dividing cells

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11
Q

What are the 3 cell-cycle checkpoints?

What is the job of each?

A
  1. G1/S- check precursors and DNA damage
  2. G2/M- make sure DNA replicated okay and there is no damage
  3. Spindle Checkpoint in M - make sure microtubules are connected properly
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12
Q

Why do cancer cells most often have to have lesions in more than one critical molecule to actually cause cancer?

A

Most mutations disrupt the cell-cycle (LOF of tumor repressors or GOF of proto-oncogenes).
There is redundancy in controlling cell proliferation so often there must be 2 mutations

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13
Q

What are the three major strategies used for non-toxic, curative chemotherapy?

A
  1. gene therapy to replace defective genes (easier for LOF tumor suppressor genes than GOF oncogenes)
  2. Target drugs specifically for cancer cells by utilizing tumor-specific agents
  3. Inhibition of new blood vessel synthesis so only fast growing tumors are affected
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14
Q

What is imatinib used to treat? How does it work?

A

It treats chronic myelocytic leukemia by inhibiting BCR-ABL tyrosine kinase

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15
Q

Most anti-cancer drugs selectively kill what type of cell?

A

One that is proliferating. The shorter the doubling time of the cell, the more effective the drug

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16
Q

What are the three major problems with chemo selectively killing rapidly proliferating cells?

A
  1. Some normal cells (marrow, GI, hair follicles) also rapidly divide. When these cells are killed, chance of infection, prolonged bleeding time, emetic effects and hairloss occur.
    2 Killing all proliferating cells may not lead to long-term survival (cancer stem cells are still present)
  2. Many tumors grow slowly (colon and lung) or have a fraction of cells that are slow growing (center of solid tumors because they have less blood supply
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17
Q

What is the doubling time of colon cancer? lung cancer?

What does this mean for treatment?

A

Colon- 80 days
Lung - 90 days (except small cell)

This means that no drugs will ensure long term survival because the drugs kill proliferating cells and these cells proliferate too slowly to be killed

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18
Q

Virtually all cancer drugs are _______ specific.

However, they can be broken down further into 2 classifications. _________ specific and _______ non-specific.

A

All drugs are cell-cycle specific (do not kill cells in Go)

  1. Phase specific- kill cells in a particular phase of the cell cycle
  2. Phase non-specific = kill cycling cells regardless of what phase they are in
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19
Q

What are phase-specific drugs?

Give 2 examples.

A

Drugs that kill cells if they are exposed in a particular phase of the cell cycle

  1. Vinca alkaloids (vincristine and vinblastine) in M phase (bc they prevent spindle formation)
  2. Antimetabolites kill in S phase
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20
Q

What are phase-nonspecific drugs?

Give an example.

A

They kill cycling cells regardless of where they are in the cell cycle during exposure.
Alkylating agents modify DNA at any stage in the cell cycle but KILL the cell in S.

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21
Q

What is an example of a drug that is phase specific AND blocks the cell cycle itself?

A

Cytarabine is an S-phase agent that prevents G1 cells from entering S

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22
Q

What does it mean that cell kills are “first order”?

A

A percent of cells are killed with each cancer drug dose.
If the drug kills 99% of the cancer cells, it will NOT kill the final 1% on the next dose. It will kill 99% of the remaining 1%.
The other name for first order killing is logarithmic kills

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23
Q

What three confounding variable make the tumors difficult to kill with chemo?

A
  1. tumor does not idle between doses so it will repopulate some while the patient is recovering from the dose
  2. Cells further from the surface of the tumor grow more slowly and are less likely to be killed
  3. Tumors develop resistance to chemo
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24
Q

How do tumors gain resistance to chemotherapy?

A
  1. Induction and gene duplication of MDR pump which export a variety of cancer drugs
  2. further loss of cell-cycle control
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25
Q

How are most cancer patients treated to maximize the chance of a cure?
What are 2 specific examples?

A

Combination therapy
1. MOPP (mechlorethamine, viscristine, procarbazine, prednisone) for Hodgkin’s lymphoma

  1. CMF (cyclophosphamide, methotextrate, fluorouracil) for breast cancer
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26
Q

Antimetabolite drugs are analogs of ______, ______ or __________ that interfere with _________________________.

A

purine, pyrimidine and necleoside analogs that interfere with the synthesis of normal nucleic acid precursors by:

  1. inhibiting DNA pol or causing chain termination
  2. inhibiting synthesis of bases or nucleosides
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27
Q

What type of cancers are antimetabolites used frequently against?

A

leukemias and lymphomas

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28
Q

What is the general function of an anti-purine drug?

A
  1. They inhibit the conversion of IMP to GMP and AMP

2. Feedback inhibit the rate-limiting step of purine biosythesis, ribosylamine-5-phosphate

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29
Q

What are the pyrimidine analogs used as anti-cancer drugs?

A
  1. 5-fluorouracil

2. Cytarabine

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30
Q

What is the mechanism of action of 5FU?

A
  1. 5-FU prodrug that gets activated to 5-FdUMP.
  2. 5-FdUMP resembles dUMP (the substrate for thymidylate synthase).
  3. 5-FdUMP inhibits TS by binding it with a 1000x greater affinity than dUMP
  4. the cell can’t make dTMP (thymidine levels drop in the cell)
  5. Cells in S phase are killed
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31
Q

What are the adverse effects of 5FU?

A
  1. bone marrow depression

2. GI ulcers and oral ulcers

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32
Q

What cancers are 5FU used to treat?

A

pancreatic cancer and adenomas

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33
Q

What is the mechanism of action of cytarabine?

A
  1. Cytosine arabinoside (aka cytarabine) is a cytosine analog where the 2’ hydroxyl points up instead of down
  2. When triphosphate cytarabine gets incorporated into DNA it inhibits chain elongation and the cells in S phase die
  • It also blocks entry from G1 to S
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34
Q

What is the mechanism of action of methotrexate?

A

It is an analog of folic acid which is normally converted to tetrahydrofolic acid.
THF acid donates a C1 unit to enzymes that synthesize purines (de novo), pyrimidines (TS step) and a few AA.
In order to transfer the C1, THF must be reduced by DHFR.
Methotrexate binds DHFR inhibiting it leading to decreased building blocks for DNA and RNA and causing a buildup of DHF-polyglutamates which are toxic to cells.

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35
Q

What is the mechanism of action of leucovorin?

A

It “rescues” cells after they have been given high doses of methotrexate because it is a fully reduced folate coenzyme.
Its main function is to reduce toxicity

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36
Q

What are the short term and long term adverse effects of methotrexate?

A

Short term:
myelosuppression
GI ulceration
pneumonitis with inflammatory infiltrates

Long term:
cirrhosis

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37
Q

What was the first drug to ever give a complete cure of a cancer? What was the cancer?

A

Methotrexate cured choriocarcinoma (placental cell cancer)

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38
Q

What are the 3 ways cells have gained resistance to methotrexate?

A
  1. Altered DHFR (so it can’t bind) or amplification of the DHFR gene
  2. upregulation of salvage pathway for purines (because methotrexate blocks de novo)
  3. Decreased methotrexate import
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39
Q

What is the mechanism of action of alkylating agents?

A

They are mono, bi or multi-functional
They have CH2-CH2-CL groups that cyclize, generate + charged reactive intermetiates that then can be attacked by lone pairs of electrons on nitrogen or oxygen.
N7 lone pair on guanine is a main target.
The result is crosslinking of DNA strands

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40
Q

What makes alkylating agents so toxic?

A

1.They do not discriminate between DNA targets on normal vs. cancer cells.
They CAN be administered, however, so normal cells can repair their DNA, whereas rapidly dividing cells (tumors) enter S phase with messed up DNA , replication is prevented, and the cell dies.
2. They are phase-non specific so they can attack cells anywhere in the cell cycle

41
Q

What is an example of an orally administered alkylating agent?

A

Cyclophosphamide can be given orally because it is not active until after first pass in the liver (before first pass, delocalization of electrons doesn’t provide a good leaving group)
Once it passes through the liver, p450 oxidase activates it to a phosphamide mustard

** NOT associated with liver cancer because the liver is able to FURTHER metabolize it to a non-toxic form

42
Q

What are the adverse effects of cyclophosphamide?

A
  1. bladder irritation

2. hemorrhagic cystitis

43
Q

What are the adverse effects of alkylating agents in general? (for our purposes cyclophosphamide and mechlorethamine)

A
  1. Bone marrow suppression (nadir at 2 weeks so watch for infections)
  2. GI ulcers
  3. Development of leukemia later in life
  4. Loss of hair, periods, sperm count
44
Q

What are the therapeutic uses of alkylating agents?

A

Leukemias and solid tumors

45
Q

What is the mechanism of action of cisplatin?

A

It crosslinks DNA by a mechanism similar to cyclophosphamide and mechlorethamine.
However, instead of a CH2-CH2-Cl that cyclizes and is attacked by N7 of guanine, cisplatin Cl are replaced by water making a carbonium ion that can be attacked by nitrogen
Bi-functional agents that react with guanines on same or complementary strands

46
Q

What are the adverse effects of cisplatin?

A
  1. Ototoxic
  2. peripheral neuropathy
  3. renal toxicity
  4. nausea/vomiting
  5. myelosupression
47
Q

What cancers are cisplatin used to treat?

A

solid tumors (specifically testicular and ovarian)

48
Q

What are anthracyclines? What is their mechanism of action?

A

Anti-cancer drug that is derived from antibiotics produced from Streptomyces peucetius fungi.

  1. intercalates into DNA
  2. is reduced to semiquinones that autoxidize to make ROS that damage the DNA
  3. Inhibits topoisomerase 2 which damages DNA replication and kills the cell
  4. DNA strand breaks
49
Q

What are adverse effects of anthracyclines?

A

They produce cardiomyopathy depending on total dose administered
Damage is IRREVERSIBLE

50
Q

What class of drug is doxorubicin? What cancers is it used to treat?

A

It is an anthracycline used to treat:

  1. breast, ovary, uterus
  2. testicle
  3. lung
  4. sarcomas
51
Q

What is bleomycin and what is its mechanism of action?

A

It is a glycopeptide antibiotic derived from streptomycete.
It works by chelating Cu and Fe and covalently binds to DNA.
Metal catalyzed redox leads to toxic radicals that cause multiple strand breaks and chromosomal aberrations.
It is a G2 specific drug

52
Q

What are the adverse effects of bleomycin?

A
  1. pulmonary fibrosis that can lead to death
  2. hyperpigmentation
  3. ulceration

***one of the few drugs however without marrow suppression

53
Q

What cancers are bleomycin most effective against?

A
  1. germ cell tumors (testes/ovaries)

2. squamous cell carcinoma

54
Q

What are the differences between topoisomerase I and topoisomerase II? What drugs target each?

A

Topo I is a monomer enzyme that produces single strand DNA breaks. (targeted by irinotecan)

Topo II is a tetrameric enzyme that produces double strand breaks and requires ATP. (targeted by doxorubicin and etoposide)

55
Q

What is the method of action of camptothecins?

A

Camptothecins (like irinotecan-CPT11) bind to topoisomerase I inhibiting it.
The result is single-strand DNA breaks, then double-strand breaks during S phase when DNA pol collide with the drug/enzyme complex

56
Q

What is interesting about the pharmacokinetics of irinotecan?

A

It is metabolized to active SN-38 in the liver that is 1000x as potent and more toxic than the parent compound
SN-38 is eliminated by glucuronidation by UGT1A1 enzyme. Patients that contain less of this enzyme are more susceptible to the toxic effects of nausea and leukopenia

57
Q

What cancers are irinotecan used to treat?

A

Breast, ovary, colorectal, lung

58
Q

What is the mechanism of action of epipodophyllotoxins?

What cancers can they treat?

A

Etoposide binds to and inhibits topoisomerase II resulting in DNA breaks.
(they are different from podophyllotoxins which affect microtubules)

They treat leukemias and lymphomas

59
Q

What are the similiarities and differences between vinca alkaloids and paclitaxel?

A

Vinca alkaloids DEPOLARIZE microtubules
Paclitaxel binds to microtubles and stabilizes

Both have the same essential effect of blocking progression of cells through mitosis

60
Q

What is the mechanism of action of vinca alkaloids?
What are the toxicities?
Of the two alkaloids, what are their specificities for treatment?

A

Vincristine and vinblastine bind to tubulin alpha-beta heterodimers preventing them from forming microtubules (M phase specific)

They cause myelosuppression and are neurotoxic (numb, tingling, muscle weakness) related to transport down neuronal axons on microtubules

Vincristine- childhood leukemia and lymphoma
Vinblastine- testicular cancer and solid tumors

61
Q

What is the mechanism of action of paclitaxel?
What are the adverse effects?
What is it used to treat?

A

It binds to existing microtubules on the B subunit preventing disassembly. The dynamic equilibrium of a-b dimers is essential for microtubule function.
The drug accumulates inactive microtubules in the cell inhibiting mitosis.

Adverse:
stocking glove neuropathy

Used for breast, ovarian, head and neck tumors

62
Q

What is the mechanism of action of prednisone?

A

It is a glucocorticoid used for leukemias (specifically childhood)
It induces apoptosis.

63
Q

What is the mechanism of action of tamoxifen?
What does it treat?
What population is it more effective in?

A

It is a SERM (selective estrogen receptor modulator) used in breast cancer.
It binds competitively with estrogens to cells with ER.

It works better in post-menopausal women because there is less estrogen competition
In pre-menopausal women you would need to use a GnRH agonist to release mass amounts of LH and FSH to desensitize the receptors and feedback inhibit the release of hormones

64
Q

What are aromatase inhibitors used to treat?

How do they work?

A

Anastrozole is a nonsteroidal reversible inhibitor of aromatase used to treat estrogen-sensitive breast cancers in post-menopausal women.

Post-menopausal women synthesize estrogen from androstenedione in peripheral tissue instead of from testosterone in the ovaries. Aromastase converts androstenedione to estrogen.

Anastrozole blocks the production of estrogen

65
Q

What is the mechanism of action of flutamide? What does it treat?
What drug is it often used in combo with?

A

Flutamide is an anti-androgen used to treat testicular cancer and prostate cancer.
They are often used with lueprolide (a GnRH agonist) to desensitize receptors and feedback inhibit testosterone release.
“chemical castration” so they don’t need orchiectomy

66
Q

What is the mechanism of action of Leuprolide?

A

GnRH agonist that causes transient release of LH and FSH followed by strong feedback inhibition and desensitization of receptors so testosterone is not produced

67
Q

What are the two ways inhibitors of protein kinases work?

A
  1. Monoclonal antibodies bind at cell surface to inhibit dimerization
  2. small molecules enter the cells and bind to kinase active sites inhibiting activity
68
Q

What are

  1. inib drugs
  2. umab drugs
  3. ximab drugs
A
  1. Inib are drugs that go into the cell and inhibit by binding TK active sites
  2. umab are humanized monoclonal antibodies
  3. ximab are mice cells chimerized to contain human Fc regions
69
Q

What drug inhibits BCR-ABL?

A

Imatinib- enters the cell and inhibits bcr-abl oncogene (a tyrosine kinase)

Mutations in bcr-abl have developed so now there is some CML relapse

70
Q

How do EGFR inibitors work?

What is an example?

A

They bind competitively to the ATP binding site of the epidermal growth factor tyrosine kinase.

Herceptin (Trastuzumab) binds HER-2/NEU tyrosine kinase. It is used with paclitaxel to treat breast cancer.

71
Q

What is VEGF?

A

vascular endothelial growth factor that is required for the growth of new blood vessels by binding to VEGFR (a tyrosine kinase)
By blocking VEGF, the tumor is denied blood supply and nutrients

72
Q

What is Bevacizumab?

What are the side effects?

A

It is a humanized monoclonal antibody that binds to VEGF itself blocking it from binding to VEGFR.

Used for breast, colorectal, and lung cancer (solid tumors)

Adverse effects:

  1. increased bleeding time
  2. slow wound healing
73
Q

How is Interleukin-2 used as a cancer treatment?

A

It stimulates the generation of killer T cells to help treat malignant metastatic melanoma

74
Q

What is the mechanism of action of bortezomib?

A

It inhibits the proteosome (which degrades ubiquitinated proteins)
Growth is stimulated by degrading IkB to free up NFkB which can go to the nucleus and activate genes.
If the proteosome can’t degrade IkB, NFkB will NOT be freed.

Used for multiple myelomas

75
Q

What is the mechanism of action of tretinoin?
What cancer does it treat?
What are the serious side effects?

A

It is an all trans retinoic acid (ATRA)
ATRA binds retinoic acid receptor (RAR) that dimerizes with RXR to displace a transcription activator (an inhibitor of differentiation)
ATRA will promote differentiation.

It is used in acute promyelocytic leukemia (APL) which has a mutated RAR with low ATRA affinity. By giving a lot of ATRA it can overcome this.

Side effects are pulmonary infiltration and respiratory distress (which can be prevented with glucocorticoids)

76
Q

What is the mechanism of action of thalidomide?

What kind of cancer does it treat?

A
  1. inhibits angiogenesis by blocking VEGF
  2. stimulates the immune system by blocking TNF and blocking production of IL-6 (which adheres tumor cells to bone marrow stroma)

It treats multiple myelomas

77
Q

How does a histone deacetylase inhibitor help treat cancer?

A

In cancer cells the HAT/HDAC ratio is altered
(acetyltransferase/deacetylase)
By inhibiting HDAC, you can cause apoptosis, cell cycle arrest and differentiation

78
Q

What is the mechanism of action of L-asparaginase?

A

It degrades asparagine, an essential AA. Rapidly dividing cells have a larger need for AA than quiescent cells thus the drug starves the cancer cell of AA.

Slows progression of leukemia

79
Q

What is CSF? How does it treat cancer?

A

It is colony-stimulating factor . It is used to increase the number of normal blood cells so you can use more aggressive cytotoxic agents with less bone marrow suppression.

Erythropoietin- RBC
GCSF- granulocytes
GMCSF- granulocyte-macrophage

80
Q

What 3 cancer drugs have toxicity in the lungs?

A
  1. ATRA (tretinoin) causes pulmonary distress
  2. Bleomycin - pulmonary fibrosis
  3. Methotrexate - pneumonitis
81
Q

What anticancer drug causes cardiomyopathy?

A

Doxorubicin overdose

82
Q

What drug causes nausea and leucopenia? Why?

A

Irinotecan in patients that have less active UGT1A1 alleles

83
Q

What is the goal of drug combination therapy for anticancer drugs?

A
  1. use drugs of different mechanisms of action

2. non-overlapping toxicities

84
Q

What four drug combination would be used for treating Acute Lymphoblastic leukemia Cycle 1A?

What 2 drugs are used for cycle 1B?

A

Cyclophosphamide- alkylating agent that kills in S phase
Vincristine- vinka alkaloid that kills in M phase
Doxorubicin- DNA intercalator and topoII inhibitor (S phase kill)
Dexamethasone- lympholytic

Cycle 1B-
Methotrexate- DHFR inhibitor
Cytarabine- cytosine analog

85
Q

When treating Acute lymphoblastic leukemia, __________ and _________ both cause nasuea and leucopenia so doses should be limited together. ______________ is NOT emetogenic or myelosuppressive so it is given safely with the first two drugs.

A

cyclophosphamide and doxorubicin are nausea agents but vincristine is not so it can be given with them

86
Q

What drug is often given following large methotrexate doses to reduce adverse side effects?

A

Leucovorin- a reduced folate that can compete with methotrexate DHFR inhibition to rescue normal cells

87
Q

What does polyglutamation allow methotrexate to do?

How does it affect leuvocorin rescue?

A

It allows it to remain in the cell for prolonged periods. If leucovorin is administered 36 hours after methotrexate dose, it will be polyglutamated and will not be able to rescue cells.

88
Q

What is adjuvant treatment?

A

Treatment that is utilized to reduce risk of recurrence and increase cure rate after primary treatment

89
Q

What drugs are given as adjuvant treatment for breast cancer after surgical removal of a tumor?

If the cancer recurs or is metastatic, what is the mode of treatment?

A
  1. doxorubicin- intercalator and topo II inhibitor
  2. cyclophosphamide- alkylator
  3. tamoxifen- SERM

If metastatic, combo therapy does not improve survival so use paclitaxel (spindle stabilizer to disrupt M phase)

90
Q

What is a relatively common site of relapse for breast cancer patients? Why?

A

The brain because a lot of the chemo drugs do not have good CNS penetration.
You must treat this with radiation

91
Q

What is dose-dense treatment?

A

When you administer the same dose and number of cycles but in a shorter time period. This gives the tumor less time to repopulate between treatment (it is the equivalent of accelerated fractionation with radiation)

92
Q

When treating rectal cancer, what 3 drugs are given as adjuvant therapy?

A

5FU
oxaliplatin
leuvocorin

93
Q

What is the relationship between leuvocorin and 5FU?

A

5FU inhibits thymidilate synthase (TS) by forming a ternary complex between 5FdUMP, TS and methylene tetrahydrofolate.
Leucovorin increases intracellular folate thus increasing the pool of methylene tetrahydrofolate available for the complex.

Leuvocorin enhances 5FU activity

94
Q

If a patient develops metastatic disease from rectal cancer, what is the mode of treatment?

A
  1. bevacizumab - block VEGF
  2. 5FU - antimetabolate
  3. irinotecan - topo I inhibitor
95
Q

Long term toxicities are more likely in _________________ patients with ____________ .

A

younger patients with curable malignancies (like Hodgkins) because they live longer after treatment with chemo

96
Q

What is secondary leukemia?

A

After a patient receives chemotherapy (like MOPP for Hodgkins) or especially from alkylating agents , epipodophyllotoxins and anthracyclines they will develop another leukemia.

97
Q

When would a secondary leukemia due to alkylating agents occur?
What is associated with it?
What are the chromosomal abnormalities most commonly associated with it?

A

5-7 years after treatment and there is a period of pancytopenia secondary to myelodysplasia due to deletions on chromosome 5 or 7

98
Q

When would a secondary leukemia due to an epipodophyllotoxin or anthracycline occur?
What is associated with it?
What are the chromosomal abnormalities?

A

2-3 years after treatment
It is NOT associated with a pancytopenia
They are due to chromosome abnormalities on chromosome 11

Fundamentals 3- Heme (19 decks)

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