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OS 217 Oncology > Lec 03 Cancer Chemotherapy > Flashcards

Lec 03 Cancer Chemotherapy Flashcards

1
Q

Mechanism of action of Cytotoxic Chemotherapy

A 
affect macromolecular synthesis and
function (DNA, RNA, Proteins)
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2
Q

What type of drug is Cytosine?

A

ANTI-METABOLITE

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3
Q

What type of drug is Paclitaxel?

A

MITOTIC INHIBITOR

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4
Q

What type of drug is Doxorubicin?

A

ANTIBIOTIC

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5
Q

What type of drug is Chlorambucil?

A

ALKYLATING AGENTS

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6
Q

Why do we look at proliferating tissues more than normal

tissues affected by cytotoxic agents?

A

DNA becomes sensitive when the double helix is
unwound and open. Unwinding occurs only during the
time of cell proliferation. That is why proliferating cells
are more sensitive.

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7
Q

Example of Cycle non-specific drugs

A

nitrosylureas and steroids

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8
Q

Example of Cycle specific drugs

A

Alkylating agents and anti-tumor antibiotics

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9
Q

How do you improve effectivity of a phase specific agent?

A

Increase time of exposure. This is to allow the rest of the cells in different phases to enter the sensitive phase.

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10
Q

Antimetabolites work only on?

A

S phase

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11
Q

Vinca alkaloids work only on?

A

M phase

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12
Q

Anti-tumor antibiotics work on?

A

most of S phase including late phases of G1 and early phases of G2

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13
Q

Alkylating agents work on?

A

all throughout the cell cycle

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14
Q

Taxoids work on what phase?

A

Taxoids are spindle poisons so they only work on M phase.

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15
Q

What is the usual mode of administration for cytotoxic drugs?

A

IV because they are poorly absorbed in the GIT and some drugs are irritants and contact to GI tissues may lead to lysis or giant ulcers that may not heal

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16
Q

Name one cytotoxic drug that can be given orally

A

Cepacitabine - a prodrug converted to 5FU by enzymes in the liver

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17
Q

What are the reservoir areas in males?

A

Brain and testes

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18
Q

What is the result of poor nutrition in distribution?

A

Poor nutrition -> less protein -> more free drug

DANGEROUS

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19
Q

What is the FRACTIONAL CELL KILL HYPOTHESIS?

A

States that each cycle of chemotherapy is capable of

destroying the same proportion of tumour cells.

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20
Q

What is the minimum recovery time for chemotherapy?

A

3 weeks

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21
Q

What are the assumptions of the Fractional cell kill hypothesis?

A

o All cells are rapidly dividing and are thus sensitive to
chemotherapeutic agents
o There is constant blood supply to be able to administer the drugs
o First order kinetics (meaning ALL cells are rapidly dividing)

22
Q

Tumours in which the logarithmic part of the curve is

shorter with a broader plateau phase will be (resistant/sensitive) to chemo

A

resistant like thyroid CA

23
Q

tumours with steep logarithmic curve will be (resistant/sensitive) to chemo

A

sensitive like lymphomas

24
Q

What are the two types of cell populations in the tumor?

A

Micrometastases – rapidly dividing and exhibiting logarithmic growth
Primary tumor – in the plateau phase of growth, some cells may be dividing, some may not

25
Q

What does the GOLDIE-COLDMAN HYPOTHESIS state?

A

within the tumor itself, there would be small population of tumor cells that are already naturally resistant to the effects of chemotherapy because of the labile genome that the cancer has

26
Q

How do you overcome resistance due to cell kinetics?

A
  1. Debulking/Reduce tumor bulk with locoregional modalities(surgery, RT)
  2. Use combinations that include drugs that can affect resting populations.
  3. Schedule drugs to prevent phase escape or to synchronize cell populations and increase cell kill by continuous infusion instead of bolus.
27
Q

Most common cause of drug resistance in chemotherapy

A

MDR (multidrug resistance) or pleiotropic drug resistance

28
Q

What is the product of the MDR gene?

A

ATP dependent P glycoprotein that pumps the drug back outside. Hence, the drug does not reach the nucleus and cannot kill the cancer cell

29
Q

How do you overcome biochemical causes of resistance:

A

o Use combination chemotherapy
o Use biologic response modifiers
o Use a 2nd agent to rescue normal cells
o Follow marrow-lethal doses of chemotherapy with autologous bone marrow transplant
o Combine high dose chemotherapy with blood cell

30
Q

What is the definition of complete remission according to the RECIST Criteria?

A

disappearance of all target lesions

31
Q

What is the definition Progressive Disease (PD) according to the RECIST Criteria?

A

≥ 20% increase in SLD when compared to smallest SLD since treatment

OR

appearance of new lesions.

32
Q

When can you give chemotherapy to a pregnant woman?

A

late 3rd trimester

33
Q

What are the three phases of vomitting

A

1) acute (2hrs-1week)
2) delayed (1-2weeks after therapy)
3) psychogenic (triggered response)

34
Q

Most life threatening symptom of chemo

A

bone marrow aplasia

35
Q

symptom of anthracyclin use

A

Cardiotoxicity

36
Q

symptom of Bleomycin use

A

Pulmonary fibrosis

37
Q

What is the basic principle of ablative therapy?

A

the Hypothalamus-Pituitary-Organ axis should be interrupted

38
Q

When do you use Peripheral Androgen Inhibitors?

A

prostate cancer

39
Q

When do you use Selective estrogen receptor modulators ie tamoxifen?

A

Used in ER (+) breast cancer patients

40
Q

What is a side effect of tamoxifen?

A

Hot flushes, vaginal bleeding and discharge are associated with tamoxifen use. Vaginal bleeding is secondary to the induced proliferation of the endometrium and can actually lead to endometrial CA. So, if you use tamoxifen, it is advised that you also do an annual pap smear.

41
Q

What is passive immunotherapy?

A

Use of monoclonal antibodies for target cell-directed killing by antigen-antibody response

42
Q

What is adaptive immunotherapy?

A

acquisition of immunity in a naïve subject as the result of the administration of immunologically activated lymphoid cells.

43
Q

Imatinib is a selective tyrosine kinase inhibitor of?

A

KIT, Bcr-Abl, and PDGFR

44
Q

What is the mode of action of imatinib mesylate?

A

inhibit ATP phosphorylation in the BCR-ABL binding site, inhibiting the binding of tyrosine residues which further blocks the binding to the effector cell.

45
Q

GIST is dependent on what oncogene?

A

KIT oncogene

46
Q

Trastuzumab, a monoclonal antibody specific for what tumor?

A

breast tumor

47
Q

Cetuximab is specific for what tumor?

A

Lung, Colorectal, Head and Neck, GBM (glioblastoma?)

48
Q

Panitumumab is specific for what tumor?

A

colorectal

49
Q

Nimotuzumab is specific for what tumor?

A

Head and Neck, GBM

50
Q

What is the effect if mTOR is blocked?

A

If blocked: hold proliferation, starve the tumor, prevent metastasis, can make a tumor sensitive to hormonal therapy

51
Q

What is the function of the 26S proteosome

A

functions like the “anus” of the cell; takes all the proteins and degrades them so that they can be utilized again. Stopping the degradation will lead to an accumulation of toxic substances in the cell, ending in apoptosis.

OS 217 Oncology (14 decks)

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