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PHAR 557 > Intro to Cancer Tx > Flashcards

Intro to Cancer Tx Flashcards

1
Q

4 most common cancers in Canada

A

Lung, prostate, breast, and colorectal

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2
Q

“An estimated 1 out of ___ Canadians are expected to develop cancer during their lifetimes”

A

2

50%!!

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3
Q

T or F: Heart dz is the leading cause of premature death in Canada.

A

F

It’s now cancer

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4
Q

Two major reasons for rising incidence of cancer

A

increasing human lifespan, population growth

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5
Q

T or F: Cancer cells can arise only from certain cell types, such as rapidly dividing intestinal cells.

A

F

Cancer can arise from ANY cell type

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6
Q

Characteristics of a cancer cell

A
  1. unctrled growth (lack of or dysfn’al feedback mechanisms)
  2. invades surrounding tissue
  3. decreased cellular differentiation (i.e. lack of functionality found in cell of origin)
  4. metastasize
  5. MANY other diffs in biochemistry, genetics, etc. that distinguish cancer cells from benign cells
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7
Q

What does tumor GRADING tell us?

A

Cancer’s aggressiveness (i.e. how bad it looks)

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8
Q

How is a tumor graded?

A

by looking at degree of differentiation (i.e. how diff it looks from the original cell of origin) and mitotic rate (i.e. how fast it’s growing)

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9
Q

How would a tumor with a higher grade be described?

A

It has little resemblance to a normal cell and many of its cells are in active cell division

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10
Q

What does tumor STAGING tell us?

A

Extent of cancer (i.e. how far has the cancer spread)

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11
Q

How is a tumor staged?

A

by looking at size of primary lesion (T), whether lymph nodes are involved (N), and metastases (M)

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12
Q

How many stages are there?

A

5: Stage 0 to stage IV

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13
Q

Tx modalities for cancer:

A

surgery, radiation, drugs (chemo and more), immunotx

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14
Q

What do cytotoxic drugs do?

A

interfere with or damage cellular DNA, leading to cell death

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15
Q

How does immunotx tx cancer?

A

It activates pt’s immune sys against cancer cells

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16
Q

Define growth fraction

A

Fraction of cells that’re undergoing mitosis in a given tissue/tumor

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17
Q

How does growth fraction change as tumors get bigger?

A

Growth fraction decreases

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18
Q

Why does the growth fraction change as a tumor gets larger?

A

growth fraction decreases because: more and more cells are growing farther away from blood vessels, there’s an accumulation of toxic metabolites, and there’s less cell-to-cell communication

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19
Q

Clinically detectable mass size

A

1 gram of tissue = 1x10^9 cells = 1 cm^3

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20
Q

MOA of cytotoxic drugs

A

interfere w/ production and fn of DNA/RNA > apoptosis

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21
Q

What specifically do cytotoxic drugs target?

A

Processes within the cell cycle

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22
Q

What is the “guardian of the genome”?

A

p53 suppressor gene

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23
Q

What is the job of the “guardian of the genome”?

A

to sense genomic damage and attempt reparation > if DNA can’t be repaired, it initiates apoptosis

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24
Q

What is a significant mechanism for drug resistance in cancer?

A

mutant p53 suppressor genes > no more apoptosis

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25
Q

List the 5 categories of cytotoxic agents

A

alkylating agents

anti-metabolites

antitumor antibiotics

antimitotic agents

topoisomerase inhibitors

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26
Q

What’re cell cycle specific drugs?

A

cytotoxic drugs that’re effective against cells that’re in the process of dividing

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27
Q

What kind of tumors are cell cycle specific cytotoxic drugs most effective against?

A

Tumors w/ high growth fraction

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28
Q

What’re the two types of cell cycle specific drugs?

A

Phase-specific and phase non-specific agents

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29
Q

What’re cell cycle non-specific drugs?

A

Cytotoxic drugs that have activity against RESTING cells

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30
Q

What kind of tumors are cell cycle non-specific cytotoxic drugs most effective against?

A

lg tumors w/ low growth fraction

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31
Q

What kind of cytotoxic drugs are most effective in multiple repeated dosing?

A

Phase-specific agents

32
Q

What kind of cytotoxic drugs are most effective in a dose-dependent manner?

A

phase non-specific agents and cell cycle non-specific drugs

33
Q

What’re the three possible goals of cancer systemic tx?

A

cure, improve survival, or palliation

34
Q

What is induction chemotx?

A

Primary treatment for cancer

35
Q

What kind of malignancy is induction chemotx usually used in?

A

It’s used for mostly hematologic malignancies

36
Q

What is adjuvant chemotx?

A

Use of anti-cancer drugs AFTER primary tumor is destroyed/removed in order to destroy micrometastatic cells that may be lingering

37
Q

Consolidation tx is similar to THIS type of tx.

A

Adjuvant chemotx

38
Q

What is consolidation tx used to tx?

A

hematologic malignancies that have been tx’ed, but may still have some residual cells remaining

39
Q

What’s neo-adjuvant chemotx?

A

Using systemic anti-cancer drugs BEFORE local tx (i.e. before tumor removal/radiation)

40
Q

What’s maintenance tx?

A

long term, low-dose tx used to reduce recurrence or progression

41
Q

What’s salvage tx?

A

Tx of relapsed (recurrent or persistent dz

42
Q

What kind of tx is used to access tumors that’re located in relatively inaccessible sites?

A

Local chemotx

43
Q

What’s one advantage of local chemotx?

A

avoid systemic toxicity

provide high local conc > more killing power

44
Q

When does dose intensification of anti-cancer drugs become necessary?

A

To overcome resistance of tumor to chemotx

45
Q

What should also accompany chemotx drug dose intensification?

A

Patient rescue procedures, such as bone marrow transplant

46
Q

What’re the advantages of combining multiple anti-cancer drugs?

A
  1. higher cell kill
  2. different MOAs for dealing w/ heterogeneity of tumor
  3. slow or prevent tumor resistance from developing
47
Q

What’re the disadvantages of combining multiple anti-cancer drugs?

A

multiple toxicities, dose reduction in combos (reduced efficacy), complicated administration, cost

48
Q

What must be balanced when giving combos of anti-cancer chemotx?

A

activity/efficacy and toxicity/safety

49
Q

How’re anti-cancer drugs chosen when considering combo tx?

A
  1. activity against tumor alone
  2. diff MOAs (NEVER the same MOA)
  3. minimally overlapping toxicities
  4. no cross resistance b/w drugs
  5. synergistic in combo
50
Q

How is dosage calculated for anti-cancer drugs?

A

It’s calculated based on BSA (mg/m^2)

51
Q

What should the initial dose be for anti-cancer drugs (in general)?

A

Maximum w/ tolerable AEs

52
Q

Why would chemotx dosages be changed?

A

the drug is causing intolerable AEs and/or the drug isn’t working)

53
Q

Why does cancer tx fail?

A
  1. toxicity to normal cells > limits dose
  2. pt comorbidities limit effective dosing
  3. first order kinetics > only a const PERCENTAGE of cells are killed, not number (i.e. can’t get 100% kill)
  4. late detection of tumor
  5. DRUG RESISTANCE
54
Q

What is the result of tumor cell heterogeneity?

A

It leads to drug-resistant cell lines in tumor cells (due to spontaneous genetic mutations)

55
Q

T or F: Smaller tumors are more likely to have drug-resistant cell lines.

A

F

LARGER tumors since there’re more cells, and hence more likely to have mutated cells that’re drug resistant

56
Q

What’s de novo drug resistance?

A

Drug resistance that’s due to abnormal p53 suppressor gene (the gene that usually initiates apoptosis in the face of irreparable DNA > if it’s abnormal, then there’s no more apoptosis > damaged cell continues to grow and replicate > cancer and drug resistance)

57
Q

What’s selected drug resistance?

A

When drug resistant cells in a heterogenous pop become predominant (i.e. they’re “selected for” by cytotoxic drugs by having all the susceptible cells destroyed)

58
Q

What’s acquired drug resistance?

A

When cells develop mechanisms of drug resistance

59
Q

What’re some examples of acquired drug resistance?

A
  1. enzymes that inactivate drug
  2. p-glycoprotein > pumps drug out of cell
  3. enzymes that repair DNA damage done by cytotoxic drug
  4. mutation in drug’s receptor
60
Q

What kinds of cancers are treated effectively by endocrine tx’s?

A

hormone-sensitive cancers (e.g. prostate, breast, and uterine cancers)

61
Q

How do endocrine tx’s exert their effects in gen?

A

through hormone receptors or hormone deprivation

62
Q

T or F: Endocrine tx’s for cancer are cytotoxic, though work differently from classic chemotx drug.

A

F

They are NOT cytotoxic

63
Q

Why’re endocrine tx’s for cancer considered “targeted drug tx” if cytotoxic anti-cancer drugs already targeted rapidly-dividing cancer cells?

A

Because the cytotoxic drugs also attacked normally-dividing cells = collateral damage/AEs, hence, not truly “targeted”

64
Q

Which type of malignancy do we often see increased dosing for?

A

hematologic malignancies

65
Q

What’s the problem w/ increasing cancer drug doses to get better tumor killing?

A

lots of collateral damage to normal cells

66
Q

What types of drugs are used in “Molecular targeted drug tx”?

A
  1. monoclonal Abs that target tumor receptors

2. small molecule, tyrosine kinase inhibitors

67
Q

What’s the primary goal of molecular targeted drug tx?

A

improve efficacy, avoid severe toxicities to normal cells (from traditional cytotoxic chemotx) > better targeting of tumor-specific targets = less AEs

68
Q

T or F: An ideal anticancer agent target for molecular targeted drug tx includes targets that’re highly expressed in normal tissues as well as tumor tissues.

A

F

We don’t want to attack healthy tissues

69
Q

In molecular targeted drug tx, what’re the two classes of drugs used?

A

Small molecule compounds and monoclonal Abs

70
Q

In molecular targeted drug tx, how do small molecule drugs work?

A

act within a cancer cell > interfere w/ key proteins made by abnormal genes > dz progression is halted

71
Q

In molecular targeted drug tx, how do monoclonal Abs work?

A

block extracellular antigens outside the cell/on cell surface that’re involved in essential cancer cell fns

72
Q

What is angiogenesis?

A

Blood vessel growth

73
Q

Why doesn’t our own immune sys not target tumor cells?

A

bc they appear to be ‘self’

74
Q

What’re the types of immunotx’s?

A
  1. OLD: non-specific immunotx

2. NEW: immune checkpoint inhibitors

75
Q

How do old immunotx’s work?

A

OLD: non-specific > boost immune sys in general way to help get rid of cancer

76
Q

How do the newer immune checkpoint inhibitors work?

A

they take the brakes off the immune sys and help them recognize and attack cancer cells

77
Q

This newer tx involves genetically altering a pt’s own T cells by adding a man-made receptor that targets a specific cancer cell antigen

A

CAR T-cell tx (chimeric antigen receptor T-cell)

PHAR 557 (36 decks)

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