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Pharmacology: Exam 3 > Lecture 5: Cancer Chemotherapy I > Flashcards

Lecture 5: Cancer Chemotherapy I Flashcards

1
Q

What is squamous cell carcinoma of the lung caused by?

A
  • Cigarette smoking
  • Squamous cell carcinoma causes keratin pearls
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2
Q

Is adenocarcinoma caused by smoking?

A

NO

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3
Q

What is malignant melanoma?

A
  • Local invasion and lymph node metastasis
  • Deeper → worse prognosis
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4
Q

What are the most new cases of malignant cancer for males and females?

A

Males: prostate
Females: breast

pancreatic cancer is very rare but one of the most lethal cancers

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5
Q

Which cancer(s) have the highest death rate?

A

Lung and Bronchus

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6
Q

What induces mesothelioma directly?

A

Asbestos

mesothelioma → cancer covering outside lung

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7
Q

Asbestos increases the risk of what cancer?

A

Increases the risk of squamous cell carcinoma in conjunction with cigarette smoking

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8
Q

Does smoking increase the risk of mesothelioma?

A

NO

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9
Q

What are the key disposing factors of Hepatocellular carcinoma?

A
  1. Chronic Hepatitis B
  2. Chronic Hepatitis C
  3. Alcoholism
  4. Aflatoxin exposure

epithelium have a glandular appearance

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10
Q

Most cancer therapies are designed to be ____ toxic to malignant tumor cells

A

directly

try to kill tumor cells w/o injuring good normal cells

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11
Q

What do most cancer therapies affect?

A
  • affect DNA or RNA synthesis and protein synthesis downstream to affect tumor cell proliferation or survival.
  • also affect normal cells and thus, both abnormal and normal cell proliferation is blocked, leading to toxicities
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12
Q

What is a major goal of cancer therapy?

A

to remove or destroy all malignant cells and convert the malignancy into a chronic disease (i.e. palliation)

chronic disease could be HTN, diabetes, etc

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13
Q

What is a big problem with chemotherapy?

A

Tumor cell resistance

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14
Q

Because of tumor cell resistance how is chemotherapy given?

A

pt give a combination of chemotherapeutic regimens

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15
Q

Tumor cells acquire additonal ____ to resist drugs

A

mutations

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16
Q

Multidrug resistance from tumor cells can occur by what?

A

amplification of P- glycoprotein (MDR1) that pumps the drug out of the cell.

This is an ABC family co-transporter, that induces the efflux of drugs from cells in an ATP-dependent manner

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17
Q

Because tumor cells acquire additional mutations to resist drugs, what is done to minimize that?

A

resistance is minimized by short-term, intermittent therapy with drug combinations

try to treat with alternative combinations of drugs so you can try and kill the mutated tumor early on

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18
Q

What are the 4 key complications of cancer therapeutics?

A
  1. Bone marrow suppression
  2. Stomatitis
  3. Nausea and severe vomiting
  4. Hair loss
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19
Q

What are 3 specific complications (side effects) of cancer therapeutics?

A
  1. Cyclophosphamide- severe cystitis
  2. Doxorubicin- cardiotoxicity
  3. Bleomycin- pulmonary fibrosis

HIGH YIELD

cystitis: inflammation of the bladder and hemorrhage

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20
Q

Which drugs cause major and mild myelosuppression?

A

Major: Cyclophosphamide and Doxorubucin
Mild: Bleomycin

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21
Q

Side effects of Cisplatin

A
  1. Ototoxicity
  2. Nephrotoxicity
  3. Nausea/vomiting
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22
Q

Side effect of Doxorubucin

A

cardiotoxicity

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23
Q

Side effect of Bleomycin

A

Pulmonary toxicity

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24
Q

Side effects of Cyclophosohamide

A

Hemorrhagic cystitis

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25
Q

Side effect of Oxaliplatin/Vincrisitne/ Taxanes

A

peripheral neuropathy

taxol for breast cancer
microtubule inhibitor, can change stability of the tubule

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26
Q

What are the hallmarks of cancer? (what a malignant cells need to have

A
  1. Sustaining proliferative signaling ( K-RAS)
  2. Evading growth supressors (cell cycle-P53)
  3. Activating invasion and metastasis
  4. Enabling replicative immortality ( Telomerase/TERT)
  5. Inducing angiosgenesis (VEGF)
  6. Resisting cell death
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27
Q

True or false: Tumor cells interact w/ host

A

True, normal cells play a role and how they are responding to tumor cells

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28
Q

What is the greatest focus of therapeutic intervention?

A

Avoiding immune destruction

29
Q

Adenoma to Carcinoma Sequence in Colon Cancer development

A

APC + APC + RAS (Adenoma) + P53 + Telemorase (Carcinoma)

30
Q

What is Adenomatous polyposis?

A

A precursor for colonic adenocarcinoma

colonoscopy: look for polpys

31
Q

What is familial polyposis?

A

A genetic cause of colonic adenocarcinoma. Mutation of APC gene: 5q-autosomal dominant disease

mutation of APC, 100% will get colon cancer bc its 1 allele

32
Q

Conversion of normal human fibroblasts and epithelial cells into malignant tumor cells requires 4 genes. What are they?

turning fibroblasts into tumor cells

A

The 4 genes activated:
1. Ras
2. SV40 large T antigen
3. SV40 small t antigen
4. TERT (telomerase)

when these 4 are mixed, in turns into tumor cells

33
Q

List how each of these genes plays a role in being converted into a malignant state
1. Ras
2. SV40 large T antigen
3. SV40 small t antigen
4. TERT (telomerase)

A
  1. Ras → stimulates signal transduction
  2. SV40 large T antigen → blocks the cell cycle inhibitors p53 and Rb
  3. SV40 small t antigen → blocks the activity of protein phosphatase 2A (PP2A)
  4. TERT (telomerase) → allows for cell replicative immortality

Transduction of 4 individual genes into normal human cells can convert them into a malignant state.
most cancers have activated RAS and elevated TERT

34
Q

What are specific chromosomal translocation leading to malignancy for Chronic Myelogenous leukemia (CML)?

A

Chr:9:22 Bcr-Abl Philadelphia chromosome
Classic finding: Splenomegaly

35
Q

What are specific chromosomal translocation leading to malignancy for Burkitt’s Lymphoma?

A

Chr:8:14
Myc amplification, pro growth

36
Q

Chemoterapeutic agents

What is a treament for Chronic Myleogenous leukemia (CML)

A

Imatinib: an inhibitor of Abl kinsae

has profound ability to induce remission

37
Q

Imatinib MOA

A

Binds to Abl kinase in its inactive conformation and prevents its activation thus it has less toxicity

leukemic cells can become resistant to Imatinib through new mutations in Abl in the Bcr-Abl fusion protein

38
Q

What are the new generations of Abl inhibitors to treat CML?

A

Dasatinib and Nilotinib (more potent and efficacious than Imatininb in treating CML)

39
Q

What is breast cancer?

A

Invasive ductal carcinoma (invades lymph nodes very easily)

40
Q

What are key genetic changes that underlie the development of breast carcinoma?

A
  • Luminal-> ER+ and HER2-=BRCA2 and PIK3CA mutation
  • HER2 enriched->HER2+= TP53 mutation and HER2 amplification
  • Basal like-> ER- and HER2-= TP53 mutation and BRCA1 inactivation
41
Q

What can identify metastatic carcinoma to a lymph node?

A

immunostaining can identify the malignant cells

how pathologists find tumor and characterize what it is

42
Q

Explain therapeutic targeting of EGF receptors in epithelial cancers.
1. EGFR inhibitors are used for what cancers?
2. EC domain of EGFR?
3. IC domain of EGFR?

A
  1. EGFR inhibitors are particularly utilized in breast, lung, and colon cancers.
  2. Blocking monoclonal antibodies directed to the extracellular domain of EGFR
  3. Chemical inhibitors of the tyrosine kinase activity of the EGFR intracellular domain

-resistance has been observed to both the antibody and chemical EGFR inhibitors

43
Q

Examples of Combination Chemotherapeutic regimens

slide 24

A

Combination Chemotherapeutic regimens are usually different drugs that inhibit diff things + antibodies mixed together

44
Q

Key chemotherapeutic agents: targets and mechanism of action

Protein kinase inhibitors antibodies MOA

low yield

A

block activites of signaling pathways

45
Q

Key chemotherapeutic agents: targets and mechanism of action

Immune checkpoint inhibitors MOA

low yield

A

block immune evasion

46
Q

Key chemotherapeutic agents: targets and mechanism of action

Hormone antagonists MOA

low yield

A

inhibits receptor fxn and expression

47
Q

Key chemotherapeutic agents: targets and mechanism of action

Expothilones, Taxanes, Vinca Alkaloids, Estramustine MOA

low yield

A

Inhibit fxn of microtubules

48
Q

Key chemotherapeutic agents: targets and mechanism of action

ATRA, Arsenic trioxide, Histone Deacetylase inhibitors MOA

low yield

A

induce differentiation

49
Q

How do chemotherapeutic agents target the cell cycle?

A
  1. Messes up DNA, RNA, and protein synthesis
  2. Trap cells in S-phase where DNA is replicated
  3. Blocls M phase with tubulin needed for chromosome segmentation and for cells to divide
50
Q

What are the cell cycle specific drugs?

A
  • Antimetabolites
  • Bleomycin
  • Etoposide
  • Vinca alkaloids
51
Q

What are the cell cycle non-specific drugs?

A

Alkylating agents
Antibodies
Cisplatin
Nitosoureas

52
Q

Anti-metabolites chemotherapeutic agents are structurally related to what? What do they interfere with and how?

A
  • Compounds are structurally related to normal compounds
  • Interfere with the availability of purine or pyrimidine nucleotide precursors
  • This interference occurs by inhibiting synthesis or by competing with normal precursors during DNA or RNA synthesis.

enzymes picks them up thinking they are normal cmpds

53
Q

Anti-metabolites chemotherapeutic agents have maximal cytotoxic effecs during what phase of the cell cycle?

A

S-phase (dna replication)

54
Q

True or false: Methotrexate (MTX) is usually used in combination regimens

A

True

MTX is a folate-related molecule important in pregnancy and closing the neural tube. low folate-anemia (need for RBC production)

55
Q

MTX is used in which cancers?

A

ALL, Burkitt’s lymphoma, breast cancer and other solid tumors

56
Q

-5-FU anti-metabolite is used for which cancer(s)?

A

used in slowly growing tumors including colon, breast, ovarian, pancreatic and gastric cancers

57
Q

-5-FU is coadministered with what?

A

Leucovorin to enhance inhibition of thymidylate synthase

58
Q

MOA of MTX anti-metabolites

A

MTX targets dihydrofolate reductase, which is necessary to create reduced folate isoforms, FH2, FH4, and N5, N10- methylene-FH4 that are required to generate dTMP

blocks synth of folate isoforms that are required to generate dTMP

59
Q

-5-FU anti-metabolite MOA

A

5-FU targets thymidylate synthase which generates dTMP from dUMP, a reaction that also requires N5, N10-methylene-FH4

TS generates dTMP from dUMP requires N5, N10-methylene-FH4

60
Q

Leucovorin (N5-formyl-FH4) anti-metabolite MOA

A

converted to N5, N10- methylene-FH4 and bypass the effects of MTX, which can cause key side effects including megaloblastic anemia

61
Q

Function of Capecitabine

Antimetabolite

Low yield

A

Metabolized to 5-FU can show less toxicity due to more selective conversion to 5-FU within the tumor.

62
Q

Function of Cytarabine

Anti-metabolite

Low yield

A

acts as a pyrimidine analog, inhibits RNA processing, used to treat AML, inhibits DNA polymerase

63
Q

Function of Azacitidine

Anti-metabolte

Low yield

A

Is a pyrimidine analog, inhibits RNA processing, used to treat AML

64
Q

Function of Gemcitabine

Antimetabolite

Low yield

A

Used in pancreatic cancer and non-small cell lung cancer therapy, metabolites block DNA synthesis

65
Q

Which of the following chemotherapies has a side effect of pulmonary fibrosis?
a. Cyclophosphamide
b. Doxorubicin
c. Bleomycin

A

c. Bleomycin

66
Q

Which of the following describes Familial polyposis?
a. APC, 5Q autosomal dominant disease
b. BCR-ABL translocation
c. Myc amplification
d. None of the above

A

a. APC, 5Q autosomal dominant disease

67
Q

Which of the following corresponds to the translocation (9:22)(q34:q11) Abl-BCR ?
a. CML
b. AML
c. Burkits lymphoma
d.Follicular lymphoma

68
Q

Which of the following EGFR targeted therapeutic treatment binds extracellularly?
a. Cetuximab
b. Osimertinib
c. Gefitinib
d. Afatinib

A

a. Cetuximab

69
Q

What gets administered with methotrexate to prevent megablastomic anemia?
a. 5FU
b. Leucovorin
c. Cytarabine
d. Azacitidine

A

b. Leucovorin

Pharmacology: Exam 3 (8 decks)

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