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MCS > Day 16, Lecture 2: Cancer III: Chemotherapy > Flashcards

Day 16, Lecture 2: Cancer III: Chemotherapy Flashcards

1
Q

Incidence of Cancer

A
  • 1.66 million new cases annually in the U.S.
    • 0.59 million deaths annually in the U.S. each year
    • 2nd leading cause of death
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2
Q

Rank the what are the three highest types of cancers diagnosed each year (highest incidence)?

What are the 3 highest cancers that causes mortality each year?

A
  • Incidence:
    1. Prostate/Breast
    2. Lung/Bronchus
    3. Colon and Rectum
  • Mortality:
    1. Lung and Bronchus
    2. Prostate/Breast
    3. Colon and Rectum
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3
Q

Why did the male incidence rate of cancer greatly increase in 1992

A
  • Invention of PSA lead to greater number of diagnosis
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4
Q
A
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5
Q

Why might obesity lead to increase risk of cancer

A
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6
Q

Etiology of Cancer

A
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7
Q

What is Cancer?

A
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8
Q
A
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9
Q

Is cancer a genetic and epigenetic disease?

A

Yes

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10
Q

Cancer Treatment

A
  • Surgery
  • Radiotherapy
  • Chemotherapy
    • often an adjuvant therapy (with/after primary therapy)
    • Can be first line therapy
      • if surgery/radiotherapy not safe or effective
    • can be neoadjuvant therapy
      • before surgery/radiotherapy to reduce tumor burden
    • Can be mono or combination therapy
  • Immunotherapy
  • Gene therapy
  • Virotherapy
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11
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A
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12
Q
A
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13
Q

Log-Kill Hypothesis

A
  • Drug kills a constant fraction of cells
  • Multiple rounds of administration are required to eradicate all tumor cells
  • Problem arises from dormant tumor cells and cancer stem cells
    • these cells are insensitive to therapy
  • It is easier to kill dividing cells, which is why there are many cell cycle-specific drugs
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14
Q

Chemotherapy Resistance

A
  • Contributes to >50% of failure of chemotherapy
  • Types of resistance:
    • Single agent
    • Multidrug resistance (MDR)
      • resistance often builds up to many drugs after treatment with only one drug
  • Potential Mechanisms:
    • Increased influx of drug out of cell
    • decreased influx of drug into cell or nucleus
    • increased detoxification mechanisms
    • decreased activation of drug
    • amplified or altered drug target
    • increased ability to tolerate damage
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15
Q

Combination Chemotherapy

A
  • Multiple agents in specific sequence (or together) to overcome resistance and enhance antitumor effects
  • Sometimes cycled ever 2-4 weeks
    • due to side-effects of drugs
    • the worst side-effects are gone by week 4
  • Criteria for combination therapy
    • should act by different mechanisms of action
    • should have different mechanisms of resistance
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16
Q

Systemic Toxicity of Chemotherapy

A
  • Direct Toxicities
    • ​Bone Marrow
      • Myelosuppression
      • Neutropenia
      • thrombocytopenia
      • anemia
    • GI mucosa
      • mucositis
      • nausea
      • vomiting
      • diarrhea
    • Oral mucosa
    • Skin, including light sensitivity
    • Hair follicles
      • Alopecia
    • Gonads
  • Other Toxicities
    • ​Heart
    • Liver
    • Lung
    • CNS
    • Kidney
    • Bladder
  • Secondary Malignancies
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17
Q

What are the types of responses to chemotherapy

A
  • Complete response
  • Partial response
  • 5-year or 10-year disease-free is often regarded as curative
  • Quality of life
    • pain versus small gain of lifetime
18
Q
A
19
Q

Most cancer drugs treat what stage of the cell cycle?

A
  • G1
20
Q

Antimetabolites

A
  • Cancer drug
  • Agents that block the biosynthesis of metabolites required for cell growth
  • inhibits S-phase
  • Examples:
    • Methotrexate
      • folic acid analog
      • inhibits dihydrofolate reductase
        • thus retards DNA/RNA and protein synthesis
    • Thiopurines
      • e.g.
        • Mercaptopurine or 6-Thioguanine
      • prodrugs requiring activation through purine salvage pathway
      • act by inducing mutations (pair with C and T) and inhibiting de novo purine synthesis
      • also effective as anti-inflammatory and immunosuppressive drugs
    • Flurouraci (5-FU)
      • blocks thymidylate synthase
        • ​thus inhibiting thymidine synthesis
21
Q

Methotrexate

A
  • type of Antimetabolite
  • inhibits S-phase
  • folic acid analog
  • mechanism:
    • inhibits dihydrofolate reductase
      • ​thus retards DNA/RNA and protein synthesis
22
Q

Thiopurines

A
  • Type of Antimetabolite
    • ​Blocks S-phase
  • e.g.
    • Mercaptopurine
      • used to treat:
        • acute leukemia
        • CML
    • 6-Thioguanine
  • Mechanism:
    • Prodrugs requiring activation through purine salvage pathway
      • act by ​inducing mutations (pair with C and T) and inhibiting de novo purine synthesis
    • also effective as anti-inflammatory and immunosuppressive drugs
23
Q

Fluorouracil (5-FU)

A
  • Type of Antimetabolites
    • ​Inhibit S-phase
  • Mechanism:
    • Blocks Thymidylate Synthase
      • ​inhibits Thymidine synthesis
24
Q

Microtubule targeting (M-phase) drugs

A
  • Vinca alkaloids
    • ​e.g. Vinblastine
      • These agents bind to tubulin and prevent mitotic spindle formation
  • Taxoids
    • ​e.g. Paclitaxel/Taxol
    • These agents induce the polymerization/stabilization of microtubules
25
Q
A
26
Q

Vinca alkaloids

A
27
Q

Taxoids

A
28
Q

Epipodophyllotoxins

A
  • Topoisomerase II inhibitors (G1/S-phase)
  • E.g.
    • Etoposide
  • These agents lead to DNA double-strand breaks and cause errors in DNA replication (and eventually apoptosis)
29
Q

Cell cycle nonspecific drugs

A
  • Alkylating agents
    • ​cause irreversible changes in DNA
      • oftne leadin to cross-linking
    • Unwanted effects
      • mutagenic
      • teratogenic
      • carcinogenic
    • Example
      • Cyclophosphamide
  • ​Antitumor antibiotics
    • ​intercalate into DNA and inhibit gene transcription
    • many isolated from Streptomyces
    • example
      • Doxorubicin (Adriamycin)
  • Topoisomerase I inhibitors
    • ​Camptothecins
      • bind to DNA topoisomerase I
        • leads to single-strand breaks in the DNA and inhibits replication as well as transcription
    • examples:
      • Irinotecan
      • Topotecan
    • Platinum compounds
      • Induce crosslinks in DNA
        • thereby blocking DNA replication and transcription
      • Examples:
        • Cisplatin
        • Carboplatin
30
Q

Alkylating Agents

A
  • cell cylce-nonspecific drugs
  • mechanism:
    • irreversible changes especially in DNA
      • often leading to cross-linking
    • Also changes in RNA and protein
  • unwanted effects:
    • mutagenic
    • teratogenic carcinogenic
  • Example:
    • Cyclophosphamide
  • Treats:
    • Lymphoma
    • leukemia
    • prostate
    • lung
    • breast
    • ovarian cancer
31
Q

Antitumor antibiotics

A
32
Q

Camptothecins

A
  • Cell cycle non-specific drugs
  • Topoismerase I inhibitors
    • leads to single strand breaks in the DNA and inhibits replication as well as transcription
  • Examples:
    • Topotecan
      • Metastatic carcinoma of ovary
    • Irotecan
      • metastatic cancer of colon and rectum
33
Q

Platinum compounds

A
  • nonspecific cell-cylce drugs
34
Q
A
35
Q

Tamoxifen

A
  • Estrogen receptor antagonist
  • treats:
    • Postmenopausal breast cancer
36
Q

Enzalutamide

A
  • Androgen receptor antagonist
  • Treats
    • Prostate Carcinoma
37
Q

Letrozole

A
  • Aromatase inhibitor
    • Inhibit the conversion of testoterone to estrogen
38
Q

Fulvestrant

A
  • Selective estrogen receptor downregulator
    • lead to the degradation and destruction of estrogen receptors
  • given to Tamoxifen (estrogen receptor antagonist) resistant patients
39
Q

Abiraterone

A
  • inhibits CYP17A1, an enzyme involved in androgen sysnthesis
    • blocks androgen synthesis
  • used to treat castration-resistant prostate cancer patients
40
Q
A
41
Q

Tretinoin

A
  • All-trans retinoic acid/ATRA
  • acid form of Vitamin A
  • Treatment for acute Promyelocytic Leukemia (APL), which harbors PML-RARalpha gene fusion t(15;17)
  • induces differentiation of undifferentiated cancer cells

MCS (40 decks)

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