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APPE 7: Oncology > Module 1: Basic Oncology > Flashcards

Module 1: Basic Oncology Flashcards

1
Q

Hallmark of CancerL six cellular alterations (“hallmarks”) acquired during malignant transformation:

A

Self-sufficiency in growth signals
Insensitivity to antigrowth signals
Evasion of apoptosis
Limitless replicative potential
Sustained angiogenesis
Tissue invasion and metastasis

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2
Q

What is the Fractional Cell Kill Hypothesis

A

The Fractional Cell Kill Hypothesis in oncology proposes that not all cancer cells within a tumor are equally sensitive to treatment. It suggests that with each cycle of radiation or chemotherapy, a certain fraction or percentage of cancer cells is killed, expressing the relationship between dose and cell kill in a logarithmic manner. The hypothesis emphasizes the need for multiple treatment cycles to reduce the tumor burden progressively, recognizing the heterogeneity of cell sensitivity within the tumor. This concept is essential for designing effective cancer treatment regimens that consider the varying susceptibilities of different cell populations within the tumor.

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3
Q

Multimodal Therapy

A

Use of multiple treatment modalities (i.e. chemotherapy, surgery, and/or radiation) in
treatment of cancer
.
Chemotherapy may be used before, during, or after other modalities
- Neoadjuvant: given prior to surgery/radiation
- Concomitant: given during radiation
- Adjuvant: given after surgery/radiation

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4
Q

Oncology Term

Dose-limiting toxicity (DLT)

A

Toxicity that precludes further dose escalation of an agent

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5
Q

Oncology Term

Maximum tolerated dose (MTD)

A

Highest dose at which an agent doesn’t cause unacceptable toxicity

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6
Q

Oncology Term

Dose density (dd)

A

Compression of time intervals between chemotherapy cycles

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7
Q

Oncology Terms

  1. Induction therapy
  2. Consolidation therapy
  3. Salvage therapy
A
  1. Induction therapy: Initial treatment given to treat the malignancy
  2. Consolidation therapy: Treatment given after disappearance of malignancy from induction therapy
  3. Salvage therapy: Treatment given after failure of other therapies
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8
Q

Oncology Terms

  1. Partial response (PR)
  2. Complete response/
    complete remission (CR)
A

PR- Decrease in size and/or extent of the malignancy after treatment
CR- Disappearance of all signs of the malignancy

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9
Q

Oncology Terms

  1. Stable disease (SD)
  2. Progressive disease (PD)
A

SD- Malignancy is neither increasing nor decreasing in size and/or extent
PD - Malignancy is is increasing in size and/or extent

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10
Q

Traditional Chemotherapy: list the 4 classes

A

Alkylating Agents, Antimetabolites, Antimitotics, Topoisomerase Inhibitors

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11
Q

Overview of Alkylating Agents: MOA, class toxicities, mics.

A

Mechanism of Action
* Covalently bind alkyl groups to DNA
* Bifunctional alkylators result in intra- and inter-strand cross-links of DNA strands
.
Class Toxicities:
* Myelosuppression
* Nausea/vomiting
* Gonadal toxicity
* Secondary malignancies
.
Mics:
* Heterogeneous class w/ differing antitumor
activity & toxicities
* Cell cycle non-specific

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12
Q

Alkylating Agent Subclasses

A
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13
Q

Alkylating Agent: Nitrogen Mustard: Cyclophosphamide Use, Toxicities, Pearls

A
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14
Q

Alkylating Agent: Nitrogen Mustard: Ifosfamide Use, Toxicities, Pearls

A
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15
Q

Alkylating Agent: Metal Salts examples/ what are they

A
  • Platinum structure allows for bifunctional cross-linking
  • Cisplatin = prototype; Carboplatin, oxaliplatin developed to reduce toxicities
  • ~10-15% patients will develop hypersensitivity after 7-8 exposures
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16
Q

Alkylating Agent: Metal Salt: Cisplatin Use, Toxicities, Pearls

A
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17
Q

Alkylating Agent: Metal Salt: Carboplatin Use, Toxicities, Pearls

A
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18
Q

Alkylating Agent: Metal Salt: Oxaliplatin Use, Toxicities, Pearls

A
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19
Q

Overview of Antimetabolites: MOA, Misc

A

Mechanism of Action
* Incorporate into RNA/DNA to disrupt DNA synthesis, and/or
* Directly inhibit enzymes responsible for DNA synthesis
.
* Cell cycle specific for S-phase
* Purine, pyrimidine analogues require phosphorylation to incorporate as false nucleotides

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20
Q

Antimetabolite Subclasses and their drugs

A
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21
Q

Antimetabolites: PURINE ANALOGUES: Mercaptopurine (6MP) Use, Toxicities, Pearls

A
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22
Q

Antimetabolites: PURINE ANALOGUES: Fludarabine Use, Toxicities, Pearls

A
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23
Q

Antimetabolites: PYRIMIDINE ANALOGUES
: Cytarabine (AraC) Use, Toxicities, Pearls

A
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24
Q

Antimetabolites: PYRIMIDINE ANALOGUES
: Gemcitabine Use, Toxicities, Pearls

A
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25
Q

Antimetabolites: PYRIMIDINE ANALOGUES
: 5-FU Use, Toxicities, Pearls

A
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26
Q

Antimetabolites: PYRIMIDINE ANALOGUES
: Capecitabine Use, Toxicities, Pearls

A
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27
Q

Antimetabolites: ANTIFOLATES
: MTX Use, Toxicities, Pearls

A
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28
Q

Antimetabolites: ANTIFOLATES
: Pemetrexed Use, Toxicities, Pearls

A
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29
Q

MTX MOA and role of Leucovorin!

A
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30
Q

High Dose Methotrexate: Considerations and other drugs to avoid

A
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31
Q

Overview of Antimitotics: MOA, Misc

A

Mechanism of Action
* Disrupt microtubule function
* Vincas bind at +,- ends of microtubules
* Taxanes bind along interior surface of microtubules
.
MISC
* Cell cycle specific for M-phase
* Originally derived from natural products (vincristine from Madagascar periwinkle; paclitaxel from Pacific yew tree)

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32
Q

Antimitotic Subclasses/ drugs

A
  1. Vinca Alkaloid
    * Vincristine
    * Vinblastine
    * Vinorelbine
    .
  2. Taxanes
    * Paclitaxel
    * Nab-paclitaxel
    * Docetaxel
    * Cabazitaxel
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33
Q

Antimitotics: VINCA ALKALOID: Vincristine Use, Toxicities, Pearls

A
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34
Q

Antimitotics: VINCA ALKALOID: Vinblastine Use, Toxicities, Pearls

A
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35
Q

Antimitotics: TAXANES: Paclitaxel Use, Toxicities, Pearls

A
36
Q

Antimitotics: TAXANES: Docetaxel Use, Toxicities, Pearls

A
37
Q

Overview of Topoisomerase Inhibitors: MOA, MISC

A

Mechanism of Action
* Topoisomerases induce DNA strand breaks to unwind double-helix structure and allow transcription/replication (prevents supercoiling)
* Topoisomerase inhibitors result in single- and double-strand breaks
.
MISC
* Multiple topoisomerase enzymes; clinically relevant inhibitors target topoisomerases I & II (Top1 & Top2)
* More double-strand breaks = more cytotoxicity

38
Q

Topoisomerase Inhibitor Subclasses

A
39
Q

Topoisomerase Inhibitors: CAMPTOTHECIN: Irinotecan (CPT-11) Use, Toxicities, Pearls

A
40
Q

Topoisomerase Inhibitors: PODOPHYLLOTOXIN: Etoposide (VP-16) Use, Toxicities, Pearls

A
41
Q

Topoisomerase Inhibitors: ANTHRACYCLINES: Doxorubicin, Daunorubicin, Idarubicin, Epirubicin Use, Toxicities, Pearls

A
42
Q

Miscellaneous: ANTITUMOR ANTIBIOTICS: Bleomycin Use, Toxicities, Pearls

A
43
Q

Miscellaneous: ANTITUMOR ANTIBIOTICS: Dactinomycin Use, Toxicities, Pearls

A
44
Q

Miscellaneous: ASPARAGINASE
general info.

A
  • Asparagine is synthesized by ʟ-asparagine synthetase
  • Asparagine synthetase absent in lymphocytic malignancies
  • Asparaginase hydrolyzes asparagine to aspartic acid + ammonia, starving the leukemic cells of asparagine –> inhibit protein synthesis –> apoptosis
  • Most products derived from E. coli (risk for HSR and resultant loss of activity)
  • Switch to Erwinia product if grade 3-4 HSR to E. coli product
45
Q

Overview of Hormonal Therapies: Focusing on breast and prostate cancer

A
46
Q

Hormonal Therapy Subclasses

A
47
Q

Hormonal: ANTIESTROGEN: Tamoxifen Use, Toxicities, Pearls

A
48
Q

Hormonal: AROMATASE INHIBITOR: Letrozole Use, Toxicities, Pearls

A
49
Q

Hormonal: GNRH AGONIST: Goserelin Use, Toxicities, Pearls

A
50
Q

Hormonal: ANTIANDROGEN
: Abiraterone Use, Toxicities, Pearls

A
51
Q

What are Targeted Therapies?

A

Therapies directed towards a specific target on cells that affects tumor growth, proliferation, or survival
- Preferentially target tumor cells

52
Q

Targeted Therapy: Small Molecule Receptor
Tyrosine Kinase Inhibitors (TKIs) - MOA

A
  • Binds to the ATP pocket of the TKD
  • Prevents phosphorylation thus no signal transduction thus leading to apoptosis/ cell arrest
53
Q

Epidermal Growth Factor TKIs: Agents, Indications, Consideration

A
  • Agents: Gefitinib erlotinib, afatinib, osimertinib, lapatinib, neratinib (all PO)
  • Indications: EGFR-mutated metastatic NSCLC, metastatic HER2+ breast cancer (lapatinib, neratinib), pancreatic cancer (erlotinib)
  • Considerations: Major class adverse events: acneiform rash; Interactions: food, CYP3A4, smoking (CYP1A2 – erlotinib); Most agents are CYP3A4 substrates; Afatinib – irreversible EGFR inhibitor – can be used in some resistant tumors; Osimertinib – overcomes activating EGFR mutations and T790M mutations; Lapatinib, neratinib – block EGFR and Her2/NEU kinase activity
54
Q

VEGFR Tyrosine Kinase Inhibitors: Agents

A

Agents
Sorafenib, sunitinib, axitinib, cabozantinib, pazopanib, lenvatinib, regorafenib, vandetinib

55
Q

VEGFR Tyrosine Kinase Inhibitors: MOA

A

Summary; these agents constrict the blood vessels leading to lack of blood flow/ nutrients to the cancer cell, starving them.

56
Q

VEGFR Tyrosine Kinase Inhibitors: Indication and Consideration

A

Considerations
Common adverse events:
hypertension, rash, proteinuria, QTc prolongation, hemorrhagic, thromboembolic, cardiac toxicity,
wound healing complications
- CYP3A4 interactions!

57
Q

Bruton’s Tyrosine Kinase (BTK) Inhibitors: Agents, Indications, Considerations

A
  • Agents: Ibrutinib, acalabrutinib, zanubrutinib
  • Indications: CLL/SLL, mantle cell lymphoma, chronic GVHD (ibrutinib)
  • Considerations Adverse effects: hemorrhage, atrial fibrillation, infections, myelosuppression, renal toxicity, secondary cancers, lymphocytosis
    CYP3A4 substrate
58
Q

Phosphatidylinositol 3-kinase (PI3K) Inhibitors: Agents, Indications, Consideration

A
  • Agents: Idelalisib, copanlisib, duvelisib, alpelisib
  • Indications: CLL/CLL, follicular lymphoma, HR+, HER2-, PIK3CA mutated advanced breast cancer (alpelisib)
  • Consideration: hepatotoxicity, diarrhea, pneumonitis, infections, cutaneous reactions,
    hyperglycemia, and perforation; CYP3A substrate
59
Q

B-cell lymphoma (BCL) Inhibitor: venetoclax (indication, consideration)

A

Indications: newly diagnosed AML (comorbid or ≥75 yo), CLL/SLL
.
Consideration
- Dosing:
“Ramp up” to target dose for TLS risk; Requires dose-adjustment for concurrent use with CYP3A4 inhibitors (commonly used with azole antifungals)
- Adverse effects: neutropenia, anemia, thrombocytopenia, diarrhea, nausea, fatigue, upper
respiratory tract infection, tumor lysis syndrome (CLL/SLL > AML)

60
Q

Non-Receptor Tyrosine Kinase Inhibitors & Other Small Molecule Inhibitors: BCR-ABL Tyrosine Kinase Inhibitors - Idications and MOA

A
  • Indications: CML, Ph+ ALL, gastrointestinal stromal tumor (GIST)
  • MOA: Inhibit BCR-ABL kinase
    Abl: normal kinase that regulates cell growth and signaling
    BCR-abl: a translocation that occurs commonly in patients with CML t(9;22) - the “Philadelphia chromosome”
    Translocation of BCR and abl leads to
    increased abl function and cell growth
61
Q

BCR-ABL Tyrosine Kinase Inhibitors: chart

A
62
Q
A
63
Q

Small Molecule Inhibitors of mTOR: agents, indications, consideration

A
  • Agents: Everolimus and temsirolimus
  • Uses: advanced breast cancer, neuroendocrine tumors, renal cell carcinoma (RCC), non-cancer indications
  • Considerations Adverse effects: hyperglycemia, increased lipids, infection, mucositis, pneumonitis, myelosuppression, hepatotoxicity; Supportive care with steroid mouthwash typically recommended; CYP3A4 drug interactions
64
Q

CDK4/6 Inhibitors: Mechanism of Action

A
65
Q

CDK 4/6 Inhibitors: DLT/ Adverse Events

A
66
Q

PARP Inhibitors: MOA

A
67
Q

PARP Inhibitors: Agents, Indications, AEs

A
68
Q

Immunomodulatory Imide Drugs (IMiDs)/ Immunomodulators: Agents, indications, MOAs, and Consideration

A
69
Q

Immunomodulatory Imide Drugs (IMiDs): PD/ PK chart

A
70
Q

Proteasome Inhibitors: Agents, indications, AEs

A
  • Agents: Bortezomib, carfilzomib, ixazomib
  • Indications: multiple myeloma, mantle cell lymphoma
  • Adverse effects: peripheral neuropathies (most with bort), thrombocytopenia, viral reactivation, cardiotoxicity (carfilzomib), eye issue with ixazomib
71
Q

Proteasome Inhibitors: MOA

A
72
Q

IDH Mutations Represent Important Cancer Metabolism Targets: What is IDH? What are the mutations?

A
73
Q

IDH Inhibitors: Agents, indications, Considerations

A
  • Agents: Enasidenib and ivosidenib
  • Indications: IDH1 or 2 mutated AML
  • Considerations
  • Adverse events: Differentiation syndrome requiring prompt initiation of dexamethasone, hyperbilirubinemia, QTc prolongation; CYP3A4 drug interactions
73
Q
A
74
Q

Smoothened (SMO) Inhibitors: Agents, indication, consideration

A
  • Agents: Vismodegib, sonidegib, glasdegib
  • Uses: AML, basal cell carcinoma
  • Considerations: Monitor serum CK and for musculoskeletal adverse reactions, Oral agents with CYP3A4 drug interactions (sonidegib); also may interact with drugs that affect pH (vismodegib)
75
Q

Mechanism: SMO Inhibitor

A
  • The hedgehog (Hh) signaling pathway is essential for embryonic development and organ formation; mutations within the pathway result in unrestricted proliferation
  • Inhibitors bind and prevent Hh ligand binding to PTCH-1, blocking stimulation of the G protein-coupled receptor (GPCR) smoothened (SMO) leading to inactivation of Gli transcription factors and pathway biological function
76
Q

Nomenclature of Monoclonal Antibodies (mAbs): Source and target

A
77
Q

Biologic Response to Antibodies: what can mAbs do?

A
78
Q

Monoclonal Antibody Therapeutic Strategies

A
79
Q

Anti-tumor mAbs: EGFR Inhibitors: agents, mechanisms, consideration

A
80
Q

K-RAS activity: normal vs when it is mutated

A
81
Q
A
82
Q

Anti-tumor mAbs: HER-2 Inhibitors: Trastuzumab VS. Pertuzumab

A

Trastuzumab:
- Inhibits ligand-independent HER2 signaling
- Activates antibody dependent cellular cytotoxicity (ADCC)
- Prevents HER2 extracellular domain shedding
.
Pertuzumab:
- Inhibits ligand-dependent HER2 dimerization and signaling
- Activates ADCC

83
Q

Anti-tumor mAbs: HER-2 Inhibitors: Agents, indication, mechanism, consideration

A
  • Agents: Trastuzumab, pertuzumab, ado-trastuzumab emtansine (T-DM1)
  • Indications: HER2+ breast cancer, metastatic HER2+ gastric cancer
  • Mechanism: binds to cell surface HER-2; Prevents EGF, TGF-α binding and signal transduction
  • Considerations: Monitor cardiac function; Require loading doses for receptor saturation
84
Q

Ado -trastuzumab emtansine (T-DM1)? what is it?

A
  • Conjugated antibody: trastuzumab and DM1 are covalently linked via a thioether linker
  • DM1 = highly potent derivative of antimicrotubule agent maytansine
  • T-DM1 specifically targets HER2+ tumor cells by antibody-dependent cellular cytotoxicity, inhibiting HER2 signaling, and delivering emtansine to cancer cells
85
Q

Monoclonal Antibodies in Hematologic Cancers

A
86
Q
A

APPE 7: Oncology (1 decks)

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