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92 Cards in this Set

  • Front
  • Back

What is cancer

Disease characterized by a shift in control mechanisms that control proliferation and differentiation

What are factors influencing cancer

1. Gender

2. Age

3. Race

4. Genetic environmental carcinogens

What are some chemical toxins that are mutagenic

1. Azo dyes

2. Asbestos

3. Benzene

What are some infection agents that cause cancer

1. HHV-8

2. Human papilloma virus

What is a sarcoma and give examples

Cancer in connective tissue

Fat, bone, muscle

What is a carcinoma and give examples

Cancer in epithelial cell

Lung, breast, colon, prostate

What are the stages of Tumor Progression

1. Hyperplasia

2. Dysplasia

3. Carcinoma in situ (not cross basal lamina)

4. Cancer (Malignant tumors) - metastasis

When treating the tumor what do you look at

1. Type of tumor

2. Location and amount of disease

3. Health of patient

What are the objectives of cancer treatment

1. Kill cancer cell

2. Lead them to apoptosis

3. Contain/limit cell growth

What are some types of cancer treatments

1. Surgery

2. Radiation

3. Chemotherapy

Is mono therapy or combination therapy better for chemotherapy treatment

Combination therapy

What is the timing of chemotherapy

Cycles = intense tx periods followed by days of no tx

What is the MOA of Genotoxic Agents

Alkylate DNA (non cell cycle dependent)

What are some cell cycle dependent agents

1. Anti-metabolites

2. Cytoskeletal inhibitors

3. Topoisomerase inhibitors

When did the first drugs come out that cured cancer (which cancers)

1960's and 1970's

Leukemias and lymphomas

What are the genotoxic agents

1. Cisplatin

2. Doxorubicin

3. Cyclophosphamide

What happens when you alklyate DNA

1. Fragments DNA

2. Create inter/intra strand DNA cross link (affects DNA separation)

3. Induces mispairing of nucleotides (leads to mutation)

4. Forms DNA adducts (DNA polymerase can't work)

Which genotoxic agents need to be given by IV

1. Platinum based chemotherpeutics agents (i.e. Cisplatin)

2. Doxorubicin

Which genotoxic agent can be given orally every day


What are the general adverse effects of genotoxic agents

These agents affect cells that are rapidly dividing:

1. Hematopoietic effects

2. GI effects

3. Hair loss

4. Increase risk of developing cancer

What are the specific adverse effects of Cisplatin, Doxorubicin, and Cyclophosphamide

Cisplastin = renal and ototoxicity

Doxorubicin = Heart effects (Heart failure)

Cyclophosphamide = Bladder irration (hemorrhagic cystitis)

Which of the genotoxic agents has the least adverse effects


Draw out the Cell Cycle

Draw Out the Cell Cycle

Where on the cell cycle do the drug work

G1, S, G2, Mitosis (Prophase, Metaphase, Anaphase, Telophase)

Which drug class works on the S phase


How do Antimetabolites work

Similar to natural metabolites

Prevent cells from carrying out vital function and unable to grow and survive

Interfere with production of Nucleic acids, RNA, DNA

What are the 3 types of Antimetabolites

1. Folate Antagonist

2. Purine Antagonist

3. Pyrimidine Antagonist

What is the Folate Antagonist


What is the MOA of Methotextrate

Inhibit dihyrdrofolate reductase (enzyme involved in forming purine and pyrimidines by allowing Carbon donation; thus no DNA replication and growth blocked)

Which cancers are methotexrate used

1. Acute lymphocytic leukemia (most common)

2. Large cell lymphoma

3. High grade lymphoma

4. Head and neck cancers

5. Breast and Bladder cancer

6. Rheumatoid arthritis

What are the next generation of Antifolate


What is the MOA of Pemetrexed

Inhibits Dihyrdofolate

Inhibits thymidylate synthase

Inhibits glycinamide ribonucelotide formyl transferase

Where is Premetrexed used

Second line therapy for non small cell lung cancer

What is a problem with Antifolates

Problems with Hematopoeitic effects

What is Folinic Acid Rescue Therapy

Give Folinic Acid with methotrexate and antifolates to decrease myelosuppression

What is the MOA of Folinic Acid

THF analog can be used as methyl donor

DHFR insensitive

Therefore some DNA/RNA base synthesis can be carried out in normal blood and GI cells

What is the function of Purine Antagonists

Prevent continued replication of DNA and cell division

What are 2 examples of Purine Antagonists


6- Thioguanine

When do you used Purine Antagonists

1. Acute lymphocytic or myelocytic leukemia

2. Lymphoblastic leukemia (kids)

3. Acute myelogenous and myelomonocytic leukemias

4. Inflammatory bowel disease

5. Organ transplant

What are some ways cells can metabolize MP and TG and inactivate them

Xanthine oxidase

TPMT (Thiopurine S-Methyltransferase)

What is the TPMTP Polymorphisms of Extensive, intermediate, and poor metabolizers

wt/wt (90%) = extensive metabolizer

wt/mut (10%) = intermediate metabolizer

mut/mut (1/300) = poor metabolizer

How do you determine TPMT Phenotype

Metabolism of MP in blood samples then look at the metabolism/drug ratio

Do poor metabolizers need more or less drugs

Less drugs

What is the MOA of Pyrimidine Antagonists

Block synthesis of pyrimidine containing nucleotide

What are the 2 Pyrimidine Antagonists

5-Fluorouracil (5-FU)


What is the MOA of 5-Fluorouracil

Inhibits Thymidylate Synthase

When would you use 5-FU

Colorectal Cancer

What is the drug class used in Mitosis

Cytoskeletal inhibitors (inhibit microtubule function)

What are the 2 groups of cytoskeleton and the drugs in each class


1. Paclitaxel

2. Docetaxel (anaphase)

Vinca Alkaloids

1. Vincristine

2. Vimblastin

3. Vindesine (metaphase)

When do you use Cytoskeletal Chemotherapies

1. Breast

2. Testicular

3. Hodgkin

4. Kid leukemia

5. Rhabdomyosarcoma

6. Lung cancer

7. Neuroblastoma

Which phase of the cycle do Topoisomerase I inhibitors work

G2 Phase

What is the function of Topoisomerase

nicks DNA strands and allows the tension to relax and also reseals the DNA so replication can occur

What are the 2 Topoisomerase I inhibitors

1. Topotecan

2. Irinotecan

What are the Topoisomerase II inhibitors

1. Etoposide

2. Teniposide

Which phase does Hormonal therapy work


What is the MOA of Hormonal therapy

Starve cancer cells from hormonal signals needed for growth

Block hormones on target cell and prevent hormone production

Where would you use hormonal therapy

1. Breast

2. Ovarian

3. Prostate

4. Endometrial

What are the 3 types of hormonal antagonists

1. Selective estrogen receptor modulator (SERM)

2. Selective androgen receptor modulator (SARM)

3. Aramatase inhbitor

What are the 2 types of Estrogen Receptors

ER alpha

ER beta

Compare and Contrast ER alpha to ER beta

Look at chart

Which cancer does SERM target

Breast cancer cells

What is the MOA of SERM

Changes gene expression preventing cell division

What are the 3 SERM drugs

1. Tamoxifen

2. Raloxifene

3. Toremifene

How do SERMs work

Drug goes in blocks estrogen receptor and inhibits estrogens growth stimulation effect

What are the issues with Tomaxifen and its Drug Interactions

1. Tamoxifen is a pro drug and it needs CYP2D6 to turn it into the active metabolite Endoxifen

2. CYP2D6 has variable metabolism activity (i.e. poor, moderate, extensive metabolizers)

3. Problems with Serotonin Uptake Inhibitors (Paroxetine, Fluxoetine, Bupropion)

What type of metabolizer works best with Tamoxifen

Extensive metabolizer

What do Aromatase inhibitors do

Inhibit the production of estrogen and estrodiol

What are the 3 Aromatase Inhibitors

1. Exemestane

2. Anastrozole

3. Letozole

What are the SERM an Aromatase Inhibitors indications

1. Advanced or Metastatic breast cancer

2. High risk population for invasive breast cancer

What do Specific Androgen Receptor Modulators (SARM) work

Block androgen receptors

What are the 2 SARMs

1. Flutamide

2. Bicalutamide

Why does Chemotherapy Fail

A lot of side effects

Which drug causes bone marrow depression


Which drugs cause nephrotoxicity

Platinum analog (Cisplatin, Carboplatin)

Purine Antagonists (6-Mercaptopurine)

Which drugs cause hepatotoxicity

Vinca Alkaloids (Vincristine, Vinlastine)


Which drugs cause Nausea and vomiting

Topotecan cpds

Which drugs cause Alopecia


Vinca Alkaloids

Which drugs cause Cardiotoxicity

Anthracyclines (Doxorubicin, Daunorubicin)


Which drugs cause Hemorrhagic cystitis


Which Drugs cause Neuropathy

Platinum Analogs (Cisplastin, Carboplatin)

Vinca Alkaloids (Vincristine, Vinblastine)

Taxol Based Chemotherapeutics

What are 4 mechanisms related with Resistance and Chemotherapy

1. Increased expression of target proteins therefore need higher amount of cancer drug, but that amount will kill all cells

2. Failure of drugs to enter cancer cell or increased rate of removal of drug from cancer


3. Drugs fail to reach target cell/target molecule no longer present

4. Target Molecule is Altered

What causes a failure of drugs to enter cancer cells (increases efflux)


1. What are the Biological Response Modifiers (2)

2. What are its MOA

3. Where are they primarily used for

4. What is the route of administration

5. What are the side effects

1.a. Interferons

b. Interleukin 2

2. Modify immune system response

3. Hematopoietic neoplasias (blood cancer)

4. Parenteral routes

5. Flu-like symptoms (mild) to fever and capillary leak syndrome (Sever)

What is the Monoclonal Antibody Therapy Drugs


Trastuzumab (herceptin)

1. What is the MOA of Rituximab

2. Function

3. Side effects

1. Binds to CD20 antigen (receptor) on the surface of B lymphocytes which activates phagocytosis and antibody dependent apoptosis

2. Inhibits proliferation of lymphocytes and lymphoma cells

3. Hypersensitivity reaction and anaphylactic shock

1. What is the MOA of Trastuzumab

2. What are the side effects

3. Which patients does it work really well for

1. Binds to epidermal growth factor receptor protein (HER2) (over expressed in some cancers like breast)

2. Allergic rxn, heart muscle damage, pulmonary toxicity

3. HER2+ metastatic breast cancer and early stage HER2+ breast cancer

1. What is the Angiogenesis inhibitor

2. Which cancers is it used for

3. What is its MOA

4. What are its advantages

5. What are its disadvantages

1. Bevacizumab (Avastin)

2. Metastatic colorectal and NSCL

3. Endothelial cell growth into the tumor

4. Fewer side effect, less chance of resistance

5. Angiogenesis is important in wound healing and normal development, long term effect no yet known

1. What are the 3 Protein Kinase Inhibitors

1. Imatinib

2. Erlotinib

3. Ruxolitinib

1.What is the function of Imatinib

2. Which cancer is it used for

1. Prevents phosphorylation of specific proteins involved in cell growth and differentiation

2. Chronic Myelogenous Leukemia

1. What is the function of Erlotinib

2. Which cancer is it used for

1. EGFR tyrosine kinase inhibitor

2. Lung and pancreatic cancer

1. What is the function of Ruxolitinib

2. What cancer is it used for

1. JAK-1 and JAK-2 inhibitor

2. Myelofibrosis

What are the benefits of the New Generation of Chemotherapeutics

less side effects

oral medication