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74 Cards in this Set

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A group of diseases:

1.) uncontrolled cellular growth

2.) local tissue invasion

3.) distant metastases

Most commonly diagnosed cancer in men?


Most commonly diagnosed cancer in women?


Most common cause of cancer death in women?


Most common cause of cancer death in men?


Age group for which cancer is the leading cause of death?

> 85 years of age

Lifetime probability of developing cancer for men and women?

men = 1 in 2

women = 1 in 3

Top 3 causes of cancer death in children and adolescents?

0-14 years: 1.) Brain, 2.) Leukemia, 3.) Soft Tissue

15-19 years: 1.) Leukemia, 2.) Bone/Joints,

3.) Brain

The 2 major influences in the development of cancer in Americans?

1.) Cigarette smoking

2.) Age

Obesity is a risk factor for which 3 cancers?

1.) Colon

2.) Prostate

3.) Ovarian

What lack in diet is associated with higher rates of cancers?

5 or more servings of vegetables daily

4 Processes in Carcinogenesis

1.) Initiation

2.) Promotion

3.) Conversion

4.) Progression



irreversible damage to normal cells caused by exposure to carcinogenic substances



carcinogens alter the environment to favor growth of the mutated cells

possibly reversible



the transformation of a normal cell to a cancerous cell

may take 5-20 years



further genetic changes leading to increased cell proliferation



the development of new blood vessels by the tumor in order to grow

Who do we screen for cancer?

Asymptomatic people with risk factors for certain kinds of cancer because...

- of the low cure rate of metastatic cancer if discovered too late

- the expense of screening

Describe the screening schedule for breast cancer.

Clinical Breast Exam:

- starting at age 20

- at least every 3 years, then annually prior to mammograms


- starting at age 40

- annually

Describe the screening schedule for cervical cancer.

Pap Smear:

- starting at age 21 to 29

- every 3 years

HPV and Pap Tests:

- starting at age 30 to 65

Describe 5 screening schedules that both men and women should follow starting at age 50.

1.) Fecal Occult Blood Test - annually

2.) Flexible Sigmoidoscopy - every 5 years

3.) Double Contrast Barium Enema - every 5 yrs

4.) Colonoscopy - every 10 years

5.) CT Colonography - every 5 years

Goals of Cancer Treatment

1.) Cure

2.) Prolong Life

3.) Palliation

Adjuvant Therapy


systemic therapy that is administered to treat any existing micrometastases remaining after surgical excision of localized disease.

Neoadjuvant Therapy


treatment given prior to the definitive local treatment, usually prior to surgery.

What order of kinetics do cancer treatments follow?

1st order

(cancer drugs kills a constant proportion of tumor cells)

What kind of cells do most cancer treatments target?

Rapidly proliferating cells, whether cancerous or no. (Ex: mucus membranes, hair follicles, bone marrow)

How are cancer treatments dosed?

The Maximum Tolerated Dose (MTD) is the most effective, but requires several cycles with resting periods in between.

The MTD is given up to the Dose Limiting Toxicity (DLT) for any one anticancer drug at which point it's too dangerous to continue.

Gompertzian Growth Curve-Log-Kill Hypothesis

Cancer cells are clinically undetectable til 10^5

- immunotherapy = greatest benefit

10^5 - 10^12 cells = symptomatic, diagnosis possible, bulk reduction of tumor is necessary

10^12 cells = plateau growth phase, 1 kg tumor, incapacitating symptoms, death

Why Combination Chemotherapy?

1.) Maximal cell kill within tolerated toxicity

2.) Broader range of coverage

3.) Prevent development of resistant lines

Metronomic Therapy


For molecularly-targeted drugs only.

Taken continuously until disease progression or unacceptable adverse events occur.

4 Classes of DNA-Damaging Drugs

1.) Alkylating Agents

2.) Antibiotics

3.) Topoisomerase Inhibitors

4.) Anti-Metabolites

Characterization of DNA-Damaging Drugs

Interfere with transcription and reduplication

- Affected cells undergo cell cycle arrest and apoptosis

* Mutagenic, Teratogenic, and Carcinogenic

Affect rapidly proliferating cells

Alkylating Agents

(Mechanism of Action)

Overall: Attach alkyl groups to DNA

* groups on DNA bases prevent DNA synthesis, RNA transcription = fragmentation

* crosslink DNA strands = no DNA separation for reduplication or transcription

* groups induce mispairing leading to mutations

8 Alkylating Agents

1.) Nitrogen Mustards *

2.) Nitrosureas *

3.) Triazenes and Hydrazines

4.) Ethylene Imines and Methylmelamines

5.) Benzoquinone-containing

6.) Alkyl Sulfonates

7.) Illudins

8.) Platinum drugs *

Nitrogen Mustards

1st Gen: Mechlorethamine *, N-0xide

2nd Gen *: Chlorambucil, Melphalan, Bendamustine, Spiromustine

3rd Gen: Uramustine

Steroid-Coupled: Estramustine phosphate, DHEA mustard, Prednimustine

Phosphoramide *: Cyclophosphamide, Ifosfamide

Which nucleotide is most susceptible to alkylation?


Phosphoramide Mustards

(Mechanism of Action)

Prodrugs metabolized by CYP450 to phosphoramides and acrolein

Phosphoramides alkylate DNA

Acrolein alkylates proteins (AE: Bladder Toxicity)



Uses: solid and hematologic tumors, bone marrow transplant (BMT)

AE: hemorrhagic cystitis (bladder toxicity)

(not as much as Ifosfamide, may give Mensa)

DLT: leukopenia = 8-14 days



Uses: sarcomas, testicular cancer, lung cancer

AE: *hemorrhagic cystitis (Mensa mandatory)


(Mechanism of Action)

Carmustine (BiCNU), Lomustine (CeeNU), Streptozocin (Zanosar)

Lipid Soluble, often oral dosing, long nadir



Uses: brain tumors, Hodgkin's Dx, mycosis fungoides, cutaneous T-cell lymphoma

*Dosage Forms: Injection (in EtOH), topical, Gliadel wafer (brain implantation)

*Long time to nadir (21-28 days)

*Administer every 6 weeks



Uses: primary brain tumors

Dosage Forms: oral capsule (10 mg increments)

Long time to nadir (dose every 6 weeks)

Platinum Compounds

(Mechanism of Action)

Crosslink DNA like mustards

- intrastrand (bind twice, same strand)

- interstrand (bind twice, crosslink)

- monoadduct (bind once)

- intermolecular (bind to DNA and protein)


(Adverse Effects)


Nausea/Vomiting (acute and delayed)


Myelosuppression (slight)



(Adverse Effects)

Uses: broad spectrum

AE: nephrotoxicity, ototoxicity, neuropathy, N/V

(less than cisplatin)


DLT: Thrombocytopenia



Calvert Formula

Target AUC (6mg/mL/min) * [GFR + 25]

(25 = constant representing non-renal Cl)


Uses: colorectal cancer, GI tumors

Often used in combo with 5-FU or Capecitabine

Dose: 135 mg/m^2


(Adverse Effects)

Hypersensitivity rxn

*DLT: Neurotoxicity (acute and delayed)





Pulmonary Fibrosis *rare


(DLT elaborated)

Acute Neurotoxicity: peripheral neuropathy, visual changes, auditory toxicity, *pharyngolaryngeal dysesthesia

Delayed Neurotoxicity: cumulative peripheral sensory neuropathy

Proph: Avoid cold temperatures and food/drink! (pharyngolaryngeal dysthesias)


(N/V tx)

5-HT3 antagonist (setron drug) + dexamethasone

(ex: Ondasetron, Granisetron, Palonosetron, Dolasetron, Metaclopramide)



Alkyl Sulfonate

Affect early WBC precursors

Uses: chronic myeloid leukemia (CML), BMT

Dosage Forms: oral

*Prolonged nadir time

AD: "Busulfan lung" = pulmonary fibrosis, seizures (proph. with phenytoin)

2nd Gen Nitrogen Mustards

Chlorambucil, Melphalan, Bendamustine

More stable with inclusion of 6-member ring and long hydrocarbon/carboxyl tail



Uses: chronic lymphocytic leukemia (CLL), non-Hodgkin's Lymphoma (NHL)

Dosage Form: 2 mg oral tabs

Dose every 2-4 weeks

AE: bone marrow suppression, N/V, pyrexia



Uses: multiple myeloma, BMT

Dosage Forms: oral and IV

9 mg/m^2 PO x4-7 days Q4-6 weeks

(BMT = 100 mg/kg)



Uses: Chronic lymphocytic leukemia (CLL), non-Hodgkin's Lymphoma (NHL)

AE: bone marrow suppression, N/V, pyrexia

(more than chlorambucil)

Topoisomerase Inhibitors

(Mechanism of Action)

Prevents Topoisomerase 1 or 2 from uncoiling the supercoiled DNA for transcription and reduplication

Topoisomerase 1 inhibitors: Camptothecins, Indolocarbazoles, Indenoiseoquinolines

Topoisomerase 2 inhibitors: Podophyllotoxins, Quinoxalines, Antibiotics



Camptothecin (T1)

Uses: Colorectal cancer

AE: Diarrhea (acute and delayed), neutropenia (dose dependent), N/V, dehydration, alopecia, mucositis, acute pulmonary toxicity?


(Diarrhea tx)


- atropine 0.25 - 1 mg IVP


- loperamide 4 mg PO LD, then 2 mg PO Q2h ATC until resolved for 12 hours


(VP-16, Vepesid)

Epipodophylotoxin (T2)

Uses: Lung cancer, NHL, BMT

Dosage Form: in EtOH, IVPB (hypotension), 50 mg PO capsules (F= 50%)

5 Classes of Antitumor Antibiotics

1.) Cyclopropylpyrroloindole

2.) Minor-Groove DNA-binding

3.) Aminoquinone

4.) Polycyclic Aromatic (anthracyclines)

5.) Enediyne

2 Broad Classes of Antitumor Antibiotics

1.) Alkylate DNA

(Cyclopropylpyrroloindoles, minor groove

binding, aminoquinones)

2.) Redox Cycling

(Polycyclic aromatics, enediynes)

Redox Cycling Antibiotics

(Class Adverse Effects)




4 different proteins from bacteria

Uses: testicular, NHL, head/neck cancers

AE: pulmonary toxicity, pyrrexia, mucositis

Polycyclic Aromatics

(aka Anthracyclines)

Doxorubicin, Amrubicin, Epirubicin, Valrubicin, Pirarubicin, Berubicin

MOA: intercalates between DNA base pairs and generates free oxygen radicals using the carbonyls on its B ring



Uses: solid and hematologic tumors

AE: cardiotoxicity (max = 550 mg/m^2 for life), myelosuppression, N/V/D, red urine, vesicant, alopecia, radiation recall, mucositis

Dose: 25-60 mg/m^2 IVP



MOA: Metal Chelator

Uses: Cardioprotection in women with metastatic breast cancer who have received 300 mg/m^2 doxorubicin

AE: myelosuppression, N/V, alopecia, LFT elevation



Uses: breast cancer, NHL, acute leukemia, ovarian cancer, metastatic prostate cancer (+ prednisone)

AE: cardiomyopathy, N/V, alopecia (less than other anthracyclines), blue/green secretions

Dose: 10-12 mg/m^2 IVP or IVPB


(Classes and Subclasses)

1.) Anti-Folates

- Dihydrofolate Reductase inhibitors

- Thymidylate Synthase inhibitors

- Glycinaminde Ribonucleotide Formyl

Transferase inhibitors

- Dihydropteroate Synthase inhibitors

2.) Anti-Pyrimidines

- Uracil analogs

- Cytidine analogs

3.) Anti-Purines

- 1st and 2nd generation


(Mechanism of Action)

1.) Serve as false building blocks

2.) Inhibit synthesizing enzymes

- prevent synthesis of DNA and RNA

Non-selective, therefore best localized


(Trexall, Rasuvo)

MOA: Anti-Folate (Dihydrofolate Reductase-i)

Uses: solid and hematologic tumors (ex: breast, lung, head/neck cancers, sarcomas)

Dosage Forms: injection including intrathecal

Dose: 12 mg/m^2


(Adverse Effects + Risk Factors)

AE (dose dependent) myelosuppression, N/V, mucositis, hepatotoxicity, neuro/nephrotoxicityRisk Factors: renal dysfunction, prior use of nephrotoxins, pleural effusion, ascites, GI obstruction, poor hydration, acidic urine

Dose > 100/m^2 requires leucovorin rescue



Low Risk:

T1/2: < 3.5 H

C24H: < 5 x 10^-6 M

Leucovorin = 10 mg/m^2 Q6H for 72H (standard low dose)

High Risk:

Monitor until < 1 x 10^-8 M and escalate leucovorin as needed



Uses: GI tumors, colorectal cancer, pancreatic

2nd line in breast, lung and head/neck

Dose: 500-1000 mg/m^2 IVP or 24H CIVI


(Adverse Effects)

CIVI: mucositis, diarrhea, hand-foot syndrome

IVP: neutropenia

Elevated LFTs, coronary artery spasm, photosensitivity

Proph: Ice chips and oral hygiene (mucositis)

Loperamide or lotomil (diarrhea)