CHEMOTHERAPY right after tumor is removed.

OR IN
COMBINATION.

 One of the modalities used in treatment of

cancer px PX IS ADVISED FOR:
 conjunction w/ surgery and radiation therapy
 adequate rest
 the cells in the body grow and divide accord to
 nutritious diet
normal cell cycle, control by nucleus that
 medication to minimize the side
contains the DNA of the cell, so when a DNA is
effects
damaged, it may grow rapidly or may die , this
causes the cell to grow rapidly making
 Tumor- as this continues to develop in size
multiple copies of itself, equals to cancer cells
it also develops its own blood supply, as
that displaces normal cells into a tumor.
cancer cells do not adhere to each other
 THIS WORKS, it is attacking the cancer cells
very well comparing to normal ones. So
and the tumor begins to shrink the cancer
they tend to break away and enter the
cells = decreased cell division
bloodstream therefore spreading across
 AFFECTS SYSTEMICALLY – enters bloodstream the body.
and enters media statics cancer cells, can’t  Metastasis- a process, has sites like the
differ a normal and cancer cells, it attacks all lungs, liver, bone, and brain. May also
of it like the sites of BONE MARROW, occur in the lymphatic system, with cancer
DIGESTIVE SYSTEM, HAIR FOLLICLES. cells entering the nearest lymph vessel in
which they migrate to nodes and the rest
of it spreading it all over the body.
SIDE EFFECTS:

 Frequent infections
 Diarrhea CHEMOTHERAPY- chemo + therapy.
 Nausea and loss of appetite  The use of drug (chemical entity/
 Hair loss substance derived form
 Bruising and anemia microorganisms) with selective
toxicity against infections/ viruses,
bacteria, protozoa, fungi and
OBJECTIVES OF IT: helminthes is called as this.
 To eliminate or reduce the tumor or INTRO:
cancer cells at the original site (and side
with mestasis)  modern chemotherapy begun in 1948
 Can be primary or secondary treatment with the introduction of nitrogen
alongside with radiation therapy, and mustard
surgical incision.  The use of chemicals to treat cancer
 These drugs can be given via IV, IM and began in the early 1940's
Orally in pills, capsules and liquid,  It is only in the last 10 to 15 yrs,
systemically. For locally, can be catheters, however, that chemotherapy has
also injected of csf, or dissolving vapors become a major treatment modality.

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OBJECTIVES

 To maximize the death of malignant CELL CYCLE

tumor cells
-Understanding the cell cycle is necessary in
 To cure the client with cancer
cancer chemotherapy
 Control the tumor growth when cure
is not possible -It is a series of events that takes place in a
 To extend the life span and improve proliferating cell (normal and malignant)
the quality of life of client with cancer leading to its division and duplication

DEFINITIONS

CANCER: A group of disease involving

abnormal cell growth with the potential to
invade or spread to other part of the body.

CHEMOTHERAPY: the term chemotherapy is

describe as the use of chemicals or drugs to
treat cancer

CYTOTOXIC DRUG: lysis both normal and

cancer cells

GOALS OF CANCER CHEMOTHERAPY

Phases of cell cycle
- Curative: eradication
G0 Phase l resting phase)
» induction: Given with the intent of inducing
complete remission (eliminate clinical o Spend much of their lives in this
evidence) when initiating a curative regimen phase.
o Have not started dividing
» Consolidation: Repetition of the induction o When the cell get a signal to produce
regimen in a patient who has achieved a they move into the G. Phase
complete remission. o Limitation to successful eradication of
many tumurs by chemotherapy They
» Maintainance: Long-term, low-dose, single
re-enter the cycle after the therapy.
or combination chemotherapy in a patient
who has achieved a complete remission. To
prevent recurrence.
G1 PHASE(Pre-synthetic phase)

o The cell starts to produce proteins and

Palliative: ensym necessary for DNA synthesis
o During this phase RVA synthesis occur
» Provide comfort
o This phase lasts about 18 to 30 hours
» Improve/prolong quality of life

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S-PHASE (synthetic phase) - Shorter time results in higher kill when
exposed to - specific agents.
o DNA synthesis
o Cellular DNA is duplicated in
preparation in - preparation for
Growth fraction
cellular division.
o Length of time S phase is - The percentage of cells actively dividing at a
approximately 18-30hrs. given - point in time. High growth fraction
o A weak link, and large number of results in higher cell kill with exposure to
anticancer agent - act. specific agent.

G₂ Phase (pre-mitotic phase)

Tumour burden
o The cell checks the DNA
o Gets ready to start splitting into 2 - The size of the tumour as determine by the
cells. number of cells present. The cancer with a
o Here both protein, RNA, and the small tumour burden are usually more
precursors to the mitotic spindle responsive to therapy. Higher tumour burden
apparatus are produced. the greater the greater the probability of
o This phase is very short 1-2hrs. development of resistance.

MITOTIC PHASE REGULATION/CHECK POINTS

- In this phase, which last only 30-60min, the • To repair DNA damage, Regulation is lost in
cell actually split into 2 new cells. cancer cells.

Significance: - INHIBITORS:

 -Drugs works mainly on cells that are • Cyclin dependent kinase inhibitors lead
active(not in the Go) generation of PS3, Rb which inhibits at
 Some drugs specifically attack cells in G₁/S(restriction point), G₂/M and M phase.
a particular phase
 Determine drug combination
 How often drug is given base on PROMOTERS:
timing. Cyclin dependent kinase + proteins → E2F,
cyclin D1, and B drives the cycle at S and G2
phase
CELL CYCLE TIME/GENERATION

-The amount of time required for cell to move

from - one mitosis to another (time to
complete one cycle)

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  According to chemical groups

o Alkylating agents

Eg: Buzalfan, Cyclophosphamide, Carboplatin

o Antimetabolites

Eg: Cladribine, Methotrexate Sodium, 5

flurouracil

o Anti tumor antibiotics

Fg: Bleomycin Sulfate, Dactinomycin,

Chemotherapeutic drugs act through variety Epirubicin
of mechanism
o Nitrosureas
-Limiting DNA synthesis and expression
Eg: Carmustine, Lomustine, Semustine
-Cross linking polymer DNA
o Plant alkaloids
-ADNA double stand breaks
Eg: Docetaxel, Etoposide, Paclitaxel
-Preventing formation of mitotic apparatus
o Hormonal agents
o Miscellaneous agents
Classification of chemotherapeutic drugs: Fg: Altetramine, Amsrcrine, Asparaginase

 According to activity on cell

1. Cell cycle phase specific:

-G1 phase :Bleomycin, Corticosteroids,

Hormones

-G2 phase: Bleomycin, Eloposide, Topotecan,

Taxol etc.

-S phase: Cytarabin, 5-fluorocil, Methotrexate

-M phase: Vinblastin, Vincristine, Paclitaxel

2. Cell cycle phase non-specific

-Basalfan
Administration of chemotherapy:
-Cisplatin
 Planning drug doses and schedules
-Cyclophosphamide  Doses: drugs are measured in milligrams
(mg) and doses are determined based on:
 Body weight in kilograms

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 Body surface area

Step A

Schedule (cycles): All procedures involved in the preparation of

cytotoxic drugs should be performed in a class
-Chemotherapy is generally given at regular
2,type A or type B
intervals called cycles
*Laminar flow biological safety cabinet
-One dose followed by several days or weeks
without treatment

Step B

Administration: The work surface of the cabinet should be

covered with plastic backed absorbent paper
✓Oral route

✓Intravenous route
Step C
-Angiocatheter, PICC line, non tunneled
catheters, tunneled catheters and port a-cath Personnel preparing the drugs should wear
PPE (Gloves,gown, facial protection
✓Subcutaneous routes respiratory protection apparatus, caps and
✓Intraventricular/ Intrathecal route: ommaya shoe covers)
reservoir *Gloves should be changed regularly and
✓Intra-arterial routes immediately if torn or punctured

*Skin contact: Thoroughly wash the area with

✓ Intraperitoneal route
soap and water do not abrade. Flush
✓ Intravesicular route eye(s),while holding back the eyelid(s) with
copious amount of water for at least 15
✓Intrapleural route
minutes. Then seek medical evaluation

Safe preparation, handling and disposal:

Step D
*Aseptic preparation of parenteral products Reconstitution should be done with a venting
should be followed
device using a 0.22 micron hydrophobic filter
*Only properly trained personnel should (reduce the probability of spraying and
handle cytotoxic drugs spillages)

*Safe preparation has been divided into 3

sections
Step E
- Steps A,B,C If a chemotherapy dispensing pin is not used
- Steps D,E,F,G ,a sterile alcohol pad should be carefully
placed around the needle a vial top during
-Steps H,I,J,K,L withdrawal from the septum

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Step E Step L

The external surface contaminated with a Cytotoxic drugs are categorized regulated
drug should be wiped clean with an alcohol wastes and therefore, should be disposed of
swab prior to transfer or transport according to National, state and local
requirements

Step G

for glass ampule, wrap it and then snap it at

the break point using an alcohol pad to reduce
the possibility of injury and to contain aerosol
produced

Step H

syringes and I.V bottles containing cytotoxic

drug should be labeled and dated

Step I

After completing the preparation process,

wipe down the interior of the safety cabinet
with water (for injection or irrigation)
followed by 70% alcohol using disposable
towels

Step J

Contaminated syringes,I.V tubing, butterfly

clips etc. should be disposed of intact to
prevent aerosol generation and injury

*Do not recap

*Labeled "cytotoxic waste only"

Cont*
Step K
• Exposure can be occur through
Hand should be washed between glove
changes and after glove removal - Inhalation of aerosols

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-Absorption through the skin Treatment:

- Ingestion of contaminated material -Stop administration

- Aspirate any residual drug and blood in IV

tubing, needle, and infiltration site.
Safe handling of chemotherapy drugs:
- Instill IV antidote
Protect patient
- Apply cold or warm pack for 24 hrs
-Care should be taken to protect skin All
connection b/w drug and patient should occur
away from patient skin
Alkylating agent - sodium thiosulfate

Antitumor antibiotics - hydrocortisone

Protect environment
Plant alkaloids - hyalouronidase
-Use Leur lock connection use air inlet device
for preparation of drugs "discard gloves after
each use and wash hand Hypersensitivity reactions:

*HSR are rare,can be serious and life

threatening
Protect your self
*The antineoplastics agents
-Minimize exposure by inhalation by skin
contaminants by ingestion -L-asperginase

- Carboplatin
Extravasation: -Bleomycin
The inappropriate or accidental leakage of -Cisplatin
intravenous drugs from the vein into the
surrounding healthy tissue. -Teniposide

Vesicant Chemotherapy: The reactions:

Drugs that cause blistering and other tissue -Dyspnea

injury that may be severe and can lead to -Tachycardia
tissue necrosis (tissue death).
- Chest tightness or pain

- Dizziness

- Pruritis

- Anxiety

- Inability to speak

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- Nausea • Neurotoxicity

- Abdominal pain • Gonadal suppression

- Hypotension •Cardiotoxicity

- Cloudy sensorium •Alopecia

- Fused appearance and cyanosis •Taste changes

•Skin changes:

Precautions to ensue client safety: -Hyper Pigmentation, Nail Discoloration,

✓Obtain allergy history -Dermatitis

✓Test dose -Fingertip Ulceration and Photosensitivity

✓Be with the client

✓Emergency equipment and drugs Antibiotics and Antimicrobials

✓Baseline vital signs • Antibiotics: Antibiotics are substances

produced by microorganisms, which
selectively suppress the growth of or kill other
microorganisms at very low concentration.

• Antimicrobials: (chemotherapeutic agent +

Antibiotics) Any substance of natural,
synthetic or semisynthetic origin which at low
concentrations kill or inhibits the growth of

Side effects of chemotherapy.

• Myelosuppression

• Fatigue

• Nausea and vomiting

microorganisms but causes little or no host
• Stomatitis and mucositis damage

• Pulmonary toxicity

• Renal toxicity

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 Tetracyclines: Broad spectrum Erythromycin
gram (+)
Principles of antimicrobial therapy

Principles of antimicrobial therapy:

-Frequency and duration of administration:

Inadequate dose may develop resistance,
Intermediate dose may not cure Infection,
optimize dose should be used for therapy.

-Continue therapy: Acute infection treated for

5-10 days. But some of the bacterial infection
exceptions to this. E.g.: Typhoid fever,
tuberculosis and infective endocarditis (after
clinical cure, the therapy is continued to avoid
relapse).

-Test for cure: After therapy, symptoms and

signs may disappear before pathogen
eradicated.
Diagnosis: Site of infection, responsible
organism, sensitivity of drug
-Prophylactic chemotherapy: To avoid surgical
site infections.
• Decide - chemotherapy is necessary: Acute
infection require chemotherapy whilst chronic
infections may not. The chronic abscess
Classification of antimicrobials
respond poorly, although chemotherapy cover
is essential if surgery is undertaken to avoid a A. Chemical structure
flare-up of infection.
*Sulfonamides and related drugs: Dapsone
(DDS), Sulfadiazine, • Sulfonamides and
Paraaminosalicylic acid (PAS)
Select the drug: Specificity (spectrum of
activity, antimicrobial activity of drug), *Diaminopyrimidines: Trimethoprim,
pharmacokinetic factors (physiochemical Pyrimethamine
properties of the drug), patient related factors
*Quinolones: Nalidixic acid, Norfloxacin,
(allergy, renal disease)
Ciprofloxacin • Beta lactam antibiotics:
Selfonamide gran (-)/{} Penicillins, Cephalosporins

Quielones gram (-) *Tetracyclines: Oxytetracycline, Doxycycline

Penicillin gram (+) *Nitrobenzene derivative: Chloramphenicol

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*Aminoglycosides: Streptomycin, Gentamycin, C. Type of organisms (against which primarily
Amikacin, Neomycin active)

*Macrolides antibiotics: Erythromycin, • Antibacterial: Penicillins, Aminoglycosides,

Clanthromycin, Azithromycin Erythromycin, etc.

*Lincosamide antibiotics: Clindamycin • Antiviral: Acyclovir, Amantadine B,

Zidovudine, etc.
*Glycopeptide antibiotics: Vancomycin
• Antifungal: Griseofulvin, Amphotericin B,
*Polypeptide antibiotics: Polymyxin-8,
Ketoconazole, etc.
Bacitracin, Tyrothridin
• Antiprotozoal: Chloroquine, Pyrimethamine,
*Nitrofuran derivatives: Nitrofurantoin •
Metronidazole, etc.
Nitroimidazoles: Metronidazole, Tinidazole
• Anthelminthic: Mebendazole, Niclosamide,
*Nicotinic acid derivatives: Isoniazid,
Diethyl carbamazine, etc.
Pyrczinamide, Ethionamide

*Polyene antibiotics: Amphotericin &

Nystatin, Hamycin

*Azole derivatives: Miconazole, Clotrimazole,

Ketoconazole, Fluconazole

*Others: Rifampin, Ethambutol, Griseofulvin

B. Mechanism of action

D. Spectrum of activity

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E. Type of action (bacteriostatic and Toxicity
bactericidal)
Local irritancy:

• exerted site of administration. E.g.: Gastric

irritation, pain and abscess formation at the
site of i.m. injection, thrombophlebitis of
injected vein.

Systemic toxicity:

Dose related organ damage.

 High therapeutic index agents may not

damage host cells, E.g.: penicillin,
erythromycin.

F. Source of antibiotics

 Fungi: Penicillin, Griseofulvin,

Cephalosporin
 Bacteria: Polymyxin B, Tyrothricin,
Colistin, Aztreonam, Bacitracin
 Actinomycetes: Aminoglycosides,
Macrolides, Tetracyclines, Polyenes,
Chloramphenicol

Systemic toxicity:

Toxicity

• Very low therapeutic index drug is used

when no suitable alternative AMAs available,

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 *Natural resistance: Some microbes have
resistant to certain AMAS. E.g.: Gram negative
bacilli not affected by penicillin G; M.
tuberculosis insensitive to tetracyclines.

*Acquired resistance: Development of

resistance by an organism (which was
sensitive before) due to the use of AMA over a
. E.g.: Vancomycin (hearing loss, kidney period of time. E.g.: Staphylococci, tubercle
damage, "red man' syndrome) bacilli develop resistance to penicillin
(widespread use fo >50 yr). Gonococci quickly
And polymyxin B (neurological and renal developed resistant t sulfonamides in 30 yr.
toxicity)

Resistance
Hypersensitivity reaction
Development of resistance
. All AMAs are capable to causing
hypersensitive reaction, and this this reactions • Resistance mainly developed by mutation or
are unpredictable and unrelated to dose. E.g.: gene transfer

• Mutation: Resistance developed by

mutation is stable and heritable genetic
changes that occurs spontaneously and
randomly among microorganism (usually on
plasmids).

. Mutation resistance may be single step or

multistep.

Penicillin induced anaphylactic shock (prick Single gene mutation may confer high degree
skin testing) of resistance. E.g.: enterococci to
streptomycin

Resistance

• Unresponsiveness of a microorganism to an
AMA, and is similar to the phenomenon of
drug tolerance.

- Natural resistance

- Acquired resistance

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- Multistep mutation may modify the more
number of gene that will decreases the
*The nonpathogenic organisms may transfer
sensitivity of AMAs to pathogens.
'R' factor to pathogenic organisms, which may
become wide spread by contamination of
food and water.

The multidrug resistance has occurred by

conjugation.

-Chloramphenicol resistance to typhoid bacilli

- Penicillin resistance to Haemophilus,

gonococci

-Streptomycin resistance to E coli

Development of resistance Gene transfer

-Transduction: Transfer resistance gene

through bacteriophage (bacterial virus) to
another bacteria of same species.

- E.g.: Transmission of resistance gene

between strains of staphylococci and between
strains of streptococci.

Drug Tolerant

• Loss of affinity of target biomolecule of the

microorganism with particular AMAS, E.g.:
Penicillin resistance to Pneumococcal strain
(alteration of penicillin binding proteins)

Development of resistance

Gene transfer - Conjugation:

*Cell-to-cell contact; transfer of chromosomal

or extrachromosomal DNA from one
bacterium to another through sex pili. The
gene carrying the resistance or 'R' factor is
transferred only if another resistance transfer
factor" (RTF) is present. This will frequently
occurs in gram negative bacilli.

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Superinfection (Suprainfection) Choice of an antimicrobial

A new infection occurring in a patient having a +Patient related factors

preexisting infection. Superinfections are most
+Drug factors
difficult to treat.
+Organism-related considerations
Superinfection

 Development of superinfection
associated with the use of broad/  Patient age
extended-spectrum of antibiotics, such
tetracyclines, chloramphenicol, ampicillin Patient age (chloramphenicol produce gray
and cephalosporins. as newer baby syndrome in newborn; Tetracyclines
 More common when host defence is deposition in teeth and bone-below the age of
compromised. 6 years)
 Generally most difficult to treat.  Renal and hepatic function
 Bacterial superinfection in viral (aminoglycoside, vancomycin renal failure;
respiratory disease infection of a chronic erythromycin, tetracycline- liver failure)
hepatitis B carrier with hepatitis D virus  Drug allergy (History of known AMAs
 Piperacillin-tazobactam may cause allergy should be obtained).
superinfection with candida  Syphilis patient allergic to penicillin-drug
of choice is tetracycline Fluoroquinolones
cause erythema multiforme
Treatment for superinfection:  Impaired host defense
 Candida albicans: Monilial diarrhoea,
Candidal vulvovaginitis or vaginal thrush  Drug factor:
(an infection of the vagina's mucous Pregnancy
membranes) treat with nystain or
clotrimazole - All AMAs should be avoided in the pregnant
 Resistant Staphylococci: treat with
- many cephalosporins and erythromycin are
coxacillin or its congeners -
safe, while safety data on most others is not
Pseudomonas: Urinary tract infection,
available.
treat with carbenicillin, piperacillin or
gentamicin.
 Superinfections minimized by
 Genetic factors
 using specific (narrow-spectrum) AMA
(whenever possible) - Primaquine, sulfonamide fluoroquinolones
 avoid using (do not use) antimicrobials to likely to produce haemolysis in G-6-PD
treat self-limiting or untreatable (viral) deficient patient)
infection
 avoid prolong antimicrobial therapy.
 Drug factor:

- Spectrum of activity (Narrow/ broad

spectrum)

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-Type of activity travelers to endemic area may take
chloroquine/ mefloquine)
- Sensitivity of the organism (MIC)
• Prevention of infection in high risk situations
- Relative toxicity
• Prophylaxis of surgical site infection
- Pharmacokinetic profile
• Prophylaxis against specific organisms
- Route of administration
• Prevention of infection in high risk situations
- Cost
Prophylaxis of surgical site infection

*Organism-related considerations:
Failure of antimicrobial therapy
-A clinical diagnosis should first be made, and
• Improper selection of AMAS, dose, route or
the choice of the AMAS selected
duration of treatment.
-Clinical diagnosis itself directs choice of the
• Treatment begun too late
AMA
• Failure to take necessary adjuvant measures
-Choice to be based on bacteriological
examination (Bacteriological sensitivity • Poor host defense
testing)
• Trying to treat untreatable (viral) infections

• Presence of dormant or altered organisms

Combined use of antimicrobials which later give risk to a relapse

• To achieve synergism, Rifampin+ isoniazid

for tuberculosis
CLASSIFICATION
• To reduce severity or incidence of adverse
Base on
effects, Amphotericin B+ rifampin (rifampin
enhance the antifungal activity of - The phases of cell cycle (Bruce and
amphotericin B) colleagues 1966)
• To prevent resistance (Concomitant • Non-phase dependent
administration of rifampin and ciprofloxacin
prevents Staph. resistance ciprofloxacin) • Phase dependent
aureus

• To broaden the spectrum of antimicrobial - Mechanism of action/biochemical activity

action (cotrimoxazole:
Trimethoprim/sulfamethoxazole) • Cytotoxics

• Immunotherapeutic agents

Prophylactic use of antimicrobials • Targeted therapy

• Prophylaxis against specific organisms

(Cholera: tetracycline prophylaxis; Malaria: for

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• Steroids and Non-steroidal Hormones +METHODS

- Clinical evaluation

- Laboratory test

PRE-CHEMOTHERAPY ASSESSMENT

• CLINICAL EVALUATION

- History

• Detail history

• Systemic involvement

. Co-morbidities

• Performance status

+AIM

- Establish diagnosis

- Fitness of patient

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Chemotherapy II

 Laboratory test
- Diagnostic: Histology
- Extent
o Imaging; CXray, CT, MRI, PET,SPET
o Uss
o LFT
PRE-CEMOTHERAPY ASSESSMENT
 Baseline
o FBC
- PCV-30%
-WBC<2.5,2.5-3.9>4.0x10^9/L
-PLT<75,75-150x10^9/L
o U&Ecr
o Stool microscopy-Strogiliodes
Stercoralis
 Others, depend on the type of cancer e.g
tumuor markers.

COUNSELING

 Adequate counseling
- Disease explained in simple terms that
 Physical assessment
 The extent of primary and metastatic can be understood
disease via the general and thorough - Extent
systemic examination
- Plan of treatment
 Body surface area
- Side effect expected
- Fair idea of prognosis

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 Opportunity given to ask adequate ADMINISTRATION
questions and get accurate answers.  Choice of Agents
 A professional counselor/psychologist  -type of cancer
should be involved.  -the stage
 The aim of the therapy must clearly be  -age
stated to the patient and relative  -clinical state of patient
-curative  -co-morbidities
-paliative  -treatment in the past
 Modalities of treatment  -drug interactions

 INFORMED CONSENT Obtained  The ORDER is written and signed.

- Name, diagnosis, drug combination,
number of cycles and duration.

DOSE
MODALITIES
- Calculate the body surface area
 Modalities is selected based on the type
- Dose prescription
and stage of the cancer.
o Standard dose; anticipate mild side
 Neoadjuvant effect, minimal supportive care
 adjuvant o High dose; above standard,
 Multimodality anticipated side effect requires
-surgery supportive care; G-CSF, blood
-chemo-radiation transfusion
o Ablative dose; ablation of tumuor

OPTIMIZATION and stem cells, in conjunction with

stem cell transplantation
 -Anemia
o Adjusted dose; reduced dose in
 -Dehydration
renal impairment.
 -De-worming
 -Malnutrition
ROUTES OF ADMINISTRATION
 -Control of Infection o Oral
 -Dialysis-Uremia o Intravenous (Bolus, Infusion)
o Arterial infusion

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 o Extracorporeal limb perfusion
o Intracavitory
o Intrathecal
o Subcutaneous
o Intramuscular
o Topical

 Pre-chemotherapy medications
-IV Fluids (allopurinol, alkylanization of
urine) – Prevent risk of tumour lysis
syndrome
-Antiemetric: Ondansetron 0.15mg/kg
given 30 min before commencement.
-Antidotes; leucovorin andtidote for
antifolate-metothraxate. (Co-
administered, after administration.

 MODES/METHODS
COMBINATION CHEMOTHERAPY
o single agent continuous therapy
Superior to single drug chemotherapy
-little value in modern cancer
considerations:
management
o Drug should be active as a single agent
-low response rates
o Avoid drugs with similar toxicity
-complete remissions were infrequent
o To reduce toxicity
-kill small fraction of tumour cell
o Use drugs with different mech. of
-potentiates the development of drug
actions
resistance
o Use maximum therapeutic doses

CYCLICAL CEMOTHERAPY
 Monitoring
 Drug is given in cyclical fashion
-Premedication vital signs take, then
 To prevent drug resistance
regular monitoring
 This gives normal cells time to recover
-Mainly cardiovascular-Cardiotoxicity
from the drug’s side effects.
o Tachycardia

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 o Arrhythmias o Treatment; (easily prevented-good vein,
o S3 gallop ensure no leakage before chemo,
o Chest pain, tightness – acute, set fresh not pre-existing line,
coronary syndrome monitor line, start with vesicant.)
o Esp anthracyclins, trastuzumab, -Stop immediately
cyclophosphamide, paclitaxel -Antihistamine
-Nausea, vomiting -Hydrocortisone
-Breathing pattern -Analgesics
-Antidotes and emergency drugs -Care of ulcer when developed
 SAFETY  Systemic
-Chemotherapeutic agents are hazardous o Haemopoietic; Myelosuppression –
o Mutagenic treatment emergencies (Anemia,
o Teratogenic thrombocytopenia, treat infection,
o Carcinogenic treatment with CSF
o Skin irritation o Gastrointestinal; nausea, vomiting,
-Gloved, goggle and gowns when anorexia, constipation, diarrhea, 5-HT
administering. In good ventilation to prevent antagonist-ondaserton
inhalation of droplets when preparing. o Hyperglycemia – Biophosphonate,
-Care in handling patient urine and feces. corticosoid
o Urinary – hemorrhagic cystitis-mesna
MANAGEMENT OF SIDE EFFECTS o Neurologic – peripheral neuropathy
 Local o Cardiovascular – pulmonary fibrosis
o Flare reaction/thrombophlebitis – o Reproductive – infertility, menorrhagia
irritation along the tracts.
Triggering inflammation along the FOLLOW UP
tract and surrounding skin.  Complication
o Vesiculation – from extravasation into -History
surrounding subcutaneous tissue -Physical examination
leading to vesicles with -Laboratory investigation- repeat
subsequently ulcerates. Chemical baseline and histology, tumour
burns. marker
-Treat complication as they arise

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  Response -CMF
 Resistance -CAF/VAC-P
-TAXANE BASED eg
RESPONSE >paclitaxel and xeloda
WHO >paclitaxel, cyclophosphamide and
 Objective response – change in longest doxorubicine
diameter of the target lesion  Gastric

 Complete; disappearance of all known -ECF

disease, confirmed at _> 4weeks  Wilm’s
 Partial; _>50% decrease from baseline, -Methotrexate or dactinomycin,
confirmed at _> 4 weeks douxorubicin and vincristine

 Progressive; _>25% increase in one or

more lesions or appearance of new FUTURE TRENDS

lesions  Tumour vaccine – stimulate the body to

 Stable; no change produce CD4 cells which suppresses

tumour cells e.g sipuleucel-T, prostate

CHEMORESISTANCE G-vax still under investigations

 Reduction in the effectiveness or failure  Gene therapy

of response could be primary or

secondary
 Depend on grade of tumour, type of
drug and dose use
 Mechanisms
-overexpression of adenosine
triphosphate binding cassette
-Inactivation of apoptosis
-Inactivation of nuclear factor-kb
transcription factor
-Cancer stem cell MODALITIES OF TREATMENT
1. Local therapy:
COMMONLY USED ANTICANCER REGIMEN o Surgery
 Breast cancer o radiation therapy

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 2. Systemic treatment  Success depend on the difference in the
o chemotherapy sensitivity between the tumor and
o hormonal therapy normal tissue.
o monoclonal antibodies  It involves the administration of ionizing
o radioactive material radiation in the form of x-ray or
3. Supportive care gamma rays to the tumor site.
4. Non-conventional therapy  Method of delivery: External beam
(Teletherapy). Internal beam therapy
(Brachytherapy)
SURGERY  Radiation therapy is planned and
 surgery was the first modality used performed by a team of nurses,
successfully in the treatment of cancer. dosimetrists, physician and radiation
 It is the only curative therapy for some oncologist.
common solid tumors.  A course of radiation therapy is
 The most important determinant of a preceded by a simulation session in
successful surgical therapy are the which low- energy beam are used to
absence of distant metastases and no produce radiographic images that
local infiltration. indicate the exact beam location.
 Microscopic invasion of surrounding  Usually delivered in fractionated doses
 Normal tissue with necessitate multiple such as 180 to 300 cGY per day, five
frozen section. times a week for a total course of 5-8
 Resection or sampling of regional lymph weeks.
node is usually indicated.  Radiation therapy with curative intent is
 Surgery may be used for palliation in the main treatment in limited stage
patients for whom cure is not possible. Hodgkin’s disease, some NHL, limited
 Has significant role in cancer prevention. stage CA prostate, gynecologic tumors
 E.g familial polyposis coli. & CNS tumor.
 Also can be used in palliative &
RADIATION THERAPY emergency setting.
 Radiation therapy: is a local modality
used in the treatment of cancer. COMPLICATION OF RADIATION

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  There are two types of toxicities – acute o Nobel prize 1908
and long term toxicity. o Magic bullet concept
 Systemic symptoms such as fatigue,
Historical perspective
local skin reaction, GI toxicity,
 >Nitrogen mustards were a product of the
oropharyngeal mucositis, xerostomia secret war gas programs in both world
& myelosuppression wars
 >In WWII, an explosion at Bar Harbor
 Long-term sequelae: may occur many exposed seamen to mustard gas – they
months or years after radiation developed severe marrow and lymphoid
hypoplasia
therapy.  Led to the use of these agents to treat
 Radiation therapy is known to be Hodgkins and non-Hodgkins lypmhomas at Yale
in 1943
mutagenic, carcinogenic, and having  In the 1950’s, folic acid was shown to
increased risk of developing both accelerate the progression of childhood
leukemias; led to development of folic acid
secondary leukemia and solid tumor. antagonists
 In the 1960’s, combination chemotherapy for
childhood leukemias and Hodgkins lymphoma
NUCLEAR MEDICINE began to be used.
> Radionuclides
 For decades have been used
CHEMOTHERAPY
systematically to treat malignant
o Systemic chemotherapy is the main
disorders.
treatment available for disseminated
 They are administered by specialists in malignant diseases.
nuclear medicine or radiation oncologist. o Progress in chemotherapy resulted in cure
for several tumors.
 Radioactive iodine in the form of 131 is
o Chemotherapy usually require multiple
effective therapy for well differentiated cycles.
thyroid ca.
MODES OF CHEMOTHERAPY
 Strontium-89. Is used for the treatment of
Primary Chemotherapy – chemotherapy is use as
bony metastasis. It is alkaline earth element the sole anti-cancer treatment in a highly sensitive
in the same family as calcium. tumor types. Example; CHOP for non-Hogdkins
lymphoma

 Adjuvant chemotherapy – treatment is given

Paul Ehrlich 1854
after surgery to mop up microscopic residual
disease. Example; Adriamycin,
o Father of chemotherapy
cyclophosphamide for breast cancer.
o Salvarsan for treatment of syphilis

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 Neoadjuvant chemotherapy – treatment is given
before surgery to shrink tumor and increase
chance of successful resection. Example;
Adriamycin, ifosfamide for osteosarcoma.
 Concurrent chemotherapy – treatment is given
simultaneous to radiation to increase sensitivity
of cancer cells radiation. Example; Cisplatin, 5-
fluorouracil, XRT for head and neck tumors

CANCER CHEMOTHERAPY

>After completion of mitosis, the resulting daughter

cells have two options

1. They can either enter GI & repeat the cycle or

2. They can go into G0 and not participate in cell

cycle.

>Growth fraction – at any particular time some cells

CANCER CHEMOTHERAPY PRINCIPLE are going through the cell cycle whereas other
cells are resting.
1. The “Silver Bullet” isn’t out there.
>The ratio of proliferating cells to cells in G0, is
2. Conventional chemotherapy targets have been
the cell cycle, microtobules and DNA called the growth fraction.
3. Combination chemotherapy improves responses >Tissue with a large percentage of proliferating cells
over single agent, but dose intensity must be
& few cells in G0 has a high growth fraction
maintained.
4. It is better to treat micrometastatic disease >Conversely, a tissue composed of mostly of cell G0
5. Phase I trials define an MTD – a maximum
has a low growth fraction.
tolerated dose – this may not equate to the
maximum therapeutic.
MECHANISMS OF CHEMO THERAPY
6. For classical therapy to be effective, cell
proliferation is required. Indolent (slowly  Damage the DNA of the affected cancer cells. It
growing) cancers are typically resistant. If
is not always possible to be selective, but
therapy is ineffective, tumor indolence
determines survival. selectivity is the ultimate goal of any drug. e.g
7. Almost all who die with cancer have been cisplatin (platinol), daunrubicin (cerubidine)
treated with chemotherapy

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 doxorubicin (Adriamycin), and etoposide HEMATOLOGICAL CONSIDERATIONS FOR DOSE
(VePesid) SCHEDULING
 Inhibit the synthesis of new DNA – strands
 Lifespan
to stop the cell from replicating, because
>Platelet 7-10 days
the replication of the cell is what allows the
>RBC 120 days
tumor to grow. e.g methothrexate
>Neutrophils 6-12 hours
(Albitrexate) mercaptopurine (purinethol),
 Time from stem cell to mature neutrophil 7-
fluorouracil (adrucil) and hydroxyurea
10 days.
(hydrea)
 Stop the mitotic process of a cell – stopping DECIDING ON TREATMENT INTERVALS

mitosis stops cell division (replication of the

 As short as possible
cancer and may ultimately halt the
 Recovery of bone marrow
progression of the cancer. e.g Vinblastine
>supplies mature cells for 8-10 days
(velban), vincristine (oncovin), (taxol)
>onset 9-10th day

PLANNING DRUG DOSES AND SCHEDULES >lowest (nadir) 14-18th day

>recovery by day 21-28
o Doses
 Usual schedule is q21-28 days
- based on boy surface area
- differ between children and adults COMPLICATIONS OF CHEMOTHERAPY
- adjusted for people who are elderly, have
 Every chemotherapeutic will have some
poor nutritional status, have already taken
deleterious side effect on normal tissue.
or taking other medications, have already
 E.G; Myelosuppression, nausea & vomiting.
received or are currently receiving
Stomatitis, and alopecia are the most
radiation therapy, have low blood cell
frequently observed side effects.
counts, or have liver or kidney diseases
o Schedule (cycles)
- A cycle = one dose followed by several days
or weeks without treatment for normal
tissues to recover from the drug’s side
effects
- The number of cycles = based on the type
and stage of cancer, and side effects.

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  Antiestrogen
 Progestins Aromatase inhibitor
 Gonadotropin-releasing hormone agonist:
Somastostatin
 Analogues

ADRENOCORTICOSOIDS

 Are frequently used in combination

regimen for the treatment of lymphocytic
leukemia and lymphoma.
 Thy function by binding to glucocorticoid-
CRITERIA USED TO DESCRIBE RESPONSE ARE: specific receptors present in lymphoid cells
and initiate programmed cell death.
 Complete response (complete remission) is
 They most commonly used agent are
the disappearance of all detectable
prednisone, methylprednisone,
malignant disease.
dexamethasone.
 Partial response is decrease by more than
50% in the sum of the products of the ANTIADROGENS
perpendicular diameters of all measurable
 Flutamide: effectively blocks the binding of
lesions.
androgen to its receptor in the peripheral
 Stable disease: no increase in size of any
tissue. It is used in the treatment of
lesion nor the appearance of any lesions.
disseminated prostate ca
 Progressive disease: means an increase by
atleast 25% in the sum of the products of BIOLOGIC THERAPY

the perpendicular diameters of measurable  Immunotherapy

lesion or appearance of new lesions. >Cytokines

ENDOCRINE THERAPY >Cellular therapy

>Tumor Vaccine
 Many hormonal antitumor agents are
 Hematopoietic factors
functional agonist or antagonist of the
steroid hormone family. TARGETED THERAPIES

 Adrenocorticosoids: Antiandrogen  New technology and drugs that allow the

 Estrogen cancer treatment to “target” a certain

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 cancer cell by interfering with the natural this is taken into account when determining a
functions of tumor growth. chemotherapy schedule. The next dose of
chemotherapy should be given only after a
 How they work. They ‘target’ specific parts of a
person’s blood counts have increased to safe
cancer cell or its actions; hand in a glove
levels after the nadir period. This happens
analogy.
gradually and typically takes 3-4 weeks.
 What it means in cancer treatment; Potentially
fewer side effects

WHITE BLOOD CELLS

NADIR: A common side effect of chemotherapy
 WBC generally drop to their lowest count
 Nadir is a term that refers to the lowest point of about seven to 14 days after a chemotherapy
anything. treatment.
 In medical terms, nadir could mean the lowest  WBC’s, especially a specific type called
concentration of a drug in the body. With regard neutrophils, are a vital component of the
chemotherapy specifically, it describes the point immunes system as they keep invading
at which blood cell counts are at their lowest bacteria at bay. Because of this, you are at a
after a chemotherapy treatment. heightened risk of developing infections when
 It is commonly referred to as the “nadir” period counts are low.
or simply “nadir” among healthcare workers  A normal neutrophil count is 2,500 – 6,000.
and patients. Lower than that and the immune system is said
to be compromised- and the risk of infection
Why NADIR occurs
increases. If neutrophils are abnormal below
o While chemotherapy directly targets cancer 500, the condition is called neutropenia and
cells, it also affects other normal rapidly dividing infection can occur.
cells in the process, including those found in the
RED BLOOD CELLS
gut, lining of the mouth, hair, and bone marrow
where the blood cells are produced.  RBC generally live longer than WBC and
o During chemotherapy, bone marrow activity reach a nadir period several weeks after
may be decreased, including red blood cells, treatment. Their job is to carry oxygen
white blood cells and platelets. from the lungs to tissues throughout the
o With each chemotherapy treatment comes a body.
nadir period, so people who have more  RBCs xontain hemoglobin, an iron-rich
frequent treatment may experience lowered protein that transports oxygen and also
counts more than those treatments are spaced gives blood its red color. When red blood
further apart. cell counts are too low, the result is called
anemia.
TIMELINE AND RISKS
PLATELETS
 Each blood cell type reaches nadir at different
times. Low counts have varying effects as well.  Generally reach their Nadir period at about
 Because permanent damage to bone marrow the same time as WBC. Platelets serve an
can occur if chemotherapy is given too often,

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 important function by helping the blood to  Vitamin B-12 (cobalamin): Found in organ
clot, which prevents bleeding. meat, beef, tuna, trout, salmon, sardines,
 When the number of platelets in the body clams and eggs.
fall too low, the condition is called  Vitamin C: Found in citrus fruit, cantaloupe,
thrombocytopenia. It is marked by bruising, kiwi, papaya, strawberries,, sweet
nosebleeds, excessive bleeding from cuts potatoes, tomatoes, bell peppers, broccoli,
and fatigue. A reddish-purple skin rash that cauliflower and kale
looks like small dots is also a symptom of a  Copper: Found in shitake mushrooms,
low platelet count. spirulina, almonds, cashews, sesame seeds,
lobster, oyster, organ meats, swiss chard,
MANAGING LOWERED BLOOD CELL COUNTS
spinach, and kale.
 When blood counts become too low,  Vitamin E: Found in salmon, trout, shrimp,
WBCs, RBCs, and platelets can be increased goose, spinach, broccoli, turnip greens,
through drugs that boost cell production, squash, avocados, wheat, olive oil,
as well as through transfusions. Upping sunflower seeds, almonds, hazelnuts,
your consumption of certain healthy peanuts, brzail nuts, mango, and kiwi.
meats, fruits, and vegetables can also help
MANAGING LOWERED BLOOD CELL COUNTS
boost the body’s natural production of
blood cells. • Vitamin C: Found in citrus fruit,
 Protein sources like poultry and fish may cantaloupe, kiwi, papaya, strawberries,
promote the production of WBCs. Platelets sweet potatoes, tomatoes, bell peppers,
can be increased by eating foods rich in broccoli, cauliflower, and kale
vitamins B-9 and B-12. • Copper: Found in shitake mushrooms,
 The following vitamins and mineral help spirulina, almonds, cashews, sesame
increase they body’s production of RBCs. seeds, lobster, oyster, organ meats,
Consider adding supplements and/or Swiss chard, spinach, and kale.
eating foods that are rich in the following. • Vitamin E: Found in salmon, trout,
 Iron: Found in leafy green vegetables like shrimp, goose, spinach broccoli, turnip
kale and spinach, organ meats, lean red greens, squash, avocados, wheat(diko
meat, egg yolks, beans and legumes. nagets yakan ni maam), olive oil,
 Vitamin A (retinol): Found in cod liver oil, sunflower seeds, almonds, hazelnuts,
sweet potatoes, spinach, broccoli, black pine nuts, peanuts, brazil nuts, mango
eyed peas, carrots, squash, pumpkin, and kiwi
cantaloupe, mango, and apricots. • Precautions to Take During Nadir
 Vitamin B-6 (pyridoxine): Found in salmon, • It’s important to avoid infection or any
poultry, eggs, potatoes, sweet potatoes, activities that could induce bleeding, as
bananas, avocado, pistachios, peanuts, WBCs that fight infection and platelets
whole grains, and brown rice. that help with clotting are diminished.
 Vitamin b-9 (folate): Found in citrus fruit, Follow some simple tips including:
banana, papaya, beets, asparagus, Brussels Washing hands often
sprouts, avocado, walnuts, and flax seeds.

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 • Thoroughly washing and cooking food -Ensure adequate fluid intake being consumed
before consuming
& retained
• Avoiding contact with those who may
carry an infection, as well as pet waste • Low fiber and residue diet (Eg. Fresh
fruits. Vegetables, seeds and nuts)
• Avoiding getting scratches or cuts
should be recommended to patient as
• Help boost your immune system by:7
these foods can cause diarrhoea
• Getting enough sleep
-Fried food should be avoided as they
• Eating a healthy, balanced diet rich in produced gas
fruits and vegetables
• Patient should be taught to maintain a
• Avoiding caffeine and alcohol
record of episodes of diarrhoea & foods
• Drinking plenty of water that cause diaarhoea
-Rectal area of patient should be kept clean &
dry to maintain skin integrity.
When to Consult a Doctor
• For oral mucositis: patient should be
• Seek immediate medical attention if taught to do oral assessment and
you have bleeding that won’t stop or a characteristics of saliva
fever of 100 degrees or higher, as that & ability to swallow
could indicate the presence of a serious -Patient should be taught to do tooth brushing
infection. & flossing before and after each meal and bed
time.

Nursing management of patient undergoing -Patient should feed with soft non irritating
chemotherapy high protein and high calorie foods -Tobacco
and alcohol should be avoided
• Patient should be protected from
infections Body weight should be measured at least
twice a week. If patient is malnourished, give
-Wash hands regularly with antibacterial agent
parental nutrition
-Avoid crowd with, flu or infections
• For alopecia: patient should be
-Avoid raw fruits and vegetables addressed to use turban, cap or wig as
hair loss is very stressful to patient
• Help the patient to identify period of
more fatigue and activeness -Advice the patient that hair will grow after
-Patient should take rest prior to an activity - chemotherapy treatment
Maintain good nutritional status an hydration
status by taking balanced diet • Patient should be carefully assessed for
pulmonary side effects (pulmonary
• Antiemetics should be administered one edema) & cardiovascular effects
hr prior to chemotherapy (ventricular dysfunction & hear failure)
-Patient should take light meal of non- • Patient should be taught
irritating food before treatment about management of adverse

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 effects and interventions are planned and begins to proliferate abnormally,
so patient can self-manage the illness ignoring growth-regulating signals in the
and facilitate coping strategies with environment surrounding the cell
help with of support groups. • Hyperplasia
• Metaplasia
CONCLUSIONS • Dysplasia
• People with cancer are living longer • Anaplasia
• The focus is on quality of life in addition • Neoplasia- new growth; tumor; can
or quantity benign or malignant; uncontrolled cell
• People surviving cancer want to live growth that follows no physiologic
normal lives demand
• New treatment of various kinds are • Benign- not malignant; an abnormal
available and there is no need to suffer growth that is stable, treatable and
generally not life- threatening
• Cancer chemotherapy is an important
component in cancer management singly • Malignant- cancerous; cells that are
or in multi-modal therapy. They are toxic invasive and tend to metastasize,
to normal tissues hence require uncontrollable or resistant to therapy;
knowledge of drugs, early recognition, rapidly spreading
and management of side effect • Invasion- refers to the growth of the
• Adequate counseling is required for primary tumor into the surroundings host
compliance to treatment. tissues

• Metastasis- the dissemination or spread

of malignant cells to distant sites by direct
spread of tumor cells to body cavities or
through lymphatic and blood circulation

CANCER

• Derived from Greek word for crab,

karkinoma
• Malignant tumor
• Tumor- Also reffered to as neoplasm
new growth

TERMS

• Cancer- disease process that begins when

an abnormal cell is transformed by the
genetic mutation of the cellular DNA In
cancer the abnormal cell forms a clone

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Benign vs Malignant Tumors - Epithelial malignant tumors that
have not broken through BM or
Benign Malignant
Grow slowly Grow rapidly
Well-defined capsule Not encapsulated
Not invasive Invasive
Well differentiated Poorly differentiated
Low mitotic index High mitotic index
Do not metastasize Can spread distantly Stage of Cancer Spread Viruses and
Cancer
(metastasis)
• Implicated
• Stage 1: Confined to organ of origin
Mitotic index = rate of growth Hepatitis B and C viruses
• Stage 2: Locally invasive
Classification and Nomenclature
Epstein-Barr virus (EBV)
• Benign tumors- Named according Stage 3: Spread to lymph nodes –
to the tissues from which they
arise, and include the suffix “-oma” Kaposi’s sarcoma herpesvirus (KSHV)

• Lipoma • Stage 4: Spread to distant sited

• Hemangioma Human papillomavirus (HPV)
• Leiomyoma Chondroma
• CIS special case
• Malignant tumors- Named
• Human T cell leukemia-lymphoma
according to the tissues from which
virus (HTLV)
they arise
• Malignant epithelial tumors are
referred to as carcinomas

-Adenocarcinoma (from glandular

epithelium)

• Malignant CT tumors are referred

to as sarcomas
-Rhabdomyosarcomas (from
skeletal muscle)

• Cancers of lymphatic tissue are

lymphomas
• Cancers of blood-forming cells are
leukemias
• Carcinoma in situ (CIS) Bacterial Cause of Cancer
• Helicobacter pylori
- Chronic infections are assiociated with:

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• Peptic ulcer disease Stomach
carcinoma
• Mucosa-associated lymphoid
tissue lymphoma

Tumor Markers Inflammation and -Cellular multiplication

cancer -Tumor cell markers (biologic
markers) • Mitotic rate vs. cellular death
rate
Chronic inflammation is an
important are substances produced -Mechanical pressure
by cancer cells factor in
-Release of lytic enzymes
development of cancer or that are
found on plasma cell Cytokine -Decreased cell to cell adhesion
release from inflammatory
membranes, in the blood, CSF, or -Increased motility
urine cells.
• Intravasation Extravasation
hormones (Epi- in blood, adrenal
Free radicals medullary
tumor Mutation promotion
-invaded by surrounding stroma

-Enzymes

>Decreased response to DNA

damage Three-Step Theory of invasion
-Genes
• Tumor cell attachment
-Antigens (PSA- in
-Fibronectin and laminin
blood, prostate
Local Spread • Degradation or dissolution of the
cancer) matrix
-Enzymes
Antibodies
• Locomotion into the matrix
Invasion

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 -Invadopodia (pseudopodia) • HeLa cells were used by Jonas Salk to
test the first polio vaccine in the
HeLa cell
1950’s
• a cell type in an immortal cell line
used in research

• one of the oldest, most commonly

used human cell lines
• derived from cervical cancer derived
from cervical cancer cells taken from
Henriett Lacks
• Patient eventually died of her cancer
on
October 4,1951

• Cell line was found to be remarkably

durable
• Cells propagated by George Otto
Gey
• First human cell line to prove
successful in vitro, which was a
scientific
achievement for the benefit of
science

• Neither lacks nor her family gave

Gey permission (at that time was
neither required or sought)

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 Examples:

Invasion and mestastasis

TERMINOLOGY

Carcinoma - term used for malignant tumors

of epithelial in origin (bronchogenic
carcinoma, invasive ductal carcinoma,
endometrial carcinoma, adenocarcinoma,
squamous cell carcinoma, basal cell

a. APC, MEN1, p53, RB, and WT1 - affect DNA

transcription

b. BRCA1 and BRCA2 - play roles in DNA repair

C. RB, p16 and TP53 - critical for the operation

of the c cycle, suggesting that many tumor
suppressor genes "gatekeeper" genes

carcinoma)

Sarcoma-term used for malignant tumors of

mesenchymal/connective tissue in origin
(rhabdomyosarcoma, liposarcoma,
leiomyosarcoma, angiosarcoma)

Note: benign tumors usually end with the

suffix "om except for lymphoma,
hepatoblastoma, neuroblastoma, myeloma,
melanoma. These are already malignant

TUMOR SUPPRESSOR GENES

Hallmark characteristic of a mutated tumor

suppressor gene is loss of function through:

1. Loss of genetic material

2. Loss of information

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 DMCIR - melanoma

SOME EXAMPLES OF GENES IN CANCER

SUSCEPTIBILITY

ALDH2- related cancers

DAPC-colorectal cancer

□CCND1 - head and neck cancer

□ COMT-breast cancer

CYP1A1 - lung, oral, and breast cancers,

childhood leukemias

GSTM1

- bladder and breast cancers; lung cancers

HRAS-breast, ovarian, lung and colorectal

cancer ris

OLTA- myeloma

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L,A&B,A