Cancer Chapter 16

A group of 200 diseases (uncontrolled and controlled)

Tumors can be classified as benign or malignant.
Ability of malignant tumor cells to invade and metastasize is the major difference
between benign and malignant neoplasms.
Appearance of cells and degree of differentiation are evaluated to determine how
closely cells resemble tissue of origin.
Poorly differentiated tumors have a worse prognosis than those closer in
appearance to normal cells.
Cancer is higher in men than women
o Prostate 28 percent and Lung cancer 14% in men
o Breast cancer 29% and Lung cancer 14% in women
Men more than women die from cancer each year
o Interesting fact is Lung cancer is likely to develop more in women than men
Nonsmoking women than men are at risk for developing cancer

Nursing Care
Assist the client (Patient) to decrease their risk for cancer (and yes this means
that you have to educate them about risk factors the benefit of good nutrition etc)
Help the patient comply with cancer management and regimen (Please dont think its
ok to drag them to chemo when they refuse)
Support the patient and their families (Yes youre not only a Nurse but youre a dam
shrink too minus the money)
OK PAY ATTENTION GUYS!!! In order to assist these patients and their
families you have to
1. Be knowledgeable about the type of cancer, the treatment and the
management option that is available to the patient.
2. Be knowledgeable of the side effects of the therapy that the patient
will receive.
3. And Last but not least Cancer patient NEED SUPPORTIVE THERAPY
& DONT FORGET THE FAMILIES

Please remember
C hange in bowel or bladder habits
A sore that does not heal
Unusual bleeding or discharge from any body orifice
T hickening or a lump in the breast or elsewhere
I ndigestion or difficulty in swallowing
Obvious change in a wart or mole
Nagging cough or hoarseness

OK PAY ATTENTION BECAUSE SHIT WILL GET CRAZY !!!!!!

CANCER THE BREAKDOWN
Stem Cell are undifferentiated Cells now these cell proliferate only by cell
degeneration, death or by an increase in WBCs. (this to maintain Equilibrium)
These newly differentiated cell entire the cell cycle and go through cell division
After the cell cycle proliferation of the cell occurs
o Now you dont want the cancer cells to proliferate too much so the body has
a mechanism for stopping that
I.
Contact InhibitionNormal cell respect boundaries & territory of the
other cells close by. Loss of contact inhibition means your ass has
cancer and that shit is on the move !!!!!! sorry
Cells with rapid proliferation--- Bone Marrow, hair Follicles, Epithelial of the GI
tract.
Slow Cell Proliferation --- Myocardium & Cartilage
Permanent Cells--- Cardiac
Cancer cells proliferate at the same time as normal cells as the tissue from which
they arise (dont get confused all this means is that it enters the cell cycle the
same time as any normal cell)
o Remember up top I mentioned Contact Inhibition, well cancer cells has no
dam respect for boundaries, that means you can say bye bye (Nsync) to
dynamic equilibrium.
OK PAY ATTENTION TO THE LINGO FROM NOW SHIT JUST GOT REAL
Cancer affects Proto-oncogenes (normal cell with all the genetic codes). Cancer
promotes growth of these cells and that the thing keeps growing.
Normal cells have what is known as the genetic lock which keeps the cell in the
mature function state.
o When this genetic lock gets affected by carcinogens, oncogenic virus, or
genetic alterations then mutation occurs
INTERESTING FACT (TUMOR 1CM (0.4 INCH IS PALPABLE & HAS 1
BILLION CELLS)

Some cancer cells produce protein on the cell membrane similar to that of the
embryonic & fetal period of life (Remember nursing 290??)
o Carcinoembryonic antigenCEA (Breast and GI cancer) (normal VALUES
<5MG/ML) (this test is very important because it tells you is treatment is

successful !!!! if treatment unsuccessful this level will be high after

treatment
Alpha Fetoprotein---AFP (Primarily in liver cancer) (normal VALUE
<40NG/ML)

Tumor suppressor genes BCRA 1 & BCRA 2 these prevent cancer cells from going
through the cell cycle which means no daughter cells will be created.
o These suppressor genes can be suppressed by carcinogen or by protein that
is secreted by some cancer cells..
o APC gene increases the risk for FAP (colorectal cancer)
NOW REMEMBER THE STAGES OF CANCER IMPORTANT FOR USE LATER !!!!
1. Initiantionthis ivolve the genetic mutation of the genetic structure
a. Remember before this is caused by Viral infection (HPV, HIV, HEP B
etc.)
b. Carcinogens--such as, well you know what they are. However please
remember this DRUG for future chapters (Cyclophasphate
(Cytoxan)this is particulary dangerous because has the possibility to
cause myelogenous leukemia
c. Inheritedhis is from generation to generation and and accounts for
5 percent of all cancers.
d. Lets not forget the good old radiation
2. PromotionTHIS STAGE IS REVIRSABLE. I mean reducing agents such as
fat, obesity, cigarette smoking and for all you alcoholics it does contribute
to alcohol.
3. ProgressionSimply means your doomed, increased growth rate of the
tumor, increase metastasis, invasiveness and spread to the distant site
SIDE NOTELATENT PERIOD INCLUDES THE INITIATION AND THE PROMOTION
PHASE !!!!

Dont worry because the variation depends on the mitotic rate (in short it
depends on the cell division so it you were to introduce say a CELL CYCLE
SPECIFIC DRUG you could control that rate in turn slow down the growth of
cancer.)

Cancer survival is based entirely on that fact that they receive blood supply this is
refered to as TUMOR ANGIOGENESISthis means that blood vessels are formed
by the tumor survival
Hematogenous MetastasisPrimary tumor is penetrating the blood vessels and
moved around.
a. Some tumors do die during this movement VIA turbulence Blood Flow
b. Others are protected via platelets and fibrin deposits.

IMMUNE SYSTEM VS CANCER

Immunological surveillanceEach cell surface antigen is checked; the abnormal cells
are prevented from turning into detectable tumors.
If a tumor is detected then the cytotoxic T cells, natural killer cells, macrophages
& B cells are sent to the rescue to eliminate them.
1. Cytotoxic T CellsKills the tumor by the production of cytokines
(Stimulates NK cells & T cells)
2. Natural Killer CellsThey directly lyse the tumor cell spontaneously without
prior sensitization (remember above we talked about Immunological
surveillance)
o Alpha- Interferon arguments the killing ability of the NK cells
3. Monocyte & MacrophagesThese can be activated by Y-interferons (TCells) no this cause a non-specific lytic agent to secrete cytokines including
Interleukin and Tumor necrosis factor
4. B- Cells---they produce specific antibodies that binds to the tumor cell
these are detectable in the patients serum or saliva
The how!!! LOL I mean how tumor cell evade being slaughtered by the Immune system
A blocking antibody bind to the tumor associated antigen on the tumor, this
prevents the cytotoxic T-cell from recognizing the tumor as foreign and destroying
them.
Examples of oncofetal antigens
CA 15-3, CA 27-29, HER-2 (breast
CA-125 (ovarian carcinoma)
cancer)
CA-19-9 (pancreatic &
kRAS (colon cancer
gallbladder cancer)
oncogenes)
PSA (prostate cancer)

EGFR (lung cancer

 Type of Cancer
CarcinomaEmbryonal ectoderm (skin Glands)& endoderm (Mucous membrane lining
and respiratory tract GI. GU
SarcomaEmbryonic mesoderm (connective tissue, bone & fat )
LymphomasLymphomas and leukemia originate from the hematopoietic system
(blood System)
Clinical Staging
Stage 0Cancer in Remission
Stage 1Tumor limited to the tissue of origin/localized tumor
Stage 2Limited local spread
Stage 3Extensive local and regional spread
Stage 4Metastasis (movement)
Clinical Grading Four Grade
Grade I
o Cells differ slightly from normal cells and are well differentiated.
Grade II
o Cells are more abnormal and moderately differentiated.
Grade III
o Cells are very abnormal and poorly differentiated.
Grade IV
o Cells are immature and primitive and undifferentiated.
o Cell of origin is difficult to determine.

TNM ( Primary tumor, Reginal lymph node, Distant metastasis)

Primary Tumor
o T0No evidence of primary tumor
o Tistumor in SITU
o T1-4Ascending degree of increase in tumor size
o TxTumor cannot be measured or found
Reginal Lymph nodes
o N0No evidence of disease in the lymph nodes
o N-1-4 Ascending degree of nodal involvement
o NxReginal lymph nodes unable to be assessed clinically
Distant Metastasis
o M0--No evidence of distant metastasis
o M1-4--Ascending degree of metastasis, involvement, including distant nodes
o Mx--Cannot be determined
PATHOLOGICAL EVALUATION OF THE TISSUE IS THE MOST DEFINITIVE
MEANS OF DX FOR MALIGNANCY!!!!! (biopsy)
So how do we treat Cancer
o The goal of treatment is to

a. Cureto get rid of the thing of course

b. ControlIf the cancer cannot be eradicated then at least try to control the
thing
c. PalliationThis is in an attempt to maintain the quality of life If controlling
is not an option.
SurgicalThe oldest form of treatment in an attempt to cure. This is effective if
the tumor is relatively small or localized.
Debulking/Cytoreductive procedurethis may be used if the tumor cannot
be completely removed
ChemotherapyThe use of chemical in the aim of curing the cancer/ Chemo Drrugs
include
Cell phase specificthis has an effect on the cell cycle during specific
phases of interphase eg Cell replication & proliferation.
Cell phase non-specificThis has an effect on the cell during all the phases
of interphase
CHEMO DRUGS
Alkylating Agents
Cell Cycle PhaseNonspecific
Agents

Damage DNA by causing breaks

in the double-stranded helix. If repair
does not occur, cells will die
immediately (cytocidal) or when they
attempt to divide (cytostatic).

Nitrosoureas
Cell Cycle PhaseNonspecific Agents
Like alkylating agents, break DNA helix,
interfering with DNA replication.
carmustine (BiCNU, Gliadel), lomustine
(CeeNU), streptozocin (Zanosar) Cross
blood-brain barrier.
Platinum Drugs
Cell Cycle PhaseNonspecific Agents
Bind to DNA and RNA, miscoding
information and/or inhibiting DNA
carboplatin (Paraplatin), cisplatin
(Platinol-AQ), oxaliplatin (Eloxatin)
replication, and cells die.
Antimetabolites
Cell Cycle PhaseSpecific Agents

bendamustine (Treanda), busulfan

(Myleran), chlorambucil (Leukeran),
cyclophosphamide (Cytoxan, Neosar),
dacarbazine (DTIC-Dome), ifosfamide
(Ifex), mechlorethamine (Mustargen),
melphalan (Alkeran), temozolomide
(Temodar), thiotepa (Thioplex)

carmustine (BiCNU, Gliadel), lomustine

(CeeNU), streptozocin (Zanosar)

carboplatin (Paraplatin), cisplatin

(Platinol-AQ), oxaliplatin (Eloxatin)

cladribine (Leustatin), clofarabine

(Clolar), fludarabine (Fludara),
mercaptopurine (Purinethol), nelarabine
(Arranon), pentostatin (Nipent),
thioguanine

Mimic naturally occurring substances,

thus interfering with enzyme function
or DNA synthesis. Primarily act during
S phase. Purine and pyrimidine are
building blocks of nucleic acids needed
for DNA and RNA synthesis.
Interfere with purine metabolism.
Interfere with pyrimidine metabolism.
Interfere with folic acid metabolism.
Interfere with DNA synthesis

Antitumor Antibiotics
Cell Cycle PhaseNonspecific Agents
Bind directly to DNA, thus inhibiting
the synthesis of DNA and interfering
with transcription of RNA.

Mitotic Inhibitors
Cell Cycle PhaseSpecific Agents
Taxanes.
Antimicrotubule agents that interfere
with mitosis. Act during the late G2
phase and mitosis to stabilize
microtubules, thus inhibiting cell
division.
Vinca Alkaloids
Act in M phase to inhibit mitosis.
Others
Microtubular inhibitors.
Topoisomerase Inhibitors
Cell Cycle PhaseSpecific Agents
Inhibit topoisomerases (normal
enzymes) that function to make
reversible etoposide breaks and repairs
in DNA that allow for flexibility of
DNA in replication

capecitabine (Xeloda); cytarabine (araC [Cytosar-U, DepoCyt]), floxuridine

(FUDR), 5-fluorouracil (5-FU [Adrucil]),
gemcitabine (Gemzar)
methotrexate (Rheumatrex, Trexall),
pemetrexed (Alimta) hydroxyurea
(Hydrea, Droxia)

bleomycin (Blenoxane), dactinomycin

(Cosmegen), daunorubicin (Cerubidine,
DaunoXome), doxorubicin (Adriamycin,
Rubex, Doxil), epirubicin (Ellence),
idarubicin (Idamycin), mitomycin
(Mutamycin), mitoxantrone
(Novantrone), plicamycin (Mithracin),
valrubicin (Valstar)

albumin-bound paclitaxel (Abraxane),

docetaxel (Taxotere), paclitaxel (Taxol)
vinblastine (Velban), vincristine
(Oncovin), vinorelbine (Navelbine)

estramustine (Emcyt), ixabepilone

(Ixempra), eribulin (Halaven)

etoposide (VePesid), irinotecan

(Camptosar), teniposide (Vumon),
topotecan (Hycamtin)