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Oncology- Nursing VI
Dilum Weliwita
B.Sc. Nursing(U.K.)
The biology of cancer
This session....... Questions to
answer
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How do cancers Arise?
What is the differences between normal
and abnormal cell changes?
What are the biological processes
involved?
What are cancer ‘promoters’?
How do cancer advance and disrupt
body function
Oncology defined
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Branch of medicine that deals with
the study, detection, treatment
and management of cancer and
neoplasia
What is neoplasia?
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Neo- new
Plasia- growth
What is cancer?
Cancer
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Set of diseases.
Abnormal growth of cells.
Regulation of cell growth and maturity
is disturbed
Ability to invade adjacent tissue and
even distant organs.
Many different types of cancer
Cont....
i)
ii)
Same cancers can also behave
differently
Eventual death of the affected patient if
tumor has progressed beyond the stage
when it can be successfully removed
Cont.....
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Changes in cell and development are
governed by genetic control
Genetic alterations: a multistep process
Cancer Terminology
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Cancer - A group of diseases
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Anaplasia - Lack of differentiation
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Dysplasia - Abnormal size, shape
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Hyperplasia - Increase in number of
cells
Start from a cell......
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‘Where a cell arises, there must be a
previous cell, just as animals can only
arise from animals and plants from
plant.......’
Virchow, 1858
Cell structure
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Nucleus- information
Mitochondria- power
Cytosol- molecule and chemical soup
Golgi apparatus- processing and
packing
Lysosomes- digestion
Vesicles- transporters
Cytoskeleton- movement and structure
Different cells...... Diffrent
jobs
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Diverse range of cells
Size and structure depends on its job
Think about the structure of sperm,
bacteria, nerve cell, neutrophils
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But ..........
cells have similarities..... Such as
the storage of genetic instructions (
genes) in DNA molecules
DNA
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DNA is the cell’s blueprint
Chemical building blocks
Carrier of genetic information
Located in chromosomes
Each cell’s nucleus has 23 pairs
Duplicated to pass on genetic
information to daughter cells
Genes
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Segment of DNA
Determines the structure and job of a
protein for development, growth,
chemical function
Each gene tells a cell to make a
different protein
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Genes--------- ‘ on ‘------ RNA-------information to make new proteins
Protein maybe structural, hormone,
growth factors, inhibitors, regulators
Process of cell division
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Response to a signal
E.g. Hormonal signals in blood loss
growth factor (erythropoetin)
produced in the kidney circulates in the
bloodstream to tell bone marrow to
manufacture more blood cells
Cell Division
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Mitosis
A type of cell division that result in
two daughter cells each with same
number as chromosomes as the parent
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Meiosis
cell division that results in daughter
cells with half the chromosome number
of the parent e.g. Eggs and sperm
Hyperplasia
Dysplasia
Carcinoma in Situ
Tumor Development
Cell cycle check points
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G1:
is the cell big enough?
is the environment favourable?
is DNA damaged?
G2:
is all DNA replicated?
is the cell big enough?
Cellular behaviour
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All these events are responses to social
controls and signals from chemical or
other cells:
Cell division
Cell differentiation (specialisation)
Cell proliferation (rate of division )
Cell senescence (limits)
Cell survival
Programmed cell death
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i.e. To regulate cell development only
when it is needed
Cancer cells
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Cancer cells ignore the signals and
social controls
Characteristics:
Reproduce in defiance of the normal
constraints
Invade and colonize territories
normally reserve for other cells
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Can grow even as far as outstripping
their blood supply and destroying the
host
Difference between benign and
malignant?
Benign Tumor
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Characteristics typical of tissue of origin
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Slow rate of growth
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Slowly progressive; Not fatal if
untreated
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Encapsulated growth
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No tissue destruction
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Rare recurrence
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Poor prognosis only if unable to remove
Malignant Tumor
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Characteristics atypical of tissue of
origin
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Slow or rapid rate of growth
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Usually progressive; Fatal if untreated
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Growth by infiltration or metastasis
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Tissue destruction is common
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Recurrence is common
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Fatal prognosis if uncontrolled
Features of cancer cells
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Immortality:
- Do not have limits on cell cycle
(does not enter senescence)
Possible diminished requirements of
growth factor
Loss of ‘point of no return’ in cell cycle
- End of G1 related to the ‘ brake’
protein pRb – activated by cyclin and a
cyclin dependant kinase (cdk)
Cancer cells may lack enough pRb
Differences in cell structure
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Change in cell surface and membrane
Changes in glycoproteins
-changes of cell adhesion, contact
inhibition, loss of growth control, and
apoptosis
Changes in cell surface antigens
- Tumour antigens
Increased nutrients uptake
Differences in differentiation
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Cells have same DNA content
But.... Only section of it is expressed for
different structure and function
i.e. A distinct ‘personality’
The more differentiated a cell , the more
specialised
Cancer cells are less differentiated from
surrounding normal tissue....
The transition to Malignancy
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They may be.....
-Metaplastic ( mildly less differentiated)
-Dysplastic(deranged cell growth)
-Carcinoma insitu ( cancer in place with
no extension or spread)
-Invasive cancer
Carcinoma
Adenoma
Remember some cancers so
poorly differentiateddifficult to ascertain the
origin
The Causes of Cancer: Role of
DNA
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DNA mutations and cancer
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Oncogene = gene involved in the
transformation of
a normal cell into a cancer cell
Cancer promoters = compounds that accelerate
cell growth
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A mutated gene no longer contains the proper
code for producing its protein
A genetic disease......
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Two types of genetic
mutations
Oncogenes
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Mutation of the proliferation gene (
proto- oncogene)
This gene encourages cell division
DNA alteration (e.g. Due to exposure to
chemical carcinogen)
Result in hyperactive cell multiplication (
accelerated) without regard to the usual
cell cycle regulation or apoptosis
Tumour suppressor gene
mutation
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Mutation of a ‘ tumour suppressor gene’
E.g. An antiproliferation gene ( a TSG )
which controls cell multiplication
Mutation of this may result in no
restraints (brakes) on proliferation and
cell multiplication is out of control
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TSG mutations are often called
recessive mutations
Each cell has a pair of TSG’s on each
chromosome
Both need to be inactivated for a
cancer to develop
Important in genetic mapping, inherited
cancer
E.g. In a carrier – one gene is mutated
already , but the other needs to be lost
for a cancer to develop
Genetic Regulation
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Oncogenes/Proto-Oncogenes
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normal exons which when mutated
promote oncogenesis
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wt = proto-oncogene (no tumor promoting
effect)
mutant = oncogene
Tumor Suppressor Genes
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Genes which regulate cell proliferation and
prevent cell from dividing ‘out of control’
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wt = ‘prevent’ cell from becoming a tumor
mutant = unable to prevent tumor-genesis
Gatekeeper Genes(Vogelstein
& Kinzler)
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Genes that produce proteins to directly
regulate tumour growth
Inhibit mitosis
Promote apoptosis
E.g. APC, p53
Caretaker Genes
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Genes that maintain the integrity of the
genome
Inactivation leads to genetic instability
and directly promotes tumour growth
by causing increased mutation
E.g. BRCA1 with heredity breast and
ovarian cancers
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-p53 can be both a gatekeeper
and a caretaker and is
becoming increasingly
important in treatment
development
Initiators and Promotors
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Initiator agents
-Produce a permanent change such as
gene mutation in the cells they are in
contact with
-May be able to be repaired by the cell
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Promoters
- Produce transient changes to cell only
causing cancer when repeatedly in
contact
Work over a long period of time
E.g. Diet, Smoking
Metastatic cancer
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Infiltration of cancer into surrounding
tissues- lymph/blood vessels
Dispersal of cancer cells to sites distant
from the primary origin
Affected by enzymatic
activity/pressure/loss of contact
inhibition/ cell proliferation/resistance to
control mechanisms
Metastasis
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Process by which tumor cells are spread to distant
parts of body to distant parts of body
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Occurs several different ways:
 Direst spread of cells by diffusion
 Circulation by way of blood and lymph
 Accidental transplant during procedures
Invasion and Metastasis
1Cancer
1Cancer
cells
cells
invade
invade
surroundin
surroundi
gng
tissues
tissues
and
andblood
blood
vessels
vessels
Finally to summarise
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One cell to start the process
Genetic changes and mutations
Chemical changes to the cell
Chain of event
Affected by promoters
No regard for rules or regulations
Important developments for
understanding the processes
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Any Questions
Diagnosis
Aims & Objectives the session
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To understand how the cancer is
diagnosed
To have an awareness of the tests
performed to determine an accurate
diagnosis
To understand how cancersare stage
Early Cancer May Not Have
Any Symptoms
How do you diagnose cancer?
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Patient explanation
Physical examination
Pathology
Radiology
Staging
Histopathology
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Blood test
Bone marrow Aspiration
Urine test
Cervical smear
Cervical Cancer Screening
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Surgical procedure
Biopsy
FNAC
EUA
........ Scopies (bronch, gastro)
Lumber puncture
Radiology
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X - Ray
Mammography
Computerised Tomography (CT)
Magnetic Resonance Imaging (MRI)
Ultra sound scan (USS)
Nuclear medicine
Isotope scanning
Positron Emission Tomography (PET )
Biopsy
MRI: metastatic
adenocarcinoma
Staging
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Staging is a way of describing a cancer,
such as the size of the tumor and where it
has spread
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Staging is the most important tool doctors
have to determine a patient’s prognosis
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The type of treatment a person receives
depends on the stage of the cancer
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Clinical diagnostic staging
Bone and liver scan
Ultrasonography
Computed tomography
MRI
Surgical StagingDescribe extent of the disease after biopsy
or surgical exploration
Grading and Staging of Tumors
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Grading: based on the degree of
malignancy, how alike the cells are to the
parent tissue or “differentiated”
Grade 1 – most differentiated
Grade 4 least differentiated, most
malignant
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Staging: general extent of cancer and
spread of disease rather than cell
appearance
Stage 1 – No invasion of other tissues,
localized
Stage IV – Metastasized to distant parts
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Staging consists of three main
classifications
T= PRIMARY TUMOUR
N=LYMPH NODE SPREAD
M=DISTANT METASTASES
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T- tumor
N- Node
M- Metastasis
TNM
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These are then subdivided:
T- related to tumour size and depth
N-related to number and mobility of
nodes ( can they be removed)
M- related to number of distance of
metastases
TNM
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Each subdivision is graded into four
Grade 1- well differentiated
Grade 4- poorly differentiated
TNM have differing levels of importance
for different cancers
T=Primary Tumor
Size
N=lymph node
involvement
M = distant
metastases
T0- no evidence of
metastasis
Tis – tumor is in
epithelial tumor is in
epithelial
N0- indicates no
abnormal lymph nodes
detected
M0 = no evidence
metastasis
T1 T1 –minimal size
and extension
T2, T3, T4–
progressively larger
and extensive larger
and extensive
N1– minimal
involvement
N2,N3,N4
progressively more
involvement more
involvement
M1 – distant metastasis
present (specify site/s)
Different staging
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Some cancers have their own staging
system,
Dukes carcinoma (Cuthbert Dukes
1930)
Dukes A- confirmed to bowel wall
Dukes B- extends through bowel wall
and may involve near organs
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Dukes C – SPREADTO LYMPH NODES
Dukes D - distant spread eg: liver
A diagnosis of cancer
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The emotional impact of cancer
will depend upon the
experiences of communication
leading up to a diagnosis of
cancer ( Wells 1999)
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Cancer Screening and
Rapid Access,
Prevention
Screening
Screening
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“ Is a public health service in which
members of a defined population, who
do not necessarily perceive they are at
risk of, or are already affected by a
disease or its complications, are asked
questions or offered a test , to identify
those individuals who are more likely to
be helped than harmed by further tests
or treatment to reduce the risk of a
disease or itscomplications “ DH 2003
Aim of Screening
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To Detect cancer
-at an early stage
-Before symptom start
-when it is easier to treat
- when it is more likely to be curable
-reduction in morbidity and mortality
Limitations
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Ethical differences – who can access
Risk are involved
People need to have realistic
expectation of what screening can
deliver
Low risk NOT no risk
Type of screening available
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Self screening
- breast and testicular cancer
Formal screening programme
- Cervical screening , mammography
Recent evaluated – national bowel
screening
- colorectal – FOB TEST
Breast Cancer Screening
Colon Cancer Screening
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Under consideration- ovarian- trans vaginal USS
- cancer antigen testing
Lung
- chest X-ray and sputum sampling
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Factors influencing
uptake
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Patient: high socio economic status,
sympathetic to screening,
Health beliefs, anxiety
Belief in effectiveness of screening
Way of presenting the test
Accessible setting
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Adverse effect of
screening
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Psychological- anxiety
Difficulties in communicating risk
information in an understanding way
False negative/ false positive results
Over treatment
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Rapid access
Rapid access
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Faxed referrals
Dedicated rapid access clinics
Pre booking
Direct bookings
Nurse led clinic
work of the cancer services
collaborative
Problems with rapid access
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Increased expectations
Inappropriate referrals- non cancer pt
being seen
Long wait for non- urgent referrals
Detections
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Patient should be advice DO NOT
IGNORE
Detection
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Cough over 3 wks or cough with blood
Hoarseness of voice for over 3 months
Lump that doesn't go away
A sore that won’t heal
Abnormal bleeding
Unresolved investigations
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Change in bowel habits or bladder
habits
Unexpected weight loss
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Prevention
Primary prevention
 Secondary prevention
 Tertiary prevention
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Primary prevention
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Modification of risk factors in the form
of health promotion campaigns about
---Diet
---Smoking
---Risky behaviours
Secondary prevention
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Intervention aimed at detecting
illness at asymptomatic stage
so its progression can be halted
or retarded
Tertiary prevention
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Rehabilitations of patients, or
treatment interventions once
an illness has manifested
itself
Cancer Prevention Advice to
the people
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There are many things that affect your
risk of getting cancer.
Some of those things are within your
power to control such as what you
consume, your activity level and other
life style behaviors.
1.
2.
Don’t smoke.
4
---smoking is one of the most
preventable causes of death in
our nation
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2. Keep a healthy weight.
-----Obesity has been determined to be
a risk factor in contracting colon,
breast, endometrial, kidney and
esophageal cancers.(Whitney, 2008)
3. Exercise for 45 minutes a day.
---------People with a vigorous lifestyle
have been shown to have a reduced
risk of colon cancer (Whitney, 2008)
4. Eat less red meat and more
vegetables, fruits and whole grains.
----Saturated and trans-fat have been
connected to a higher risk of
cancer while fruits, vegetables and
whole grains have a protective effect.
5.
Limit alcohol consumption to no more
than one drink per day for women, or
two for men.
------- Alcohol use has been linked to
increased risk mouth, throat, voice box,
esophagus, liver, breast, colon and
rectum and the risk increases with the
amount of alcohol consumed.
6. Protect your skin from sun exposure.
The sun's UV rays cause the vast majority of skin
cancers includi.ng melanoma,
---------which can be life-threatening. Sun screen
alone is not a good enough
preventative measure. One needs to wear
protective clothing or seek
shade as well.
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7. Practice safe sex.
----Both HPV, the most common STD,
and Hepatitis B can cause cancer.
Treatment methods
to cancer
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There are many factors that go into
deciding which treatment is the best
option. Factors include the type of
cancer, location, whether or not the
cancer has spread and the patient’s
general health as well as other things.
(Denton, 2010)
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There are several types of treatments
that can help to reduce and eliminate
cancer cells: chemo therapy, radiation
therapy, biologic therapy, surgery and
bone marrow transplant.
There are also some natural types of
treatments such as herbs and vitamins
to help boost the immune system.
Radiotherapy
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Radiation damages the DNA of cells
with high energy x-ray which kills them
or at least slows their reproduction.
Radiation also damages regular cells
but because they grow more slowly
than the cancer cells, they can more
easily repair themselves. (Abramson
Cancer Center at the University of
Pennsylvania, 2010)
Chemotherapy
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The use of chemical agents to stop
cancer cells from growing. (Abramson
Cancer Center at the University of
Pennsylvania, 2010)
Biologic Therapy
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This therapy may encourage your body to
produce more of its natural defenses, or the
therapy may be a man-made version of a
naturally occurring substance itself.
There are also therapies that use cells which
have been removed from the patient's body
and altered in a laboratory and then returned
back into the patient’s body. (Abramson
Cancer Center at the University of
Pennsylvania, 2010)
Surgery bone marrow
transplant.