Transcript Cancer: - health

What is cancer?
Cancer is not just one disease
More than 200 different types of cancer have been identified
CANCER
Defining cancer
Cancer is an accumulation of abnormal cells that multiply through uncontrolled
cell division and spread to other parts of the body by invasion and/or distant
metastasis via the blood and lymphatic system
Normal cells
Abnormal cells
Tumour growth
Metastasis
Uncontrolled
cell division
Invasion into
surrounding tissues
Spread via blood or
lymphatic system
Incidence of cancer across the globe (2008, estimate)1
Estimated number of new cancer cases
(% of total)
Africa (6%)
Asia (48%)
Europe (25%)
Latin America and Caribbean (7%)
Northern (13%)
Oceania (1%)
1. Ferlay J, Shin HR, Bray F, Forman D, Mathers C and Parkin DM. GLOBOCAN 2008 v2.0, Cancer
Incidence and Mortality Worldwide: IARC Cancer Base No.10 [Internet]. Lyon, France: International Agency
for Research on Cancer; 2010. Available from: http://globocan.iarc.fr, accessed on 06/06/2013.
Changing prevalence of cancer
Global cancer incidence and
mortality rates continue to rise1
2030
25 M
75 M
people living
with
cancer*2
predicted to
be living
with cancer2
2008
21.3 M
GROWING AND
AGEING POPULATION
13.1 M
12.7 M
7.6 M
CASES
DEATHS
ADOPTION OF
UNHEALTHY
LIFESTYLES
IMPROVEMENT IN
DIAGNOSIS/SCREENING
2002
*Diagnosed in last 5 years
2030
1. Ferlay J, Shin HR, Bray F, Forman D, Mathers C and Parkin DM. GLOBOCAN 2008 v2.0, Cancer
Incidence and Mortality Worldwide: IARC Cancer Base No.10 [Internet]. Lyon, France: International Agency
for Research on Cancer; 2010. Available from: http://globocan.iarc.fr, accessed on 14/01/2013.
2. The International Agency for Research on Cancer. World Cancer Report 2008. Available from:
http://www.iarc.fr/en/publications/pdfs-online/wcr/, accessed on 06/06/2013.
Common cancers in men and women worldwide1
Men (%)
Women (%)
Lung (16.5)
Breast (22.9)
Prostate (13.6)
Colorectum (10.0)
8.5
16.5
3
13.6
Bladder (4.4)
4.9
7.9
10
29.7
Liver (7.9)
Oesophagus (4.9)
9.7
3
4.4
Non-Hodgkin lymphoma (3.0)
Leukaemia (3.0)
Other and unspecified (27.0)
Colorectum (9.4)
Stomach (5.8)
Stomach (9.7)
27
Lung (8.5)
2.7
22.9
9.4
5.8
3.7
4.8
8.8
3.7
Liver (3.7)
Cervix uteri (8.8)
Corpus uteri (4.8)
Ovary (3.7)
Thyroid (2.7)
Other and unspecified (29.7)
1. Ferlay J, Shin HR, Bray F, Forman D, Mathers C and Parkin DM. GLOBOCAN 2008 v2.0, Cancer
Incidence and Mortality Worldwide: IARC Cancer Base No.10 [Internet]. Lyon, France: International
Agency for Research on Cancer; 2010. Available from: http://globocan.iarc.fr, accessed on 06/06/2013.
Global cancer mortality
Lung, stomach, liver,
colorectal and female
breast cancers
cause 50% of all
cancer deaths1
25
Mortality (% of all cancer types)
Approximately 7.56
million people died from
cancer in 2008,1
accounting for 13% of all
deaths (from any cause)2
Lung
20
Stomach
15
Liver
10
Colorectal
5
0
Both
sexes
Men
Women
Female
breast
1. Ferlay J, Shin HR, Bray F, Forman D, Mathers C and Parkin DM. GLOBOCAN 2008 v2.0, Cancer Incidence and
Mortality Worldwide: IARC Cancer Base No.10 [Internet]. Lyon, France: International Agency for Research on
Cancer; 2010. Available from: http://globocan.iarc.fr, accessed on 06/06/2013.
2. American Cancer Society. Global Cancer Facts and Figures 2nd Edition. Atlanta: American Cancer Society; 2011.
Common terms
Localised
Invasive
Metastatic
the cancer is still confined
to the site of origin and has
not yet invaded the
surrounding tissues or
spread to other sites
the cancer has spread
from the site of origin into
the surrounding tissues
the cancer has spread to
distant sites in the body to
form new tumours
Grade
Stage
how abnormal cancer cells appear in comparison
to normal cells and how aggressive the cancer is
Low grade – nearly normal in appearance;
slow rate of growth and metastasis
High grade – very abnormal-looking cells;
high rate of growth and metastasis
classification of the cancer,
important for treatment
decisions, based on the
size, presence or absence
of metastasis and involvement of lymph nodes
Cancer categories
Carcinoma
Sarcoma
Leukaemia
cancer of the skin or
tissues that line or
cover the internal
organs
cancer of bone,
cartilage, muscle, fat,
blood vessels, and
connective tissues
cancer of the bone
marrow affecting the
white blood cells
Lymphoma
cancer arising in the
lymph glands
Central nervous
system cancers
cancer of the brain or
spinal cord
Making sense of cancer names
Artwork originally created for the National Cancer Institute.
Reprinted with permission of the artist, Jeanne Kelly. Copyright 2013.
Risk factor definitions
013
RISK FACTOR
Intrinsic
risk factor
Extrinsic
risk factor
…is related to an
individual’s own actions
…is an integral part of
and environment
the individual and Something that increases
(tobacco, pollution,
the chances of getting
cannot be changed
diet, etc.)
a disease
(genetics, age, etc.)
Risk factors are multiple
and differ according to the cancer type
Smoking
tobacco
Radiation
Chemicals
RISK
FACTORS
Hereditary
Viruses
Age
HPV
EBV
HBV
General
health
Hormones
Diet
Obesity
Sun
exposure
Bacteria
H.pylori
Absolute risk vs. Relative risk
Absolute risk
Relative risk
The risk of an
individual
developing
cancer during
their entire
lifetime
The risk of a
group of people
developing
cancer in
comparison to
another group
Benefits of assessing risk
!
Allows the individual at risk to undertake prevention
strategies (e.g. stop smoking, avoid radiation)
!
Alerts physicians to those individuals at risk of
developing cancer
!
Enables screening procedures to detect cancer at
an early stage
!
Early detection enables physicians to initiate
treatment, whist the tumour is still in the initial stages
Emergence of a cancer cell
Genetic mutations, i.e. changes to the
normal base sequence of DNA, contribute to
the emergence of a cancer cell
Cancers originate
from a single cell1,2
A series of mutations accumulate in successive
generations of the cell in a process known as
clonal evolution
Malignant cell
First
mutation
Second
mutation
Third
mutation
Fourth or
later mutation
Eventually, a cell
accumulates enough
mutations to become
cancerous
1. Nowell, PC. The clonal evolution of tumor cell populations. Science (1976) 194:23-28.
2. Cavenee, WK & White, RL. The genetic basis of cancer. Scientific American (1995) 272:72-79.
The hallmarks of cancer
In order for cancerous cells to develop and form a tumour, mutations
and other alterations that allow the cell to acquire a succession of the
following biological capabilities must occur:1,2
Sustaining proliferative signalling
Resisting cell
death
Evading growth
suppressors
Inducing
angiogenesis
Activating invasion
& metastasis
Enabling replicative immortality
1. Hanahan D & Weinberg RA. The hallmarks of cancer. Cell (2000) 100:57-70.
2. Hanahan D & Weinberg RA. Hallmarks of cancer: the next generation. Cell (2011) 144:646-674
Sustaining proliferative signalling
Normal cells rely on positive growth signals from other cells
Cancer cells can reduce their dependence on growth signals by:1,2
- Production of their own extracellular growth factors - Overexpression of growth factor receptors - Alterations to intracellular components of signalling pathways -
Growth factors
Growth factor receptors
Cell wall
1. Hanahan D & Weinberg RA. The hallmarks of cancer. Cell (2000) 100:57-70.
2. Hanahan D & Weinberg RA. Hallmarks of cancer: the next generation. Cell (2011) 144:646-674
Evading growth suppressors
• Normal cells rely on
antigrowth signals to regulate
cell growth1,2
• Cancer cells can become
insensitive to these signals
• One way that this can
happen is by disruption of the
retinoblastoma protein (pRb)
pathway1
• pRb prevents inappropriate
transition from the G1 phase
of the cell cycle to the
synthesis (S) phase1
• In cancer cells, pRB may be
damaged, allowing the cell to
divide uncontrollably1
M
G2
Cell
division
cycle
G1
S
1. Hanahan D & Weinberg RA. The hallmarks of cancer. Cell (2000) 100:57-70.
2. Hanahan D & Weinberg RA. Hallmarks of cancer: the next generation. Cell (2011) 144:646-674
Resisting cell death
An important hallmark of many
cancers is resistance to apoptosis,
which contributes to the ability of the
cells to divide uncontrollably1,2
When normal cells become
old/damaged, they go through
apoptosis (programmed cell death)
Normal cell
division
Apoptosis
Cell damage –
no repair
Cancer cell
division
First
mutation
Second
mutation
Third
mutation
Fourth or
later mutation
Uncontrolled
growth
Hanahan D & Weinberg RA. The hallmarks of cancer. Cell (2000) 100:57-70. 2. National Cancer Institute, What is Cancer, 2010. 3.
Hanahan D & Weinberg RA. Hallmarks of cancer: the next generation. Cell (2011) 144:646-674. Artwork originally created for the
National Cancer Institute. Reprinted with permission of the artist, Jeanne Kelly. Copyright 2013.
Enabling replicative immortality
Another important hallmark of
cancer is the ability of the cell to
overcome the boundaries on how
many times a cell can divide1
Normal cells
Cell division
Cancer cells
Chromosomes
Telomeres
These limits are usually set by
telomeres (the ends of
chromosomes):1,2
• In normal cells, telomeres get
shorter with each cell division until
they become so short that the cell
can no longer divide
• In cancer cells, telomeres are
maintained, allowing the cell to
divide an unlimited number of
times
Apoptosis
No
apoptosis
1. Hanahan D & Weinberg RA. The hallmarks of cancer. Cell (2000) 100:57-70.
2. Hanahan D & Weinberg RA. Hallmarks of cancer: the next generation. Cell (2011) 144:646-674
Inducing angiogenesis
FGFR
The formation and maintenance
of new blood vessels
(angiogenesis) plays a critical
role in tumour growth.1,2
New blood vessels supply the
cancer cells with oxygen and
nutrients, allowing the tumour to
grow.
VEGFR
PDGFR
Cell wall
Smooth
muscle
Pericyte
Endothelial
Blood vessel
Nearby blood vessels grow into the tumour.
Angiogenesis is mediated
principally through vascular
endothelial growth factor (VEGF)
Other growth factors also play a role,
e.g.:
• Fibroblast growth factor (FGF)
• Platelet-derived growth factor (PDGF)
Oxygen and
nutrients
Blood vessel
1.Folkman J. Clinical applications of research on angiogenesis. N Engl J Med (1995) 333:1757-63.
2. Ellis LM, Hicklin DJ. VEGF-targeted therapy: mechanisms of anti-tumour activity. Nat Rev Cancer (2008) 8:579-591.
Activating invasion & metastasis
Eventually, tumours may
spawn pioneer cells that can
invade adjacent tissues and
travel to other sites in the
body to form new tumours
(metastasis)1
Nearby blood vessels grow into the tumour.
This capability allows
cancerous cells to colonise
new areas where oxygen
and nutrients are not
limiting1
Metastasis causes 90% of
deaths from solid tumours2
Oxygen and
nutrients
Blood vessel
Cells escape
and metastasise
1. Hanahan D & Weinberg RA. The hallmarks of cancer. Cell (2000) 100:57-70.
2. Gupta GP & Massagué J. Cancer metastasis: Building a framework. Cell (2006) 127: 679-695
Enabling characteristics and emerging hallmarks
There is evidence that a further two emerging hallmarks are involved
in the pathogenesis of cancer1
The acquisition of these hallmarks of cancer is made possible by two
enabling characteristics1
The uncontrolled growth and division of
The immune system is responsible for
Emerging
hallmarks
cancer cells relies not only on the
recognising and eliminating cancer cells,
deregulation of cell proliferation, but
and therefore preventing tumour
also on the
reprogramming
of cellular
formation.
Evasion
of this immune
Deregulating
cellular
Evading
immune
metabolism,energetics
including increased
surveillance
by weakly immunogenic
destruction
aerobic glycolysis (known as the
cancer cells is an important emerging
Warburg effect)
hallmark of cancer.
Cancer cells achieve genome instability
by increasing their mutability, or rates of
mutation, through increased sensitivity
Genome
instability
to mutagenic
agents
or breakdown of
and mutation
genomic maintenance
machinery.
Immune cells infiltrate tumours and
produce inflammatory responses, which
can paradoxically enhance
Tumour-promoting
tumourigenesis,
helping tumours acquire
the inflammation
hallmarks of cancer
Enabling characteristics
Click on each hallmark or enabling characteristic for more information
1. Hanahan D & Weinberg RA. Hallmarks of cancer: the next generation. Cell (2011) 144:646-674
How is cancer diagnosed?
‘Cancer’ is an umbrella
term for a broad group of
diseases
There is no single test
that can diagnose all
cancers1
Diagnostic tests include:
• Physical examination
• Laboratory tests
• Imaging
• Endoscopic examination
If there are symptoms
suggestive of cancer a
broad range of tests
allow HCPs to make an
accurate and detailed
diagnosis
• Biopsy
• Surgery
• Molecular testing
1. Stanford Cancer Institute, Cancer Diagnosis, 2012
Laboratory tests
Assess the general health of the body
and levels of certain compounds
Typically, blood and/or urine samples
Marker
Cancer
CA 125
Ovarian
Blood is assessed for its composition,
and can give an indication of liver and
renal function
CEA
Colorectal
AFP
Liver, ovarian, testicular
Blood, proteins and other compounds
in the urine indicate there could be a
problem
HCG
Testicular, ovarian, liver,
stomach, pancreatic, lung
CA 19-9
Colon, stomach, bile duct
CA 15-3
Ovarian, lung, prostate
CA 27-29
Colon, stomach, kidney,
lung, ovarian, pancreatic,
uterus, and liver
Tumour markers detected in blood or
urine are substances created by the
body in response to cancer cells
• Currently, markers are used to
monitor treatment efficacy and
recurrence
• May become more important in
diagnosis in the future
CEA, carcinoembryonic antigen, several cancers can raise
CEA levels; AFP, alpha-fetoprotein; HCG, human chorionic
gonadotropin; CA 15-3 and CA 27-29 are most useful in assessing
advanced breast cancer treatment
1. Stanford Cancer Institute, Cancer Diagnosis, 2012.
Imaging
Produce images of the organs
and structures
Imaging
Reveal location and extent of
disease
Transmitted
radio waves
Emitted
radio waves
Three main types:
• Transmission imaging: highenergy photons beamed through
body – the ‘opacity’ of different
structures/tissues varies > X-ray,
CT scan, bone scan, mammogram,
lymphangiogram
• Reflection imaging: high
frequency sound reflected
differentially depending on
structures/tissues > Ultrasound
• Emission imaging: atoms excited
to emit energy waves detected by
a scanner > MRI, PET
1. Stanford Cancer Institute, Cancer Diagnosis, 2012.
magnetic field
direction
Endoscopy
An endoscope is a small, flexible tube with a light, lens and tools
• Bronchoscopy
Used to examine the airways and
obtain tissue samples from the lungs
Oesophagus
• Colonoscopy and sigmoidoscopy
Used to view the large intestine or just
the sigmoid colon
Endoscope
• Endoscopic retrograde
cholangiopancreatography (ERCP)
Combined with X-ray to examine the
liver, gallbladder, bile ducts, and
pancreas
Light
• Oesophagogastroduodenoscopy
(upper endoscopy)
Used to view the inside of the
oesophagus, stomach, and duodenum
• Cystoscopy (cystourethroscopy)
Device inserted through the urethra to
examine the bladder and urinary tract
Stomach
Interior of
stomach
Endoscope
Light
Stomach
lining
1. Stanford Cancer Institute, Cancer Diagnosis 2012.
Biopsy sample
Biopsy
Biopsy type
Tissue or cells from
the body for
examination under a
microscope
Performed in the
doctor’s office or
hospital, depending
on the type of biopsy
and location of the
tumour
Description
Endoscopic
Tissue sample removed
via an endoscopy
Bone
marrow
Bone chip or cells
aspirated from the sternum
or hip
Excisional
or incisional
Full thickness of skin even
whole tumour removed
Fine needle
aspiration
(FNA)
Tiny pieces of tumour
extracted via a thin needle
Punch
Short cylinder of tissue
taken
Shave
Top layer of skin removed
Skin
Small sample of skin taken
1. Stanford Cancer Institute, Cancer Diagnosis, 2012.
Pathology
Tests on biopsies and
samples of patient
tissue or body fluids
reveal a great deal
about the cancer
Biopsy
Pathology
Blood sample
or
tissue sample
Proteomic profile
Microscopic
examination can reveal
the presence of cancer
cells, the origin of the
cancer cells (sub-type),
and information on
stage, etc.
1. National Cancer Institute, Understanding Cancer, 2009.
Artwork originally created for the National Cancer Institute.
Reprinted with permission of the artist, Jeanne Kelly. Copyright 2013.
Genomic profile
What is TNM?
!
TNM is a system for classifying malignant tumours
!
It is a cancer staging system, which describes
the extent of a person's cancer
!
Most types of cancer have TNM designations,
but some do not1
!
Most medical facilities use this system as their
main method for cancer reporting1
1. National Cancer Institute, Cancer Staging, 2010
How does the TNM system work?
The 3 parameters
of the TNM system1:
A number is
added to each letter
to indicate1:
T = extent of the tumour
the size or extent of
N = the extent of spread
the primary tumour
to the lymph nodes
M = presence of distant
the extent of cancer
spread
metastases
1. National Cancer Institute, Cancer Staging, 2010
T = extent of primary tumour
T is classified as follows:1
Tx: Primary tumour cannot be evaluated | T0: No evidence of primary tumour
Tis: Carcinoma in situ (CIS)2 | T1, T2, T3, T4: Size and/or extent of the primary tumour
T0
organ
T1
T2
T3
local tissues
1. National Cancer Institute, Cancer Staging, 2010
2. CIS – abnormal cells are present but have not spread to neighbouring tissue; although not cancer, CIS
may become cancer and is sometimes called pre-invasive cancer
N = extent of spread to lymph nodes
N is classified as follows1:
Nx: Regional lymph nodes cannot be evaluated | N0: No local lymph node involvement
N1: Tumour has spread to local lymph nodes | N2, N3: Involvement of local and distant
lymph nodes (number of lymph nodes and/or extent of spread)
N0
N1
distant
nodes
local nodes
1. National Cancer Institute, Cancer Staging, 2010
N2
M = presence of distant metastases
M is classified as follows1:
Mx: Distant metastasis cannot be evaluated | M0: No distant metastasis
M1: Distant metastasis is present
M0
M1
Mx
?
lung
bone
liver
1. National Cancer Institute, Cancer Staging, 2010
Intrinsic vs. extrinsic factors
Cancer caused by intrinsic
factors, i.e. inherited mutations,
can only be prevented by
screening and appropriate early
intervention
Cancer caused by extrinsic
factors can be prevented by
reducing or eliminating exposure
to these factors (e.g. chemicals,
tobacco, radiation, viruses)
Cancer Prevention
Radiation
Viruses
or bacteria
1. National Cancer Institute, Understanding Cancer, 2009.
Carcinogenic
chemicals
Tobacco products
The use of tobacco products
is implicated in ~33% of all cancer
deaths1
~1 person dies every 6 seconds
Lung Cancer Risk Increases with
Cigarette Consumption1
due to tobacco2
15x
The combination of tobacco
and alcohol products appears to
be particularly dangerous1
As well as lung cancer,
tobacco products have also been
implicated in cancer of the mouth,
larynx, oesophagus, stomach,
pancreas, kidney, and bladder1
Avoiding tobacco is the single
10x
Lung
Cancer
Risk
5x
0
Non-smoker
15
Cigarettes Smoked per Day
most important factor in reducing
cancer risk
1. National Cancer Institute, Understanding Cancer, 2009. 2. WHO Fact Sheet 339, 2012.
Artwork originally created for the National Cancer Institute.
Reprinted with permission of the artist, Jeanne Kelly. Copyright 2013.
30
Excessive exposure to UV radiation
Excessive UV exposure,
particularly in fairskinned individuals can
cause:1
• cutaneous malignant
melanoma
• squamous cell
carcinoma
• basal cell carcinoma
In 2000, >200,000 cases
of melanoma were
diagnosed worldwide1
Sun
exposure
Stratosphere
UV-C
Ozone
UV-B
Epidermis
Dermis
Hypodermis
1. WHO Fact Sheet 305, 2009.
UV-A
Diet
radiation and alcohol, dietary
components that influence
cancer risk have been difficult
to determine1
Limiting fat and calorie
intake appears to reduce
cancer risk1
A diet rich in meat
increases cancer risk,
especially colon cancer1
Correlation Between Meat
Consumption and Colon Cancer
Rates in Different Countries1
Number of Cases (per 100,00 People)
Unlike tobacco products, UV
40
N.Z.
U.S.A.
30
DEN.
CAN
G.B.
SWE
NETH
NOR
20
JAM
10
ISR
GERMANY
ICE
FIN P.R.
POL 15
YUG
CHILE ROM HUNG
JAPAN
COL
NIG
0
80
100
200
300
Grams (per person per day)
National Cancer Institute, Understanding Cancer, 2009.
Artwork originally created for the National Cancer Institute.
Reprinted with permission of the artist, Jeanne Kelly. Copyright 2013.
Viruses
Worldwide, 15% of all cancers
may be caused by viruses,
including:1
• Epstein-Barr virus
• Human papilloma virus (HPV)
• Hepatitis B virus
HPV Infection Increases Risk for
Cervical Cancer2
High
• Human herpes virus-8
• Human T lymphotrophic virus
type 1
• Hepatitis C virus
Cervical
Cancer
Risk
Reducing exposure to these
viruses reduces cancer risk
In the case of HPV, avoiding
unprotected sex with many
partners reduces the risk of
contracting this virus2
Low
Non-infected
women
Women infected
with HPV
1. Liao JB. Viruses and Human Cancer. YJBM 2006 (79);115-122. 2.National Cancer Institute, Understanding Cancer, 2009.
Artwork originally created for the National Cancer Institute. Reprinted with permission of the artist, Jeanne Kelly. Copyright 2013.
Strategies for prevention
Education
about cancer and risk factors (warnings on cigarette packets,
campaigns about sun and exposure to UV radiation)
Awareness pink ribbons for breast cancer,
campaigns world cancer day
Risk
avoidance
don’t smoke, stay out of the sun, avoid toxic chemicals and
polluted areas
Screening
cervical smear, mammography, colonoscopy
Vaccines
HPV vaccine to reduce risk of cervical cancer; Hep B
vaccine to reduce risk of liver cancer
Lifestyle
normal weight, healthy diet, exercise
Healthcare regular check-ups, seek medical attention early
What is screening?
Screening is the name
given to a range of tests
that can detect cancer at
an early stage before
symptoms appear
Breast Cancer Screening
Finding cancer early
usually means it is easier
to treat/cure
By the time symptoms
appear, the cancer may
have grown and spread
and therefore be more
difficult to treat/cure
1. National Cancer Institute, Cancer Screening Overview, 2012.
Screening: the rationale
For screening to be effective, two requirements
must be met:
!
A test or procedure must be available to detect
cancers earlier than if the cancer were detected
as a result of the development of symptoms
!
Evidence must be available that treatment initiated
earlier as a consequence of screening results in an
improved outcome
1. National Cancer Institute, Cancer Screening HCP, 2012.
Screening tests
A variety of tests are used in
cancer screening:
Cervical Cancer Screening
• Physical exam and history:
check general health and
review medical history
Normal
Pap smear
• Laboratory tests: investigate
samples of tissue, blood,
urine, etc.
• Imaging: visualise the insides
of the body using e.g. x-ray,
ultrasound, CT, MRI, etc
• Molecular tests: look for
specific mutations that are
linked to some types of
cancer
Abnormal
Pap smear
Biopsy
Pathology
Patient‘s blood sample
or
tissue sample
Proteomic profile
Genomic profile
National Cancer Institute, Cancer Screening Overview, 2012. Artwork originally created for the National Cancer Institute.
Reprinted with permission of the artist, Jeanne Kelly. Copyright 2013.
Screening: pros and cons
Pros
Cons
• Reduction in cancer deaths
• Some screening
procedures carry their own
risks
• 3–35% of premature deaths
due to cancer could be
avoided with screening
• Improved outcomes (does
not apply in all cases)
• False negative results –
patient wrongly assured
there is no problem
• False positive results –
patient may receive
treatment they do not need
1. National Cancer Institute, Cancer Screening HCP, 2012.
Screening and high risk populations
By focusing on high-risk
populations, screening
resources can be better
applied
Patients with a personal
history/strong family
history of cancer are
deemed to be high-risk
The ability to test for
specific genetic mutations
has further refined the
identification of high-risk
patients
Heredity and cancer
All Breast Cancer Patients
Inherited factor(s)
Other factor(s)
Genes and Cancer
Chromosomes
are DNA molecules
Heredity
National Cancer Institute, Cancer Screening HCP, 2012. Artwork originally created for the National Cancer Institute.
Reprinted with permission of the artist, Jeanne Kelly. Copyright 2013.