Cancer 2016 Large Slides

What is Cancer?
Cancer is a chronic disease

characterised by the uncontrolled cell growth and
division
ability to metastasise or spread
Likelihood of developing cancer increases with

age
Is a considerable health problem in Australia
From Cancer in Australia: An Overview, 2012, Cancer series no. 74. Cat. no. CAN 70. Canberra. Australian
Institute of Health and Welfare & Australasian Association of Cancer Registries. Pg 1 4
Cancer incidence
Males Females
1. Prostate 1. Breast
2. Colorectal 2. Colorectal
3. Melanoma 3. Melanoma
4. Lung 4. Lung
5. Head and neck 5. Uterus
6. Lymphoma 6. Lymphoma
7. Leukaemia 7. Thyroid
8. Bladder 8. Leukaemia
9. Kidney 9. Ovary
10. Pancreas 10. Pancreas
Institute of Health and Welfare & Australasian Association of Cancer Registries. From Table 3.2 5
Cancer mortality
Males Females
1. Lung 1. Lung
2. Prostate 2. Breast
3. Colorectal 3. Colorectal
4. Pancreas 4. Pancreas
5. Unknown 5. Unknown
6. Melanoma 6. Ovary
7. Liver 7. Leukaemia
8. Leukaemia 8. Other digestive organs
9. Oesophagus 9. Lymphoma
10. Lymphoma 10. Brain
From Cancer in Australia: An Overview, 2014, Cancer series no. 90. Cat. no. CAN 88, Canberra. Australian
Institute of Health and Welfare & Australasian Association of Cancer Registries. From Table 3.2 6
Rates in Indigenous and non-
Indigenous Australians
Higher incidence in Indigenous Australians of:

cervical cancer
lung cancer
Lower incidence in Indigenous Australians of:

colorectal
breast
prostate cancer
melanoma
7
Trends in 5 year survival
Institute of Health and Welfare & Australasian Association of Cancer Registries. 8
Normal Cell Division and Proliferation
Cells grow and divide according to their tissue
type
Cell size and number are regulated and
maintained
Number of cells can change

For example, during infection, the number of white blood
cells (leucocytes) increases
Cell Regulation
Approximately 100 trillion cells in the body
Cells are highly organised and regulated
Cell size and number are regulated
Cell division
Cell death
Cells which are damaged, aged, or are no
longer needed undergo apoptosis
Apoptosis
Active process (uses ATP)
May be a normal process
(eg older cells)
May be due to disease (eg
viral infection)
No inflammation
12
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 4-14B
DNA
DNA
Genetic information
Genes segments of DNA
Remains in nucleus
13
Marieb & Hoehn, Human Anatomy and Physiology, 2007, Fig 2.22
DNA, Genes and Chromosomes
14
Huether & McCance, Understanding Pathophysiology, 2008, Fig 2-6
Cell cycle
Stages from cell

formation to cell
reproduction
Two main phases:
Interphase
Mitotic phase
15
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 5-3
Cell cycle
Interphase:
From cell formation to cell division (cells not actually
dividing)
G1 (gap 1)
Main phase
Active growth and production of proteins
S (synthesis)
DNA is replicated Synthesis = production of molecules
G2 (gap 2)
proteins and enzymes needed for cell division are produced
16
Cell cycle
Mitotic phase
Mitosis: division of nucleus to form two identical
daughter cells
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015,

17
Fig 5-4
Checkpoints
G1/S checkpoint
Progresses into S phase only if:
Fully prepared to complete cycle
DNA damage has been repaired
G2/M checkpoint
Progresses into M phase only if:
DNA replication is completed
Chromosomes are intact
18
Tumour Growth
A tumour (neoplasm) is a mass or growth
which can arise from normal tissue
Tumours can be benign or malignant
Benign tumours are non-invasive and do not
spread
Malignant tumours have the capacity to invade
and infiltrate surrounding tissue, so extend
beyond the tissue of origin and can
metastasise or spread to other sites
Benign and Malignant
Benign tumours are composed of well
differentiated cells
mature cells that resemble the tissue of origin
Malignant tumours are undifferentiated

The cells lack the ability to undertake mature
cellular functions, as they are immature
Tumour classification
Malignant tumour or
Benign Tumour
Cancer
Slow growth Usually rapid growth
Have well defined capsule Lack capsule
Cells well differentiated Loss of cell differentiation
Can invade blood vessels
Not invasive
and lymph nodes
Does not metastasize Can metastasize
Good prognosis: often not Poor prognosis: usually
life-threatening become life-threatening
22
23
http://www.cancer.gov/cancertopics/understandingcancer/cancer/page9, Last accessed Sep 2014
24
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Table 36-2
25
Genetic basis of cancer
Cancer arises due to genetic mutations
(damage to DNA)
Due to:
Inheritance of mutated genes
Lifestyle and environmental factors
26
Genetic mutations
Carcinogens
Genetic
mutations
Inheritance of
mutated genes Cancer
(5% of cases)
27
Growth and antigrowth signals
Cancer cells may
stimulate their own
growth
Secrete growth factors
Increased number of
growth factor receptors
Genes that regulate
apoptosis
28
Normal regulatory genes
Proto-oncogenes:
Regulate cell growth and division
Tumour suppressor genes eg p53
Slow down proliferation
Direct cell repair when DNA is damaged
Other regulatory genes eg Caretaker genes
Help repair DNA
Induce apoptosis when repair not completed
29
30
http://www.cancer.gov/cancertopics/understandingcancer/cancer/page47, Last accessed Sep 2014
DNA damage, repair, and cancer

32
http://ittakes30.wordpress.com/2012/07/10/cellular-morse-code/, Last accessed Sep 2014
Fig 36-10 33
Mutations to regulatory genes
Proto-oncogenes become active oncogenes
Promote cell proliferation and tumour growth
Tumour suppressor become inactive tumour
suppressor genes
Eg. p53 gene
They lose their normal brake "on cell
proliferation and allow tumour growth
When other regulatory genes mutate
Apoptosis does not occur
Damaged genes are not repaired
34
Leenders & Tuszynski, Stochastic and deterministic models of cellular p53 regulation, Front. Oncol, 2 April 2013, Fig 1 35
36
Multistep development of cancer
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 36-12 37

Features of cancer development
Genetic features of cancer
Decreased tumour suppressor
Increased oncogene activity
gene activity
Cellular features of cancer

Cell division not slowed
Uncontrolled cell division
Apoptosis does not occur
Unregulated cell differentiation and growth
Cancer
38
39
40
Kumar et al, Robbins & Cotran Pathologic Basis of Disease, 8th edn, Fig 7-32
41
Cancer growth
Growth
Cells grow and multiply independently of normal cell
controls
Angiogenesis
Formation of new blood vessels
Metastasis
Spread to other distant tissues or organs
42
Cancer growth
Loss of normal arrangement of cells
Variation in cell shape and size
Increase in size of nucleus (increase in DNA)
Increase in mitotic activity (cell division)
Invasion of surrounding tissues
43
Angiogenesis
Mainly in more advanced cancers
Tumour develops its own blood supply
Due to high metabolic rate
Can facilitate metastasis
44
Majno & Joris, Cells, Tissues, and Disease,
2nd edn, 2004, Fig 26-57 45
Metastasis
Ability to migrate and spread
to distant organs
Via blood vessels (mainly
veins)
Via lymphatic vessels and
body cavities (mainly
peritoneal cavity)
46
Herlihy, The Human Body in Health and Illness, 2007, p350
Metastasis
Most common sites are liver, lungs, bone and brain
Most common sites of metastasis differ for each primary
cancer type

47
Fig 36-17
48
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Tab 36-4
Primary versus Secondary
Primary cancer: original site of the cancer
Secondary cancer: cancer which has spread to

another site
Unknown primary site: cancer diagnosed after

spreading to another site
Pathology testing can be used to identify the cell
type, which can assist in defining the primary cancer
Usually cancer is well advanced
49
Multistep nature of metastasis
50
51
Production of new formed elements
All blood cells are:
Produced in the red bone marrow
Derived from stem cells (haematopoietic stem cell)
Blood cell production

Erythrocytes; insufficiency leads to anaemia
Leucocytes; insufficiency leads to leucopenia
Platelets (thrombocytes); insufficiency leads to
thrombocytopenia
52
53
Vander, Human Physiology, Fig 12.71
Red bone marrow
54
Silverthorn, Human Physiology, 2001, Fig 16.5c
Immune system and cancer
Cytotoxic T lymphocytes
Natural killer cells
Macrophages
Inflammation
55
Macrophages
Cells that engulf and
remove debris, cells etc
Process of phagocytosis
56
Germann & Stanfield, Principles of Human Physiology, 2002, Fig 22.4
Natural killer (NK) cells
Type of lymphocytes
Lysis of cancer cells
Release chemicals that
disintegrates the cell
57
Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 12-2B
Inflammation and cancer
Chronic inflammation increases risk of cancer
Inflammatory cells release cyclo-oxygenase 2
(COX-2)
Associated with some cancers
eg colorectal
Aspirin: anti-inflammatory
58
Stress and Cancer
Stress, immunity and cancer
Excess cortisol suppresses some functions of the
immune system
Link with the development of cancer
In cancer patients, stress can increase growth and
spread of cancer
59
60
Carcinogens
Infectious agents e.g.
viruses, bacteria
Environmental factors e.g.
ionizing radiation,
iatrogenic exposure
Lifestyle factors e.g.
obesity, alcohol, physical
inactivity, nutritional
factors
61
Mann & Truswell, Essentials of Human Nutrition, 3rd edn, 2007, Table 21.2
Infectious agents
Human papillomavirus (HPV) cancer of cervix
Human immunodeficiency virus (HIV) lymphoma
Hepatitis virus cancer of liver
Helicobacter pylori stomach cancer
62
Ionizing radiation
Radiation from medical imaging

Fallout from nuclear radiation
UV radiation from sunlight and tanning booths
63
Iatrogenic exposure
Due to medical diagnostics and treatments

Chemotherapeutic drugs (for cancer treatment)
can increase development of other cancers
Hormone replacement therapy increases risk of
breast cancer
64
Lifestyle factors that increase risk
Modifiable risk factors for cancer
Obesity
Sedentary lifestyle
Alcohol consumption
Smoking
Dietary eg low fibre, low intake of fruit and vegetables, high salt,
iron, cooking process eg charring meat, aflatoxin
Hyperglycaemia, hyperinsulinaemia
Chronic inflammation
Stress
Lifestyle modifications
66
Mann & Truswell, Essentials of Human Nutrition, 3rd edn, 2007, Table 21.4
67
Clinical features
Mainly in advanced stages
Pain Local effects
Fatigue
Cachexia
Systemic effects
Anorexia
Anaemia
Thrombocytopenia
Infection
68
Pain
Usually only when cancer is well advanced
Related to
Direct pressure of tumour on sensory receptors
Obstruction
Tumour growing inside a lumen, or compressing the
lumen from outside
Inflammation
Tissue damage
69
Gould, Pathophysiology for the Health Professions, 2006, Fig 5-3
Fatigue
Persistent tiredness
Most common symptom
Sleep disturbances
Alterations in cytokines
Psychosocial factors
Nutritional status
Level of physical activity
70
Cachexia
Severe tissue wasting (fat and muscle)
Fatigue and weakness
Anorexia
Pain
71
Copstead & Banasik, Pathophysiology, 4th edn, Fig 7-18
Anorexia
Loss of appetite
(not = anorexia nervosa)
Very little appetite due to various factors
including:
Altered taste sensation
Nausea and vomiting
Psychological concerns
Some of these are due to cancer treatments
72
73
Anaemia
Oxygen-carrying capacity is low due to:
Inadequate food intake, chronic bleeding and iron loss
Cancer in bone marrow or depression of bone marrow
via cancer treatments
Causing insufficient number of erythrocytes
74
Thrombocytopenia
Low platelet count
Cancer in bone marrow or depression of bone
marrow via cancer treatments
Causing insufficient number of platelets
Prone to haemorrhage
Contributes to iron loss and anaemia
75
Infections
Immune system becomes weakened
Infection often fatal
Due to
Cancer in bone marrow or depression of bone
marrow via cancer treatments
Causing insufficient number of leucocytes: leucopenia
76
77
Treatment
Surgery
Radiation therapy
Antineoplastic medications
Cytotoxic drugs
Antibodies
Hormonal
Palliative care
78
Surgery
Removal of the tumour
Usually removal of a margin (take some
apparently healthy tissue around the growth as
well)
Removal of nearby lymph nodes
79
Radiation therapy
X-rays or gamma rays
Causes damage to cancer cell DNA, inducing
apoptosis
80
Mader, Human Biology, 2006, Fig 24.9
Cytotoxic drugs
Use of cytotoxic or antineoplastic drugs that target
rapidly dividing cells
Used after surgery to destroy any remaining cells (adjuvant
chemotherapy)
Used before surgery to decrease tumour size (neoadjuvant
chemotherapy)
Often a few drugs are used together
eg Fluorouracil in combination with other drugs
81
Antibodies,
drugs that modify the immune system
Boosts the immune defences against cancer
cells
Activate immune system components
Eg Filgrastim increases production of neutrophils
Vaccination against some viruses that cause

cancer
Eg Cervical cancer (HPV) vaccine
82
Hormonal therapy
Some cancers of the reproductive system
are hormone dependant
Drugs that block activity or production of
hormones may be used
e.g. Tamoxifen blocks effects of oestrogen
83
Palliative care
Treatment of patients symptoms when
other treatment options are not suitable
Includes pain medications
84
Side effects of cancer therapies (1)
Rapidly dividing cells are vulnerable
Hair follicles
Alopecia, usually temporary
Gastrointestinal tract
Causing nausea, vomiting, anorexia, diarrhoea
Anti-emetics eg ondansetron
Skin and mucous membranes
Resulting in infections
Prevention, early intervention
85
Side effects of cancer therapies (2)
Bone marrow
Causing leucopenia, thrombocytopenia, anaemia
Treated using transfusions, erythropoietin (EPO)
Reproductive system
Causing decreased fertility, early menopause
Addressed using sperm or embryo banking
86
Lymphatic Vessels
Marieb & Hoehn, Human Anatomy and Physiology,

87
8th edn, 2010, Fig 20.2
Secondary lymphoedema
Tissue fluid is normally returned to lymphatic vessels, then
empties into venous circulation
If lymph channels are blocked or removed,

fluid is trapped in tissues, leading to oedema
Secondary lymphoedema may arise from surgical removal or damage of
lymph nodes during cancer treatment
88
http://www.vibraq.com/images/lymph_1.jpg , Last accessed Sep 2014
89
Main cancers for Australia
Colorectal
Breast
Prostate
Melanoma
Lung
National Cancer Screening Programs
Breast cancer
Bowel (colorectal) cancer
Cervical cancer
Understanding Pathophysiology, Craft et al, 2011,

91
Fig 36-31A
Colorectal cancer
Most develop from benign growths called

polyps
Mass protruding into gut lumen
Benign, can become malignant
Risk factors
Low dietary fibre, high fat intake
92
http://www.sciencedaily.com/releases/2008/03/080324202016.htm, Last accessed Sep 2014
Colorectal cancer clinical features
Few symptoms until advanced stage
Symptoms depend on location of cancer and include

Change in bowel habits
Abdominal pain, bloating
Bleeding
Unexplained tiredness
93
Colorectal cancer detection
Currently <40% of cases detected early
No early warning symptoms
Remains confined for long period before invading
bowel wall and other organs
National Bowel Cancer Screening Program

Faecal occult blood test
94
Incidence: Colorectal
Mortality: Colorectal
Breast cancer
Usually arises from epithelial cells lining the small
ducts involved in milk production
Risk factors:
Early menarche and late menopause
No pregnancy, or first pregnancy late in life; little
breast feeding
Family history / genetics
Hormone replacement therapy
97
Breast cancer diagnosis
Self examination
Mammogram
from 40 years
MRI for younger
women in high-
risk groups
Needle biopsy
Mader, Human Biology, 2006, Fig 24.8 98

Breast cancer clinical features
Painless lump
Breast skin dimpling
Changes to nipples
Palpable nodes in axilla
http://www.cancerresearchuk.org/cancer-help/type/breast-
99
cancer/treatment/number-stages-of-breast-cancer, Last accessed Sep 2014
Prostate cancer
Most are adenocarcinomas
Risk factors
Family history / genetics
Dietary factors eg high fat intake
100
Prostate cancer clinical features
If advanced, tumour compresses urethra
causing urinary symptoms
e.g. dysuria, urinary infection, frequent urination
Metastasis to bone, pelvic lymph nodes
101
Prostate cancer diagnosis
Digital rectal examination
Prostate serum antigen (PSA) levels in the
blood
Biopsy
http://m.medlineplus.gov/ency/presentations/100046.htm?
102
page=2, Last accessed Sep 2014
Incidence: Prostate and Breast
Mortality: Prostate and Breast
Melanoma
Malignant tumour arising from melanocytes
Very rapid metastasis, resistant to
chemotherapy
Risk factors
Recurring exposure to UV light
Sunburn in childhood
Fair skin
Family history
105
Melanoma
detection
Asymmetry
Border irregularity
Colour variation
Diameter >6mm
Evolving over time
or elevation
106
Mader, Human Biology, 2006, Fig 24.8
Incidence: Lung
Mortality: Lung

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What is Cancer?

Cancer is a chronic disease

Likelihood of developing cancer increases with

Higher incidence in Indigenous Australians of:

Lower incidence in Indigenous Australians of:

Number of cells can change

Stages from cell

Craft & Gordon, Understanding Pathophysiology 2nd ed 2015,

Malignant tumours are undifferentiated

Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 36-6

Craft & Gordon, Understanding Pathophysiology 2nd ed 2015, Fig 36-12 37

Cellular features of cancer

Unregulated cell differentiation and growth

Craft & Gordon, Understanding Pathophysiology 2nd ed 2015,

Secondary cancer: cancer which has spread to

Unknown primary site: cancer diagnosed after

Blood cell production

Human papillomavirus (HPV) cancer of cervix

Human immunodeficiency virus (HIV) lymphoma

Hepatitis virus cancer of liver

Helicobacter pylori stomach cancer

Radiation from medical imaging

Due to medical diagnostics and treatments

Removal of nearby lymph nodes

Vaccination against some viruses that cause

Marieb & Hoehn, Human Anatomy and Physiology,

If lymph channels are blocked or removed,

Understanding Pathophysiology, Craft et al, 2011,

Most develop from benign growths called

Symptoms depend on location of cancer and include

National Bowel Cancer Screening Program

Mader, Human Biology, 2006, Fig 24.8 98

Metastasis to bone, pelvic lymph nodes

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