CELLULAR ADAPTATION

AND ABERRANT CELL

GROWTH

Presented by
Faustin Ntezimana
 Learning Objective
 Define Cellular adaptation.
 Define Hypoxia, Atrophy, Hypertrophy,
Hyperplasia, Metaplasia and Dysplasia
 Define Aberrant cell growth.
 Define cancer and List the characteristics of cancer
cell.
 Differentiate between benign and malignant
Tumors.
 Nomenclature of benign and malignant Tumors.
 Explore staging of tumor and grading.
Definition of Cellular adaptation

The group of changes that occur in a cell

in response to environmental stress is
called cellular adaptation
OR
Cellular adaptation refers to the
adjustments in shape, size, pattern of
growth and metabolic activity that a cell
makes in response to alterations in the
environment in which it must live.
 CELLULAR ADAPTATION TO STRESS

Adaptations are reversible changes in the number, size, phenotype,

metabolic activity or functions of cells in response to changes in their
environment

Physiologic adaptations are responses of cells to normal stimulation by

hormones or endogenous chemical mediators

Pathologic adaptations are responses to stress that allow cells to

modulate their structure and function and thus escape injury
HYPOXIC INJURY
▪ Definitions: Hypoxia, Anoxia, Hypoxemia, Ischemia
▪ Impaired gas exchange that takes place in the alveoli (between air and
blood) and at tissues (between blood and cells).
May be due to:
- Lack of oxygen in the air
- Problems with oxygen transport:
- Disease of the respiratory and/or cardiovascular system
- Narrowing of an artery or vein
- Obstruction of an artery or vein
Myocardial Infarction (MI)
▪ Acute obstruction of coronary artery leading to myocardial cell death.
▪ There is hypoxia, which progresses to anoxia if blood flow is not
restored.
- In response to hypoxia, the heart modifies its method of oxygen uptake
and utilizes myoglobin stores [Remember: Myoglobin = hemoglobin in
heart]
- Myoglobin stores are limited and eventually run out.
Hypertrophy
is an increase in the size of cells & consequently an
increase in the size of an organ.
the enlargement is due to an increased synthesis of
structural proteins & organelles
Occurs when cells are incapable of dividing

Types:
a) physiologic
b) pathologic
Causes:
a) increased functional demand
b) hormonal stimulation
Hyperplasia
is an increase in the number of cells in an organ or tissue
an adaptive response in cells capable of replication
a critical response of connective tissue cells in wound healing

Types:
a) physiologic hyperplasia
1) hormonal
ex. Proliferation of glandular epithelium of the female
breast at puberty & during pregnancy
2) compensatory – hyperplasia that occurs when a portion
of
a tissue is removed or diseased
e.g. partial resection of a liver > mitotic activity 12 hours
later
b) pathologic hyperplasia
Caused by excessive hormonal or growth factor
stimulation
Atrophy
Shrinkage in the size of the cell by the loss of cell substance
Results from decreased protein synthesis and increased
protein degradation in cells
Is accompanied in many situations by increased autophagy
with resulting increases in autophagic vacoules

Causes:
Decreased workload
Loss of innervation
Diminished blood supply
Inadequate nutrition
Loss of endocrine stimulation
Aging (senile atrophy)
Metaplasia
A reversible change in which one adult cell type ( epithelial
or mesenchymal) is replaced by another adult cell type.
Is cellular adaptation whereby cells sensitive to a
particular stress are replaced by other cell types better
able to withstand the adverse environment
Epithelial metaplasia
Examples
Squamous change that occurs in the respiratory epithelium
in habitual cigarette smokers ( normal columnar epithelial
cells of trachea & bronchi are replaced by stratified
squamous epithelial cells
Vitamin A deficiency
Chronic gastric reflux, the normal stratified squamos
epithelium of the lower esophagus may undergo metaplasia
to gastric columnar epithelium
Dysplasia:-
- Dysplasia refers to the appearance of cells that have
undergone some atypical changes in response to chronic
irritation.
- It is not a true adaptive process in that it serves no specific
functions.
- It is controlled reproduction of cells, but closely related to
malignancy in that it may transform into uncontrolled, rapid
reproduction.
- It is complete loss of normal architectural orientation of one
cell with the next both in shape and size.
- Epithelial cells are common sites for dysplastic changes.
E.g.: -Bronchial epithelium, Cervical epithelium, etc.
 Case#1
A 4 year girl has a broken arm.
After her cast is removed 6 weeks later, her
healing arm is markedly smaller than her
normal arm.
Identify the type of adaptation and also
mention its mechanism.
Type of cellular adaptation:
Disuse Atrophy
Mechanism of adaptation:
Immobilization of muscle and decrease in the
flow of blood, than normal, will lead to shrinking
 Case #2

On a routine visit to the physician, a healthy 51-

year-old man has a blood pressure of 150/95 mm
Hg.
If his hypertension remains untreated for years,
which of the following cellular alterations would
most likely be seen in his myocardium? And why?
Type of cellular adaptation:
Hypertrophy of myocardium
Mechanism of adaptation:
Increase blood pressure is a stress for myocardium
the myocardium becomes thicker in response to
bear the stress. The myocyte increase in length and
breadth.
 Case #3:
A 69-year-old man has had difficulty with urination, including
hesitancy and frequency, for the past 5 years.
A digital rectal examination reveals that the prostate gland is
palpably enlarged to about twice normal size.
Which of the following pathologic processes has most likely
occurred in the prostate? And why?
Type of cellular adaptation:
Benign Prostate Hyperplasia (BPH)
Mechanism of adaptation:
Studies show that prostate functions and structure are
maintained by testicular hormone (testosterone). With aging
the hormone become less, this leads to increase functioning of
the gland and therefore, the size of the gland increases. In
addition, aging process is also responsible for BPH
 CELLULAR INJURY
Cell Injury- pertains to the sequence of events when cells have no
adaptive response or the limits of adaptive capability are
exceeded

Types of Cell Injury

1. Reversible Injury- injury that persists within certain limits, cells
return to a stable baseline

2. Irreversible Injury- when the stimulus causing the injury persists

and is severe enough from the beginning that the affected
cells die
a. necrosis
b. apoptosis
CAUSES OF CELL INJURY
1. Hypoxia causes:
a. Ischemia
b. Inadequate oxygenation of the blood
c. Reduction in the oxygen-carrying capacity of the
blood

2. Chemical Agents
a. glucose, salt or oxygen
b. poisons
c. environmental toxins
d. social “stimuli”
e. therapeutic drugs
3. Physical agents- trauma, extremes of temperature, radiation,
electric
shock, & sudden changes in atmospheric pressure

4. Infectious agents
5. Immunologic reactions
Example: anaphylactic reaction to a foreign protein or a drug
reaction to self antigens

6. Genetic defects
Examples are genetic malformations associated with Down
Syndrome,
sickle cell anemia & inborn errors of metabolism

7. Nutritional Imbalances
NECROSIS
Refers to a series of changes that accompany cell death,
largely resulting from the degradative action of enzymes on
lethally injured cells
The enzymes responsible for digestion of the cell are derived
either from the:
1) Lysosomes of the dying cells themselves or from
2) lysosomes of leukocytes that are recruited as
part of the inflammatory reaction to the dead cells
 Patterns of Tissue Necrosis

1. Coagulative Necrosis
➢
A form of tissue necrosis in which the component cells are
dead but the basic tissue architecture is preserved for at
least several days
➢
It is characteristics of infarcts ( areas of ischemic
necrosis) in all solid organs except the brain

A wedge-shaped kidney
Infarct (yellow) with
preserva
tion of the outlines
2. Liquefactive Necrosis

➢
Seen in focal bacterial or occassionally fungal infections
because microbes stimulate the accumulation of
Inflammatory cells and the enzymes of leukocytes digest
( “liquefy”) the tissue
➢
This necrosis is characteristic of hypoxic death of cells
witnin the CNS
➢
Associated with suppurative inflammation (accumulation
of pus)
➢
The areas undergoing necrosis are transformed into a
Semi-solid consistency or state (liquid viscuous mass)
Example: abcess
Liquefactive necrosis. An infarct in the brain, showing
dissolution of tissue
3. Caseous Necrosis
➢
Encountered most often infoci of tuberculous infection
➢
Characterized by a cheesy yellow-white appearance of
the area of necrosis
➢
It is often enclosed within a distinctive inflammatory
border

A tuberculous lung with a large

area of caseous necrosis
containing yellow-white and
cheesy debris
4. Fat Necrosis
➢
Refers to focal areas of fat destruction, typically resulting
from release of activated pancreatic lipases into the
substance of the pancreas and the peritoneal cavity
➢
Occurs in acute pancreatitis

Fat necrosis in acute pancreatitis. The areas of white chalky deposits

represent foci of fat necrosis with calcium soapformation (saponification)
at sites of lipid breakdown in the mesentery
5. Fibrinoid necrosis
➢
A special form of necrosis usually seen in immune reactions
involving blood vessels.
This pattern of necrosis is prominent when complexes of
antigens and antibodies are deposited in the walls of arteries
Deposits of these immune complexes together with fibrin that
has leaked out of vessels result in a bright pink and
amorphous appearance called 'fibrinoid”

Fibrinoid necrosis in an artery

in a patient with Polyarteritis
Nodosa.
The wall of the artery shows a
circumferential bright pink
area of necrosis with protein
deposition and inflammation
6. Gangrenous Necrosis
This is not a distinctive pattern of cell death
It is usually applied to a limb, generally the lower leg, that has
lost its blood supply involving multiple tissue layers
➢
Types:
✔
A. Wet gangrene
✗
Occurs in naturally moist areas like mouth, bowels lungs
✗
Characterized by numerous bacteria.
✔
B. Dry gangrene
Begins at the distal part of the limb due to ischemia and often
occurs in the toes and feet of elderly patients due to
arteriosclerosis
✗
This is mainly due to arterial occlusion
✗
There is limited putrefaction and bacteria fail to survive.
 SUBCELLULAR RESPONSES TO INJURY

Autophagy
Refers to lysosomal digestion of the cell's ow components
It is thought to be a survival mechanism in times of nutrient
deprivation
Organelles are enclosed in vacuoles that fuse with lysosomes

Heterophagy a cell usually a macrophage ingests

substances from the outside for intracellular destruction
 Hypertrophy of Smooth Endoplasmic Reticulum
Cells exposed to toxins that are metabolized in the SER show
hypertrophy, a compensatory mechanism to maximize
removal of the toxins
Mitochondrial Alterations
* alterations in size, number, shape & function
Ex. Mitochondria assume extremely large & abnormal
shapes (megamitochondria) in hepatocytes in various
nutritional deficiencies & alcoholic liver disease
Cellular hypertrophy > of mitochondria in cells
Atrophy < of mitochondria

Cytoskeletal Abnormalities
some drugs & toxins interfere with the assembly & functions
of Cytoskeleton filaments or result in abnormal
accumulations of filaments
General Principles Relevant To Most Forms Of Cell Injury

• The cellular response to injurious stimuli depends on the type of

injury, its duration, and its severity

• The consequences of an injurious stimulus depend on the type ,

status , adaptability , and genetic makeup of the injured cell.

• Cell injury results from functional & biochemical abnormalities in

one or more of several essential cellular components
The most important target of injurious stimuli are:
1) cell membrane integrity, critical to cellular ionic and osmotic
homeostasis
2) mitochondrial, the site of adenosine triphosphate (ATP)
generation
3) protein synthesis
4) integrity of the genetic apparatus
5) cytoskeleton
 MECHANISMS OF CELL INJURY

➢
ATP depletion: failure of energy-dependent functions
reversible Injury necrosis
➢
Mitochondrial damage: ATP depletion failure of energy-
dependent cellular functions ultimately necrosis;
under some conditions, leakage of proteins that causes apoptosis
➢
Influx of calcium: activation of enzymes that damage cellular
components and may also trigger apoptosis
➢
Accumulation of reactive oxygen species: covalent modifications
of
cellular proteins, lipids, nucleic acids
➢
Increased permeability of cellular membranes: may affect plasma
membrane, lysosomal membranes, mitochondrial membranes;
typically culminates in necrosis
➢
Accumulations of damaged DNA and misfolded proteins triggers
apoptosis
APOPTOSIS (“FALLING OFF”)
➢
It is a pathway of cell death that is induced by a tightly
regulated suicide program in which cells destined to die
activate enzymes capable of degrading the cells own nuclear
DNA and nuclear and cytoplasmic proteins.

It differs from necrosis in the following characteristics:

➢

 Plasma membrane of the apoptotic cell remains

intact
 Has no leakage of cellular contents
 Does not elicit an inflammatory reaction in the host.
 Sometimes coexist with necrosis
 Apoptosis induced by some pathologic stimuli may progress
to necrosis
Causes of Apoptosis
Death by apoptosis is a normal phenomenon that serves to
eliminate cells that are no longer needed and to maintain a
steady number of various cell populations in tissues

Programmed destruction of cells during embryogenesis,

Including implantation, organogenesis, developmental
involution, and metamorphosis.


Involution of hormone- dependent tissues upon hormone
deprivation such as endometrial cell breakdown during the
menstrual cycle and regression of the lactating breast after
weaning.


Cell loss in proliferating cell populations, such as intestinal
epithelia

Causes of Apoptosis con’t

Death of cells that have served their useful purpose, such

as neutrophils in an acute inflammatory response and
Lymphocytes at the end of an immune response

Elimination of potentially harmful self-reactive lymphocytes

either before or after they have completed their maturation

Cell death induced by cytotoxic T lymphocytes, a defense

mechanism against viruses and tumors that serves to kill
eliminate virus-infected and neoplastic cells

Apoptosis eliminates cells that are genetically altered or

Injured beyond repair without eliciting a severe host
reaction, thus keeping the damage as contained as
possible.
Two Major Pathways in the Initiation of Apopotosis

1. Mitochondrial ( intrinsic) pathway

Triggered by loss of survival signals, DNA damage
and accumulation of misfolded proteins (ER stress)

2. Death receptor (extrinsic) pathway

Responsible for the elimination of self-reactive
lymphocytes and damage by cytotoxic T lymphocytes
 INTRACELLULAR ACCUMULATIONS

THREE MAIN PATHWAYS OF ABNORMAL INTRACELLULAR

ACCUMULATIONS

A normal substance is produced at abnormal or an increased
rate, but metabolic rate is inadequate to remove it

Example: Fatty change in the liver

 A normal or abnormal endogenous substance accumulates
because of genetic or acquired defects in its folding, packaging,
transport or secretion.
 Accumulation of proteins in anti-trypsin deficiency
1. Fatty Change (Steatosis)

Refers to any abnormal accumulation of triglycerides within

✔

parenchymal cells

Most often seen in the liver but may also occur in the heart,
✔

Skeletal muscle, kidney and other organs

May be caused by toxins, protein malnutrition, diabetes

✔

mellitus, obesity and anoxia

Alcohol abuse and diabetes associated with obesity are

✔

the most common causes of fatty liver

Fatty Liver
Cholesterol and Cholesteryl Esters

✔
Result of defective catabolism and excessive intake

Present in lipid vacoules of smooth muscle cells and

✔

macrophages in atherosclerosis (hardening of the aorta)

Give atherosclerotic plaques their characteristic yellow color

✔

and contibute to the pathogenesis of the lesion

✔
Xanthomas are hypercholesterolemic tumurous masses
found in the connective tissue of the skin or tendons
Proteins
✔
Less common than lipid accumulations
✔
Occur because excess are presented to the cells or
because the cells synthesize excessive amounts
✔
Examples:
1) Nephrotic syndrome there is heavy protein leakage
across the glomerular filter due to a much larger
reabsorption of albumin
2) accumulation of newly synthesized imunoglobulins
in RER of some plasma cells forming rounded,
eosinophilic Russell bodies
3) Mallory body or “ alcoholic hyalin” is an eosinophilic
cytoplasmic inclusion in liver cells highly characteristic
of alcoholic liver disease
4) Neurofibrillary tangle found in the brain in Alzheimer
disease
Protein reabsorption droplets in the renal tubular epithelium
Glycogen
✔
Accumulations of these are associated with abnormalities
in the metabolism of either glucose or glycogen
✔
Ex.
1) In poorly controlled diabetes mellitus, glycogen
accumulates in renal tubular epithelium, cardiac
myocytes, and β cells of Islets of langerhans
2) Glycogen storage diseases or glycogeneses are
Genetic disorders where glycogen accumulates in
macrophages of patients with defects in lysosomal
enzymes
 2) Melanin
✔
An endogenous, brown-black pigment synthesized
exclusively by melanocytes when the enzyme tyrosinase
catalyzes tyrosine to (DOPA) dihydroxyphenylalanine
located in the epidermis
✔
Acts as a screen against harmful ultraviolet radiation
✔
Basal keratinocytes in the skin can accumulate the
pigment (e.g. in freckles)
Melanin pigment in melanoma
3) Hemosiderin
✔
A hemoglobin-derived granular pigment that is
golden yellow to brown and accumulates in tissues
when there is a local or systemic excess of iron

✔
Iron is normally stored within cells in association with the
protein apoferritin, forming ferritin micelles
✔
Iron can be identified by the Prussian blue reaction
 ✔
Local excess of iron & consequently of hemosiderin result
from hemorrhage
Ex. Bruise

The original red-blue color of hemoglobin is

transformed to varying shades of green-blue by the
local formation of biliverdin (green bile) and bilirubin
(red bile) from the heme moiety
✔
The iron of hemoglobin accumulate as golden- yellow
hemosiderin
 Hemosiderosis
✔
a condition where hemosiderin is deposited in many organs
and tissues whenever there is systemic overload of iron
✔
It occurs in the following settings
 Increased absorption of dietary iron
 Impaired utilization of iron
 Hemolytic anemias
 Transfusions
Hereditary Hemochromatosis
✔
A condition where there is extensive accumulations of iron with
tissue injury like liver fibrosis, heart failure and
diabetes mellitus
✔
Characterized principally by
1) the deposition of hemosiderin in the following organs (in
decreasing order of severity):liver, pancreas,
myocardium, pituitary, adrenal, thyroid, joints & skin
2) cirrhosis and 3) pancreatic fibrosis
 Proliferation & cell differentiation
 Proliferation is a process by which cell divide and
reproduce itself. It maintains a balance between the
number of cells dying and the number of cells actively
dividing and this is a regulated activity.
 Differentiation is a process by which proliferating cells
are transformed into different and more specialized cells
for example RBCs takes the shape of a disc, becomes
capable of carrying oxygen and is destined to die in 120
days
 What is an Aberrant cell growth
Aberrant cell growth is defined as any abnormal cell growth
or new growth called neoplasm.
Neoplasm is an abnormal mass of tissue.
The growth beyond normal and is uncoordinated with that of
normal tissue and persist in the same excessive manner after
the cessation of the stimuli which evoked the change.
Although not synonymous, tumor and neoplasm are used
interchangeably.
Cancer: A disease process whereby cells proliferate
abnormally, ignoring growth-regulating signals in the
environment surrounding the cells
 Cancer
 A disease resulting from the uncontrolled
growth of cells, which causes malignant
cellular tumors.
 The second leading cause of death in
developed countries
 Benign & malignant neoplasm
Neoplasm that contain well differentiated cells that are
clustered together in a single mass are considered to be
benign neoplasm.

Malignant neoplasm are less differentiated and have the ability

to break loose, enter the circulatory or lymphatic system and
form secondary malignant tumors at other sites.
Cancer is a malignant neoplasm
Word cancer is derived from the Greek word “Karkinos”
meaning crab.
Malignancy is synonymous with the medical meaning of
cancer.
 Difference between Benign and
malignant neoplasm
Benign neoplasm/Tumors Malignant neoplasm/Tumors
Grow slowly Grow rapidly
Have a well-defined capsule Are not encapsulated

Are not invasive Invade local structure and

tissues
Well-differentiated; looks like the Poorly differentiated; may not
tissue from which it arises be able to tell which tissue it
arose from

Have a low mitotic index; High mitotic index; many

dividing cells are rare dividing cells
Do not metastasize Can spreads distantly, often
through blood vessels and
lymphatics
 Characteristics of Benign and Malignant Tumors

Characteristic Benign Malignant

s

Cell Well-differentiated cells Cells are undifferentiated

resemble normal cells of and may bear little
the tissue from which the resemblance to the normal
tumor originated. cells of the tissue from
which they arose.
Mode of growth Tumor grows by expansion Grows at the periphery and
and does not infiltrate the overcomes contact
surrounding tissues; usually inhibition to invade and
encapsulated. infiltrate surrounding
tissues
Rate of growth Rate of growth is usually Rate of growth is variable
slow. and depends on level of
differentiation; the more
anaplastic the tumor, the
faster its growth.
Characteristi Benign Malignant
cs
Metastasis Does not spread by Gains access to the blood and
metastasis lymphatic channels and
metastasizes to
other areas of the body
General effects Is usually a localized Often causes generalized
phenomenon that does effects, such as anemia,
not weakness, systemic
cause generalized inflammation, weight loss, and
effects unless its location CACS
interferes with vital
function
Tissue Does not usually cause Often causes extensive tissue
destruction tissue damage unless its damage as the tumor
location interferes with outgrows its blood
blood flow supply or encroaches on blood
flow to the area; may also
produce substances
that cause cell damage
Ability to Does not usually cause Usually causes death unless
cause death unless its location growth can be controlled
death interferes with vital
CACS, cancer-related anorexia-cachexia syndrome.
Adapted from Porth, C. M., & Matfin, G. (2009). Pathophysiology: Concepts of altered health states (8th ed.). Philadelphia: Lippincott Williams &
Wilkins.
 Tumor Staging and
Grading
 A complete diagnostic evaluation includes identifying
the stage and grade of the tumor.
 This is accomplished prior to treatment to provide
baseline data.
 Treatment options and prognosis are based on tumor
stage and grade.
 Staging determines the size of the tumor, the
existence of local invasion, lymph node involvement,
and distant metastasis.
 Several systems exist for classifying the anatomic
extent of disease.
 The tumor, nodes, and metastasis (TNM) system
is one system used to describe many solid tumors
 Cont…
TNM Classification System
 T: The extent of the primary tumor

 N: The absence or presence and extent of

regional lymph node metastasis

 M: The absence or presence of distant

metastasis
The use of numerical subsets of the TNM
components indicates the progressive
extent of the malignant disease
 Cont….
T (tumor) Cancer Staging
Tx Tumor cannot be adequately assessed
T0 No evidence of primary tumor
Tis Carcinoma in situ (E.g. ductal Ca of
breast)
T1—4 Progressive increase in tumor size or
involvement
N (nodes)
Nx Regional lymph nodes cannot be assessed
N0 No evidence of regional node metastasis
N1—3 Increasing involvement of regional lymph
nodes
M (metastasis)

Mx Not assessed

M0 No distant metastasis

M1 Distant metastasis present, specify sites

Adapted from Edge, S. B., Byrd, D. R., Compton, C. C., et al. (Eds.).(2010).
AJCC cancer staging manual (7th ed.). New York: Springer
 Cancer "Grading"
 "Grading is the pathologic classification of
tumor cells. Grading systems seek to define
the type of tissue from which the tumor
originated and the degree to which the
tumor cells retain the functional and
histologic characteristics of the tissue of
origin (differentiation)
 Grade I : Well differentiated.
 Grade II : Moderately differentiated.
 Grade III : Poorly to very poorly differentiated
 Grade IV : Very poorly differentiated.
Naming of benign & malignant
neoplasm
Tumors/neoplasm are named by adding the suffix-oma to
parenchymal tissue type from which the growth
originate.
E.g. benign tumor of glandular epithelial origin is
adenoma, of bone origin is osteoma.
Term carcinoma is used to designate a malignant tumor of
epithelial tissue origin. E.g. malignant tumor of
glandular epithelial origin is adenocarcinoma.
Malignant tumor of parenchymal origin is called
sarcomas (e.g. osteosarcoma)
 Nomenclature
Benign Malignant

Epithelial Tumor
Surface Papilloma Squamous cell carcinoma
Glandular Adenoma Adenocarcinoma
Connective tissue
Fibrous Fibroma Fibro sarcoma
Adipose Lipoma Liposarcoma
Cartilage Chondroma Chondrosarcoma
Bone Osteoma Osteosarcoma
Blood vessels Hemangioma Hemangiosarcoma
Lymph Vessels Lymphangioma Lymphangiosarcoma
Muscle tumors
Smooth Leiomyoma Leiomyosarcoma
Striated Rhabdomyoma Rhabdomyosarcoma
Nerve Cell Tumors
Nerve cell Neuroma
Glial tissue Glioma
Hematologic tumors
Granulocytic Myelocytic leukemia

Erythrocytic Erythroleukemia
Plasma Cell Multiple Myeloma
Lymphoid Lymphocytic
leukemia
 Causes of Cancer
 Chemical agents such as tobacco smoke,
asbestos, & coal dust account for about 75% of
cancers
 Physical and Environmental factors
Radiation
Exposure to irritants and pollutants
Exposure to sunlight
 Viruses & bacteria
DNA viruses- Hepa B, Herpes, EBV,
CMV, Papilloma Virus
RNA Viruses- HIV,
Bacterium- H. pylor
 Cont…
 Genetic and family history
Colon cancer
Breast cancer
 Dietary habits includes Low-Fiber,
High-fat, processed foods & alcohol
 Carcinogenesis
 Carcinogens cause mutations in cellular
DNA.
 Malignant transformation, or
carcinogenesis, is thought to be at least
a three-step cellular process, involving:
 Initiation,
 Promotion
 Progression
 Carcinogenesis
 Initiation
 Mutation of genetic structure
 Has potential to develop into clone of neoplastic
cells
 Promotion
 Characterized by the increased proliferation of
altered cells
 Latent period
• Initial genetic alteration to clinical evidence of cancer
 Progression
 Characterized by increased growth rate of tumor
as well as its invasiveness and metastatic
Process of Cancer Development
Characteristics of Cancer Cells
 Vary in size and shape
 Aren’t encapsulated
 Undergo abnormal mitosis
 Function abnormally
 Don’t resemble their cells of origin
 Produce substances rarely associated
with the original cell or tissue
 Can spread to other sites.
Signs & symptoms of cancer
 Change in bowel/bladder function
 Sores that do not heal
 Unusual bleeding or discharge
 Thickening or lump in breast or other
body parts
 Indigestion or difficulty in swallowing
 Recent change in a wart or mole
 Nagging cough or hoarseness