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1. What is the cancer?
2. How would you define cancer?
3. Multiple changes lead to cancer.
4. Loss of normal growth control.
5. Naming cancers.
6. Characters of cancer cells.
7. Malignant Versus benign Tumors.
8. Why cancer is potentially dangerous?
9. Metastasis.
10.Quiz.
To understand the origin of cancer and what is
meaning.
Cancer is a disease that begins when a
single cell escapes from the regulation of its
own division.
•A collection of different diseases
•Cancers display uncontrolled growth
•Metastasis=Migration from the site of origin
How would you define cancer?
Cancer=malignant growth
Malignant=ability of growth to migrate and invade surrounding tissues
Neoplasm=new growth
Tumor=benign (harmless) and malignant growths
Multiple changes lead to cancer
1. Requires multiple exposures to chemicals or radiation,
leading to changes in DNA
2. Cell can't repair some damage
3. Cell can commit suicide (programmed cell death) if
badly damaged
4. Cancers except leukemia associated with age
Carcinomas, the most common types of cancer, arise from the cells that cover
external and internal body surfaces. Lung, breast, and colon are the most frequent
cancers of this type in the United States.
Sarcomas are cancers arising from cells found in the supporting tissues of the body
such as bone, cartilage, fat, connective tissue, and muscle.
Lymphomas are cancers that arise in the lymph nodes and tissues of the body’s
immune system.
Leukemias are cancers of the immature blood cells that grow in the bone marrow
and tend to accumulate in large numbers in the bloodstream.
Cancer can originate almost anywhere in the
body:
Some common sarcomas:
Fat
Bone
Muscle
Lymphomas:
Lymph nodes
Leukemias:
Bloodstream
Lung
Breast (women)
Colon
Bladder
Prostate (men)
Some common carcinomas:
Loss of Normal Growth Control
Cancer arises from a loss of normal growth control. In
normal tissues, the rates of new cell growth and old cell
death are kept in balance. In cancer, this balance is
disrupted. This disruption can result from uncontrolled
cell growth or loss of a cell’s ability to undergo cell
suicide by a process called “apoptosis.” Apoptosis, or
“cell suicide,” is the mechanism by which old or damaged
cells normally self-destruct.
Cancer cell division
Fourth or later mutation
Third mutation
Second mutation
First mutation
Uncontrolled growth
Cell Suicide or Apoptosis
Cell damage— no repair
Normal cell division
Scientists use a variety of technical names to distinguish the many
different types of carcinomas, sarcomas, lymphomas, and leukemias.
In general, these names are created by using different Latin prefixes
that stand for the location where the cancer began its unchecked
growth. For example, the prefix “osteo” means bone, so a cancer
arising in bone is called an osteosarcoma. Similarly, the prefix
“adeno” means gland, so a cancer of gland cells is called
adenocarcinoma--for example, a breast adenocarcinoma.
Naming Cancers
Prefix Meaning
adeno- gland
chondro- cartilage
erythro- red blood cell
hemangio- blood vessels
hepato- liver
lipo- fat
lympho- lymphocyte
melano- pigment cell
myelo- bone marrow
myo- muscle
osteo- bone
Cancer Prefixes Point to Location
Characters of Cancer Cells:
1. divide when they shouldn’t
2. don’t cooperate
3. don’t respond to normal signals
4. don’t do their specialized job
5. migrate away from their original site
6. enter the blood stream
7. move to other parts of the body
Growth of a tumor depends on:
1.Nutrients
2. Blood supply
Survival of cancer cells depends on:
1. Escaping detection
2. Finding fertile ground to migrate to
Depending on whether or not they can spread by invasion and
metastasis, tumors are classified as being either benign or
malignant. Benign tumors are tumors that cannot spread by invasion
or metastasis; hence, they only grow locally. Malignant tumors are
tumors that are capable of spreading by invasion and metastasis. By
definition, the term “cancer” applies only to malignant tumors.
Malignant versus Benign Tumors
Malignant (cancer) cells invade neighboring tissues, enter blood vessels, and metastasize to different sites
Time
Benign (not cancer) tumor cells grow only locally and cannot spread by invasion or metastasis
Why Cancer Is Potentially Dangerous?
A malignant tumor, a “cancer,” is a more serious health problem than
a benign tumor because cancer cells can spread to distant parts of the
body. For example, a melanoma (a cancer of pigmented cells) arising
in the skin can have cells that enter the bloodstream and spread to
distant organs such as the liver or brain. Cancer cells in the liver
would be called metastatic melanoma, not liver cancer. Metastases
share the name of the original (“primary”) tumor. Melanoma cells
growing in the brain or liver can disrupt the functions of these vital
organs and so are potentially life threatening.
Melanoma cells travel through bloodstream
Melanoma (initial tumor)
Brain
Liver
Cells from the original tumor can break away and start
new cancers at distant locations, a process called
metastasis
Metastasis
Cancer cells can travel virtually anywhere in the body via
the lymphatic and circulatory systems. The lymphatic
system collects fluids lost from microscopic blood vessels
called capillaries. Some blood is lost from the thin walls
of the capillaries; the lymphatic system collects the lost
fluids (called lymph) and returns them to the blood. Lymph
nodes are small ducts that filter the lymph.
1. Cancer display controlled growth.
2. Malignant ability of growth to migrate and invade
surrounding tissues.
3. All types of cancer associated with age.
4. Loss of cell suicide ability related to cancer
progression.
5. Myocarcinoma related to liver cancer.
6. survival of cancer cells depends on blood supply.
7. Cancer cells can travel any where in the body via
circulatory and excretory systems.
1. Plasma Membrane
2. Nucleus
3. Cytoplasm
4. Mitochondria
5. Cytoskeleton
6. Extracellular matrix/cell junctions
To understand what goes wrong in a cancer cell, we
need to know more about the structure and function
of normal cells. In today's class we will review
some basic cell biology and point out some of
changes that occur in cancer cells.
Plasma membrane
Normal cell Cancer cell
Let nutrients and oxygen in,
wastes out
Same as normal cell
Receive/send signals to other cells Incorrectly process signals/send
wrong signals
1. forms boundary of cell
2. critical for receiving signals from outside cell and deciding
what enters cell.
3. phospholipid bilayer
4. contains embedded proteins, such as receptors
Nucleus
Nucleus = membrane bound organelle that contains the
genetic material. Changes in appearance when cell
divides.
Normal cell Cancer cell
Nucleus contains genes Some of the genes are "mutated"
Nucleus directs cell to make
proteins
DNARNA protein
Mutated genes in the nucleus
direct synthesis of altered
proteins
Nucleus receives chemical signals
from cytoplasm that alter gene
expression
Cancer cell nucleus receives the
wrong signals; tell cell to divide
or to turn on inappropriate genes
Cytoplasm
Consists of fluid (cytosol), proteins, ribosomes (sites of
protein synthesis), and membrane bound organelles
Organelles include
•Mitochondria: Energy metabolism
•Endoplasmic reticulum and Golgi body: Protein
processing
•Lysosomes: Degration of organelles and proteins
Mitochondria
Mitochondria = organelles involved in energy
metabolism and cell death
Normal cell Cancer cell
Efficiently make ATP, the energy
storing molecule
Hog ATP and starve out normal
cells
Old cells receive a signal to die
so they are replaced by new cells
Old cells not told to die; get too
many cells cancer
Cytoskeleton:
cytoskeleton=Network of fibers throughout the cytoplasm
Made of filamentous proteins: tubulin, actin, keratin
1. Provide structural support
2. Determine cell shape
3. Involved in cell movement
4. Anchor cell-cell connections
5. Move organelles around
6. Move chromosomes during cell division
Normal cell Cancer cell
Predetermined cell shape Become metastatic, able to
change shape and migrate
from original site
Divide in response to
normal signals
Cell division not regulated
Extracellular matrix/cell junctions
ECM=material outside cell that holds cell in place yet allows for
movement of nutrients, oxygen, and signaling molecules.
Includes a lot of "sticky proteins" (collagen, proteoglycan,
fibronectin).
Normal cell Cancer cell
Cells stay put Cells migrate away
Cells anchored to ECM Secrete enzymes that break
down ECM
Intercellular junctions
1. Hold cells together
2. Some allow communication between cells
3. Some prevent fluid from seeping into tissues
4. Most common in epithelia
Normal cell Cancer cell
Cells attached to each other Cells lose their attachments
Cell communication good Cell communication reduced
1. ……………….…………..……... directs cell to make proteins.
2. ……………….……….Let nutrients and oxygen in, wastes out.
3. …......… genes in the nucleus direct synthesis of altered
proteins.
4. …..………...efficiently make ATP, the energy storing molecule.
5. Cytoskeleton Made of filamentous proteins: ……….., …..…..,
………….…
1. Cancer detection and diagnosis.
2. Early cancer may not have any symptoms.
3. Biopsy.
4. Microscopic appearance of cancer cells.
5. Cancer classification.
6. Tumor grading.
7. Tumor staging.
Cancer Detection and Diagnosis
Detecting cancer early can affect the outcome of the disease for some
cancers. When cancer is found, a doctor will determine what type it is
and how fast it is growing. He or she will also determine whether
cancer cells have invaded nearby healthy tissue or spread
(metastasized) to other parts of the body. In some cases, finding
cancer early may decrease a person’s risk of dying from the cancer.
For this reason, improving our methods for early detection is
currently a high priority for cancer researchers.
Early Cancer May Not Have Any Symptoms
Some people visit the doctor only when they feel
pain or when they notice changes like a lump in
the breast or unusual bleeding or discharge. But
don’t wait until then to be checked because early
cancer may not have any symptoms. That is why
screening for some cancers is important,
particularly as you get older. Screening methods
are designed to check for cancer in people with
no symptoms.
Biopsy To diagnose the presence of cancer, a doctor must look at a sample of the affected
tissue under the microscope. Hence, when preliminary symptoms, Pap test,
mammogram, PSA test, FOBT, or colonoscopy indicate the possible existence of
cancer, a doctor must then perform a biopsy, which is the surgical removal of a
small piece of tissue for microscopic examination. (For leukemias, a small blood
sample serves the same purpose.) This microscopic examination will tell the doctor
whether a tumor is actually present and, if so, whether it is malignant (i.e., cancer)
or benign. In addition, microarrays may be used to determine which genes are
turned on or off in the sample, or proteomic profiles may be collected for an
analysis of protein activity. This information will help doctors to make a more
accurate diagnosis and may even help to inform treatment planning.
Patient’s tissue sample or
blood sample Genomic profile
Proteomic profile
Pathology
Microscopic Appearance of Cancer Cells
Cancer tissue has a distinctive appearance under the
microscope. Among the traits the doctor looks for are a
large number of irregularly shaped dividing cells, variation
in nuclear size and shape, variation in cell size and shape,
loss of specialized cell features, loss of normal tissue
organization, and a poorly defined tumor boundary.
Cancer classification
1. There are >100 different types of cancers.
2. Arise from abnormalities in cell growth and division.
3. Originate from different types of normal cells.
4. Vary in rates of growth and ability to spread.
Classification of cancers based on cell/tissue origin
Carcinomas: cancers of epithelial cells.
•Epithelia: cell that cover surfaces, for example skin, lining of digestive tract.
• Glands also are epithelia.
•Make up 90% of human cancers.
Sarcomas: tumors of connective tissues.
•Connective tissues lie below epithelia and hold things together or
support the body.
• Some examples are muscle and bone.
•Cancers are rare, because these cells do not reproduce very often.
Leukemia's and Lymphomas: Cancers of blood cells.
1. Leukemias are cancers of circulating blood cells or stem
cells of the bone marrow.
2. Lymphomas are usually solid tumors in lymphatic
organs (system that cleanses the blood).
3. Comprise 8% of all human cancers.
Further classification of cancers
site of origin: lung, breast carcinomas.
cell type: squamous cell carcinoma: cancer of flat
epithelial cell.
Cancers of glands: prefix adeno- Example adenocarcinoma
Cancers of embryonic tissues: suffix -blastoma
Neuroblastoma: Childhood cancer of neurons.
Retinoblastoma: Childhood eye cancer.
Hyperplasia
Instead of finding a benign or malignant tumor, microscopic
examination of a biopsy specimen will sometimes detect a condition
called “hyperplasia.” Hyperplasia refers to tissue growth based on an
excessive rate of cell division, leading to a larger than usual number
of cells. Nonetheless, cell structure and the orderly arrangement of
cells within the tissue remain normal, and the process of hyperplasia
is potentially reversible. Hyperplasia can be a normal tissue response
to an irritating stimulus.
Hyperplasia Normal
Dysplasia
In addition to hyperplasia, microscopic examination of a biopsy
specimen can detect another type of noncancerous condition called
“dysplasia.” Dysplasia is an abnormal type of excessive cell
proliferation characterized by loss of normal tissue arrangement and
cell structure. Often such cells revert back to normal behavior, but
occasionally they gradually become malignant. Because of their
potential for becoming malignant, areas of dysplasia should be
closely monitored by a health professional. Sometimes they need
treatment.
Hyperplasia Mild dysplasia Normal
Carcinoma in Situ
The most severe cases of dysplasia are sometimes
referred to as “carcinoma in situ.” In Latin, the term “in
situ” means “in place,” so carcinoma in situ refers to an
uncontrolled growth of cells that remains in the original
location. However, carcinoma in situ may develop into an
invasive, metastatic malignancy and, therefore, is usually
removed surgically, if possible.
Mild dysplasia
Carcinoma in situ (severe dysplasia)
Cancer (invasive)
Normal Hyperplasia
Tumor Grading
Microscopic examination also provides information regarding the
likely behavior of a tumor and its responsiveness to treatment.
Cancers with highly abnormal cell appearance and large numbers of
dividing cells tend to grow more quickly, spread to other organs
more frequently, and be less responsive to therapy than cancers
whose cells have a more normal appearance. Based on these
differences in microscopic appearance, doctors assign a numerical
“grade” to most cancers. In this grading system, a low number grade
(grade I or II) refers to cancers with fewer cell abnormalities than
those with higher numbers (grade III, IV).
General Relationship Between Tumor Grade and Prognosis
Patient Survival
Rate
Years
High grade
Low grade
100%
1 2 3 4 5
Tumor Staging After cancer has been diagnosed, doctors ask the following three
questions to determine how far the disease has progressed:
1. How large is the tumor, and how deeply has it invaded surrounding
tissues?
2. Have cancer cells spread to regional lymph nodes?
3. Has the cancer spread (metastasized) to other regions of the body?
Based on the answers to these questions, the cancer is assigned a
“stage.” A patient’s chances for survival are better when cancer is
detected at a lower stage.
Five-Year Survival Rates for Patients with Melanoma (by stage)
Stage at Time of Initial Diagnosis
100%
50%
I II III
Clinical staging of cancer
Staging specific to particular types of cancer,
1. prostate cancer—Gleason system
2. lung cancer—Stages I-IV, now correlated with TNM staging
Universal system: "TNM system"
•Developed by US and International committees
•Based on 3 considerations
T = condition of primary tumor (values usually T1-T4)
N = extent of lymph node involvement (values N0-N2)
M = extent of distant metastasis (values M0 or M1)
25
26
Grade of tumor:
Refers to the degree of abnormality of cancer
cells compared with normal cells.
Based on microscopic examination of cancer
cells.
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Grades:
• Grade I: 75 : 100 % differentiation
• Grade II: 50 : 75 % differentiation • Grade III: 25 : 50 % differentiation • Grade IV: 0 : 25 % differentiation
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Stage of tumor:
Is a descriptor of how much the cancer has
spread.
It takes into:
1. The size of tumor.
2. How deep it has penetrated
3. How many lymph nodes it has
metastasized
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Stages: Stage 0: carcinoma in situ. Stage I: usually means a cancer is small and contained with in the organ it started in. Stage II: usually means the cancer is localized. Stage III: usually means the cancer is larger and their cells in the lymph nodes in the area. Stage IV: means that the cancer has spread from where it started to another body organ.
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TNM staging
TNM Staging is used for solid tumors is an acronym for the words Tumor, Nodes, and Metastases
• Tumor (T) refers to the primary tumor and carries a number
of 0 to 4.
• N represents regional lymph node involvement and can also
be ranked from 0 to 4.
• Metastasis is represented by the letter M, and is 0 if no
metastasis has occurred or 1 if metastases are present.
Example: TNM staging of colon cancer
Stage Survival rate (5 yr) T1N0M0
T2N0M0
~90%
T3N0M0 ~80%
T4N0M0 ~60-70%
T3N1M0 ~50%
T4N1M0 ~40%
For early stage: surgery usually leads to cure
For T3, T4, N1 or N2: radiation and/or chemotherapy useful in addition to surgery
M1 stage: No longer curable; treatments can prolong life
1) Detecting Cancer early can affect the outcome of the disease for
all cancers.
2) Carcinomas are cancers of epithelial cells.
3) Hyperplasia is an excessive rate of cell division leading to a
larger than usual number of cells.
4) Carcinoma in situ refers to a controlled growth of cells that
remains in the original location.
5) Grade III refers to Cells with fewer abnormalities than grade I.
1. What Causes of Cancer ?
2. Population based studies.
3. Heredity? Behavior? Other factors.
4. Tobacco use and cancer.
5. Low strength radiation.
6. High strength radiation.
7. Lag time.
8. Viruses.
9. Bacteria and stomach cancer.
10. Heredity and Cancer .
11. Genetic testing.
12. Cancer risk and aging.
What Causes Cancer?
Heredity Diet
Hormones
Radiation Some chemicals
Cancer is often perceived as a disease that strikes for no
apparent reason. While scientists don’t yet know all the
reasons, many of the causes of cancer have already been
identified. Besides intrinsic factors such as heredity, diet,
and hormones, scientific studies point to key extrinsic
factors that contribute to the cancer’s development:
chemicals (e.g., smoking), radiation, and viruses or
bacteria.
Population-Based Studies
One way of identifying the various causes of cancer is by studying
populations and behaviors. This approach compares cancer rates
among various groups of people exposed to different factors or
exhibiting different behaviors. A striking finding to emerge from
population studies is that cancers arise with different frequencies in
different areas of the world. For example, stomach cancer is
especially frequent in Japan, colon cancer is prominent in the United
States, and skin cancer is common in Australia. What is the reason
for the high rates of specific kinds of cancer in certain countries?
CANADA: Leukemia
Regions of Highest Incidence
BRAZIL: Cervical cancer
U.S.: Colon cancer
AUSTRALIA: Skin cancer
CHINA: Liver cancer
U.K.: Lung cancer
JAPAN: Stomach cancer
Heredity? Behaviors? Other Factors? In theory, differences in heredity or environmental risk factors might be
responsible for the different cancer rates observed in different countries.
Studies on people who have moved from one country to another suggest
that exposure to risk factors for cancer varies by geographic location. For
example, in Japan, the rate of colon cancer is lower, and the rate of
stomach cancer is higher, than in the United States. But this difference has
been found to gradually disappear in Japanese families that have moved to
the United States. This suggests that the risk of developing the two kinds
of cancer is not determined primarily by heredity. The change in risk for
cancer for Japanese families could involve cultural, behavioral, or
environmental factors predominant in one location and not in the other.
100
50
5 0
Stomach Cancer (Number of new cases per 100,000 people)
U.S. Japan Japanese families in U.S.
100
70
7
0
Colon Cancer (Number of new cases per 100,000 people)
U.S. Japan Japanese families in U.S.
Tobacco Use and Cancer Some Cancer-Causing Chemicals in Tobacco Smoke
Among the various factors that can cause cancer, tobacco smoking is
the greatest public health hazard. Cigarette smoke contains more
than two dozen different chemicals capable of causing cancer.
Cigarette smoking is the main cause of lung cancer and contributes
to many other kinds of cancer as well, including cancer of the
mouth, larynx, esophagus, stomach, pancreas, kidney, and bladder.
Current estimates suggest that smoking cigarettes is responsible for
at least one out of every three cancer deaths, making it the largest
single cause of death from cancer. Other forms of tobacco use also
can cause cancer. For example, cigars, pipe smoke, and smokeless
tobacco can cause cancers of the mouth.
Low-Strength Radiation Some atoms give off radiation, which is energy that travels through
space. Prolonged or repeated exposure to certain types of radiation
can cause cancer. Cancer caused by the sun’s ultraviolet radiation is
most common in people who spend long hours in strong sunlight.
Ultraviolet radiation from sunlight is a low-strength type of
radiation. Effective ways to protect against ultraviolet radiation and
to prevent skin cancer are to avoid going into strong, direct sunlight
and to wear protective clothing. Sunscreen lotions reduce the risk of
some forms of skin cancers.
Annual Sunshine (UV radiation)
Skin Cancer
Incidence
Most
Dallas
Pittsburgh
High
Detroit
Low Least
High-Strength Radiation
Increased rates of cancer also have been detected in people exposed
to high-strength forms of radiation such as X-rays or radiation
emitted from unstable atoms called radioisotopes. Because these two
types of radiation are stronger than ultraviolet radiation, they can
penetrate through clothing and skin into the body. Therefore, high-
strength radiation can cause cancers of internal body tissues.
Examples include cancer caused by nuclear fallout from atomic
explosions and cancers caused by excessive exposure to radioactive
chemicals.
Most
High
Low Least
X-ray Dose (atomic radiation)
Lag Time
Chemicals and radiation that are capable of triggering the
development of cancer are called “carcinogens.” Carcinogens act
through a multistep process that initiates a series of genetic
alterations (“mutations”) and stimulates cells to proliferate. A
prolonged period of time is usually required for these multiple steps.
There can be a delay of several decades between exposure to a
carcinogen and the onset of cancer. For example, young people
exposed to carcinogens from smoking cigarettes generally do not
develop cancer for 20 to 30 years. This period between exposure and
onset of disease is the lag time.
4000
3000
2000
1000
20-Year Lag Time Between Smoking and Lung Cancer
Cigarettes Smoked
per Person per Year
Lung Cancer Deaths (per 100,000 people)
Year
Lung cancer (men)
Cigarette consumption (men)
1900 1920 1940 1960 1980
150
100
50
Viruses In addition to chemicals and radiation, a few viruses also can trigger
the development of cancer. In general, viruses are small infectious
agents that cannot reproduce on their own, but instead enter into
living cells and cause the infected cell to produce more copies of the
virus. Like cells, viruses store their genetic instructions in large
molecules called nucleic acids. In the case of cancer viruses, some of
the viral genetic information carried in these nucleic acids is inserted
into the chromosomes of the infected cell, and this causes the cell to
become malignant.
Virus inserts and changes genes for cell growth
Cancer-linked virus
Examples of Human Cancer Viruses
Only a few viruses that infect human cells actually cause cancer.
Included in this category are viruses implicated in cervical cancer,
liver cancer, and certain lymphomas, leukemias, and sarcomas.
Susceptibility to these cancers can sometimes be spread from person
to person by infectious viruses, although such events account for
only a very small fraction of human cancers. For example, the risk of
cervical cancer is increased in women with multiple sexual partners
and is especially high in women who marry men whose previous
wives had this disease. Transmission of the human papillomavirus
(HPV) during sexual relations appears to be involved.
Viruses are not the only infectious agents that have been
implicated in human cancer. The bacterium Helicobacter
pylori, which can cause stomach ulcers, has been
associated with the development of cancer, so people
infected with H. pylori are at increased risk for stomach
cancer. Research is under way to define the genetic
interactions between this infectious agent and its host
tissues that may explain why cancer develops.
Bacteria and Stomach Cancer
H. pylori Patient’s tissue sample
Heredity and Cancer
Cancer is not considered an inherited illness because most cases of
cancer, perhaps 80 to 90 percent, occur in people with no family
history of the disease. However, a person’s chances of developing
cancer can be influenced by the inheritance of certain kinds of
genetic alterations. These alterations tend to increase an individual’s
susceptibility to developing cancer in the future. For example, about
5 percent of breast cancers are thought to be due to inheritance of
particular form(s) of a “breast cancer susceptibility gene.”
Inherited factor(s)
All Breast Cancer Patients
Other factor(s)
Heredity Can Affect Many Types of Cancer
Inherited mutations can influence a person’s risk of
developing many types of cancer in addition to breast
cancer. For example, certain inherited mutations have
been described that increase a person’s risk of
developing colon, kidney, bone, skin or other specific
forms of cancer. But these hereditary conditions are
thought to be involved in only 10 percent or fewer of
all cancer cases.
Genetic Testing Laboratory tests can determine whether a person carries some of the
genetic alterations that can increase the risk of developing certain
cancers. For example, women who inherit certain forms of a gene
called BRCA1 or BRCA2 have an elevated risk of developing breast
cancer. For women with a family history of breast cancer, taking
such a test may relieve uncertainty about their future risk. However,
the information obtained from genetic tests is often complex and
difficult to interpret. The decision to undergo genetic testing should
therefore be a personal, voluntary one and should only be made in
conjunction with appropriate genetic counseling.
Cancer Risk and Aging
Because a number of mutations usually must occur for cancer to
arise, the chances of developing cancer increase as a person gets
older because more time has been available for mutations to
accumulate. For example, a 75-year-old person is a hundred times
more likely to develop colon cancer than a 25-year-old. Because
people are living longer today than they did 50 or 100 years ago,
they have a longer exposure time to factors that may promote gene
changes linked to cancer.
400
300
200
100
Cancer Risk and Aging
Number of
Cancer Cases
(per 100,000
people)
Age of Person (in years)
Colon
Breast
0 20 40 60 80
1) Cigarette smoking is the main cause of only lung cancer.
2) UV. Radiation from sun light is a high strength type of radiation.
3) Lag time is the period between exposure and onset of disease.
4) Viruses are the only infections agents that have been implicated
in human cancer.
5) Developing of cancer related to accumulated further mutations
1. Cell Cycle
2. Cancer as error in controlling cell cycle
3. Growth of normal cells vs. cancer cells
4. Cell death pathways
What are the normal constraints on cell growth?
•hematopoietic (blood-forming) cells
•intestinal epithelia
•skin cells
Some cells divide continuously
•Epithelia of various types
•Some connective tissue cells
Some cells divide often
Some cells never divide in adults •Nerve cells
•Cardiac muscle
Cell Cycle
What happens when cells divide?
Interphase: Preparation for next cell division.
G1 Gap 1 can vary for different cells, cell growth occurs
S Synthesis phase DNA replication occurs
G2 Gap 2 cell growth occurs
Mitosis:
Cell division of somatic (body) cells.
Replicated chromosomes are equally distributed among two daughter cells.
Checkpoints
Before proceeding around the cell cycle, the cell checks its state
G1/G0 checkpoint:
Acts like a molecular switch to decide whether the cell proceeds through the cell
cycle.
If Rb has a phosphate group added to it, the cell cycle can move forward.
If Rb has the phosphate group removed, the cell stalls in G0 of the cell cycle
Assess whether nutrients and growth factors are available for
growth
Rb (retinoblastoma) protein and its metabolic state is involved in
decision:
G2/M checkpoint
Is all DNA replicated?
Is environment good?
Are conditions in the cell favorable?
p53 plays a critical role in checking for DNA damage
Mitotic metaphase checkpoint
Are chromosomes correctly aligned in center of the cell for cell
division?
Cancer as a defect in cell cycle control
Many tumor suppressor genes and oncogenes encode
proteins important for controlling the cell cycle.
The following examples show that.
Component Role in cell cycle Defect in cancer
PDGF (platelet derived
growth factor, encoded by
oncogene c-sis)
Regulates cell growth Signal cell to reenter
cell cycle when cell
should be quiescent
Rb (retinoblastoma, tumor
suppressor protein)
Needed for quiescence Cell can proceed
through cell cycle
p53 (tumor suppressor
protein)
Surveys for DNA damage,
triggers cell death if needed
Allows cell division to
proceed, often leading
to abnormal
chromosomes
Cyclin D (cyclins are
unstable proteins involved
in the cell cycle)
Helps cell proceed through
cell cycle
Unregulated cell growth
Growth of cells in culture as model for cancer.
"Normal cells" Tumor cells
After several cell divisions, cells become
quiescent
Cells continue to divide
Require growth factors to grow Reduced need for growth factors
Require surface to grow Become anchorage independent
Die after 50-100 divisions Cells become immortalized
Chromosome # mostly stable Chromosome # may vary--unstable
Other differences between normal cells and cancer cells observed
in animal studies of cancer (in vivo):
Observation* Normal cells Cancer cells (in vivo)
Protease secretion Low High
Secretion of angiogenic
factors
Low High
Can terminally
differentiate
Able Unable
Able to undergo
programmed cell death
Able Unable
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is genetically programmed cell death, which leads to
breakdown and disposal of cells
Morphologically, apoptosis is characterized by changes
in the cell membrane (with the formation of small bodies
known as “apoptotic bodies”), shrinking of the nucleus,
chromatin condensation, and fragmentation of DNA.
Macrophages other phagocytic cells recognize apoptotic
cells and remove them by phagocytosis without
inflammatory phenomena developing.
17 all rights preserved (C) Abou-Mesalam2008
18
Systems initiate apoptosis process
Fas system Tumer necrosis factor-α (TNF-α )
P53
all rights preserved (C) Abou-Mesalam2008 19
1) Cardiac muscle cells divide continuously.
2) During Gap2 phase , cell growth occurs.
3) If Rb protien has a Phosphate group add to it , the cell cycle can
move forward.
4) P53 protein is the product of Rb gene during translation.
5) Protease secretion is low by cancer cells in vivo.
1.Genes and Cancer.
2.DNA structure.
3.DNA mutations.
4.Oncogenes.
5.Tumor suppressor genes.
6.DNA repair genes.
7.Mutations and cancer.
Genes and Cancer Chemicals (e.g., from smoking), radiation, viruses, and heredity all
contribute to the development of cancer by triggering changes in a
cell’s genes. Chemicals and radiation act by damaging genes,
viruses introduce their own genes into cells, and heredity passes on
alterations in genes that make a person more susceptible to cancer.
Genes are inherited instructions that reside within a person’s
chromosomes. Each gene instructs a cell how to build a specific
product--in most cases, a particular kind of protein. Genes are
altered, or “mutated,” in various ways as part of the mechanism by
which cancer arises.
Chromosomes are DNA molecules
Heredity
Radiation Chemicals
Viruses
DNA Structure
Genes reside within chromosomes, the large DNA molecules, which
are composed of two chemical strands twisted around each other to
form a “double helix.” Each strand is constructed from millions of
chemical building blocks called “bases.” DNA contains only four
different bases: adenine, thymine, cytosine, and guanine (abbreviated
A, T, G, and C), but they can be arranged in any sequence. The
sequential order of the bases in any given gene determines the
message the gene contains, just as the letters of the alphabet can be
combined in different ways to form distinct words and sentences.
DNA molecule
Chemical bases
G C
T A
DNA Mutation
Genes can be mutated in several different ways. The
simplest type of mutation involves a change in a single
base along the base sequence of a particular gene--much
like a typographical error in a word that has been
misspelled. In other cases, one or more bases may be added
or deleted. And sometimes, large segments of a DNA
molecule are accidentally repeated, deleted, or moved.
Additions
Deletions
Normal gene
Single base change
DNA
C
T
A G C G A A C T A C
A G G C G C T A A C A C T
A G C T A A C T A C
A G A A C T A C
Oncogenes
One group of genes implicated in the development of
cancer are damaged genes, called “oncogenes.” Oncogenes
are genes whose PRESENCE in certain forms and/or
overactivity can stimulate the development of cancer.
When oncogenes arise in normal cells, they can contribute
to the development of cancer by instructing cells to make
proteins that stimulate excessive cell growth and division.
Mutated/damaged oncogene
Oncogenes accelerate cell growth and division
Cancer cell
Normal cell Normal genes regulate cell growth
Proto-Oncogenes and Normal Cell Growth
Oncogenes are related to normal genes called proto-oncogenes that
encode components of the cell’s normal growth-control pathway.
Some of these components are growth factors, receptors, signaling
enzymes, and transcription factors. Growth factors bind to receptors
on the cell surface, which activate signaling enzymes inside the cell
that, in turn, activate special proteins called transcription factors
inside the cell’s nucleus. The activated transcription factors “turn
on” the genes required for cell growth and proliferation.
Receptor
Normal Growth-Control Pathway
DNA
Cell proliferation
Cell nucleus
Transcription factors
Signaling enzymes
Growth factor
Oncogenes are Mutant Forms of Proto-Oncogenes
Oncogenes arise from the mutation of proto-oncogenes. They resemble proto-oncogenes in
that they code for the production of proteins involved in growth control. However,
oncogenes code for an altered version (or excessive quantities) of these growth-control
proteins, thereby disrupting a cell’s growth-signaling pathway.
By producing abnormal versions or quantities of cellular growth-control proteins, oncogenes
cause a cell’s growth-signaling pathway to become hyperactive. To use a simple metaphor,
the growth-control pathway is like the gas pedal of an automobile. The more active the
pathway, the faster cells grow and divide. The presence of an oncogene is like having a gas
pedal that is stuck to the floorboard, causing the cell to continually grow and divide. A
cancer cell may contain one or more oncogenes, which means that one or more components
in this pathway will be abnormal.
Cell proliferation driven by internal oncogene signaling
Transcription
Activated gene regulatory protein
Inactive intracellular signaling protein
Inactive growth factor receptor
Tumor Suppressor Genes
A second group of genes implicated in cancer are the “tumor suppressor genes.”
Tumor suppressor genes are normal genes whose ABSENCE can lead to cancer. In
other words, if a pair of tumor suppressor genes are either lost from a cell or
inactivated by mutation, their functional absence might allow cancer to develop.
Individuals who inherit an increased risk of developing cancer often are born with
one defective copy of a tumor suppressor gene. Because genes come in pairs (one
inherited from each parent), an inherited defect in one copy will not lead to cancer
because the other normal copy is still functional. But if the second copy undergoes
mutation, the person then may develop cancer because there no longer is any
functional copy of the gene.
Normal genes prevent cancer
Remove or inactivate tumor suppressor genes
Mutated/inactivated tumor suppressor genes
Damage to both genes leads to cancer
Cancer cell
Normal cell
Tumor Suppressor Genes Act Like a Brake Pedal
Tumor suppressor genes are a family of normal genes that instruct
cells to produce proteins that restrain cell growth and division. Since
tumor suppressor genes code for proteins that slow down cell growth
and division, the loss of such proteins allows a cell to grow and divide
in an uncontrolled fashion. Tumor suppressor genes are like the brake
pedal of an automobile. The loss of a tumor suppressor gene function
is like having a brake pedal that does not function properly, thereby
allowing the cell to grow and divide continually.
Tumor Suppressor Gene Proteins
DNA Cell nucleus
Signaling enzymes
Growth factor
Receptor
Transcription factors
Cell proliferation
p53 Tumor Suppressor Protein Triggers Cell Suicide
One particular tumor suppressor gene codes for a protein
called “p53” that can trigger cell suicide (apoptosis). In
cells that have undergone DNA damage, the p53 protein
acts like a brake pedal to halt cell growth and division. If
the damage cannot be repaired, the p53 protein eventually
initiates cell suicide, thereby preventing the genetically
damaged cell from growing out of control.
Normal cell Cell suicide
(Apoptosis)
p53 protein
Excessive DNA damage
DNA Repair Genes A third type of genes implicated in cancer are called “DNA repair genes.”
DNA repair genes code for proteins whose normal function is to correct
errors that arise when cells duplicate their DNA prior to cell division.
Mutations in DNA repair genes can lead to a failure in repair, which in turn
allows subsequent mutations to accumulate. People with a condition called
xeroderma pigmentosum have an inherited defect in a DNA repair gene. As
a result, they cannot effectively repair the DNA damage that normally
occurs when skin cells are exposed to sunlight, and so they exhibit an
abnormally high incidence of skin cancer. Certain forms of hereditary
colon cancer also involve defects in DNA repair.
Cancer
No cancer
No DNA repair
Normal DNA repair
Base pair mismatch
T C A T C
A G T C G
T C A G C
A G T C G
A G T G A G T A G
T C A T C T C A T C
Cancer Tends to Involve Multiple Mutations
Cancer may begin because of the accumulation of mutations involving
oncogenes, tumor suppressor genes, and DNA repair genes. For example,
colon cancer can begin with a defect in a tumor suppressor gene that
allows excessive cell proliferation. The proliferating cells then tend to
acquire additional mutations involving DNA repair genes, other tumor
suppressor genes, and many other growth-related genes. Over time, the
accumulated damage can yield a highly malignant, metastatic tumor. In
other words, creating a cancer cell requires that the brakes on cell growth
(tumor suppressor genes) be released at the same time that the accelerators
for cell growth (oncogenes) are being activated.
Malignant cells invade neighboring tissues, enter blood vessels, and metastasize to different sites
More mutations, more genetic instability, metastatic disease
Proto-oncogenes mutate to oncogenes
Mutations inactivate DNA repair genes
Cells proliferate
Mutation inactivates suppressor gene
Benign tumor cells grow only locally and cannot spread by invasion or metastasis
Time
Mutations and Cancer
While the prime suspects for cancer-linked mutations are the
oncogenes, tumor suppressor genes, and DNA repair genes, cancer
conspires even beyond these. Mutations also are seen in the genes
that activate and deactivate carcinogens, and in those that govern
the cell cycle, cell senescence (or “aging”), cell suicide (apoptosis),
cell signaling, and cell differentiation. And still other mutations
develop that enable cancer to invade and metastasize to other parts
of the body.
Cancer Tends to Corrupt Surrounding Environment
In addition to all the molecular changes that occur within a cancer
cell, the environment around the tumor changes dramatically as well.
The cancer cell loses receptors that would normally respond to
neighboring cells that call for growth to stop. Instead, tumors amplify
their own supply of growth signals. They also flood their neighbors
with other signals called cytokines and enzymes called proteases.
This action destroys both the basement membrane and surrounding
matrix, which lies between the tumor and its path to metastasis--a
blood vessel or duct of the lymphatic system.
Growth factors = proliferation
Blood vessel
Proteases
Cytokines
Matrix
Fibroblasts, adipocytes
Invasive
Cytokines, proteases = migration & invasion
1) Viruses damage genes by introduce their own genes to cells.
2) Mutations occurred only by additions of single bases.
3) Over activity of Oncogenes may stimulate the development of
cancer.
4) Tumor suppressor genes are normal genes whose absence can
lead to cancer.
5) P53 is oncogene can trigger cell suicide.
1. Cancer prevention.
2. Avoid Tobacco.
3. Protection from sun light.
4. Diet.
5. Avoiding cancer viruses.
6. Avoiding carcinogens.
7. Industrial pollution.
8. Is there a cancer “epidemic” ?
Cancer Prevention
Since exposure to carcinogens (cancer-causing agents) is
responsible for triggering most human cancers, people can
reduce their cancer risk by taking steps to avoid such
agents. Hence the first step in cancer prevention is to
identify the behaviors or exposures to particular kinds of
carcinogens and viruses that represent the greatest cancer
hazards.
Cancer viruses or bacteria
Carcinogenic radiation
Carcinogenic chemicals
Avoid Tobacco
As the single largest cause of cancer death, the use of tobacco
products is implicated in roughly one out of every three cancer
deaths. Cigarette smoking is responsible for nearly all cases of lung
cancer, and has also been implicated in cancer of the mouth, larynx,
esophagus, stomach, pancreas, kidney, and bladder. Pipe smoke,
cigars, and smokeless tobacco are risky as well. Avoiding tobacco is
therefore the single most effective lifestyle decision any person can
make in attempting to prevent cancer.
15x
10x
5x
Non-smoker Cigarettes Smoked per Day
Lung Cancer Risk Increases with Cigarette Consumption
0 15 30
Protect Yourself From Excessive Sunlight While some sunlight is good for health, skin cancer caused by
excessive exposure to sunlight is not among the sun’s benefits.
Because some types of skin cancer are easy to cure, the danger posed
by too much sunlight is perhaps not taken seriously enough. It is
important to remember that a more serious form of skin cancer,
called melanoma, is also associated with excessive sun exposure.
Melanomas are potentially lethal tumors. Risk of melanoma and
other forms of skin cancer can be significantly reduced by avoiding
excessive exposure to the sun, using sunscreen lotions, and wearing
protective clothing to shield the skin from ultraviolet radiation.
Limit Alcohol and Tobacco Drinking excessive amounts of alcohol is linked to an increased risk
for several kinds of cancer, especially those of the mouth, throat, and
esophagus. The combination of alcohol and tobacco appears to be
especially dangerous. For example, in heavy smokers or heavy
drinkers, the risk of developing cancer of the esophagus is roughly 6
times greater than that for nonsmokers/nondrinkers. But in people
who both smoke and drink, the cancer risk is more than 40 times
greater than that for nonsmokers/nondrinkers. Clearly the
combination of alcohol and tobacco is riskier than would be expected
by just adding the effects of the two together.
40x
30x
20x
10x
Alcoholic Drinks Consumed per Day
Packs of Cigarettes Consumed per Day
Combination of Alcohol and Cigarettes Increases Risk for Cancer of the Esophagus
Risk Increase
AND
Diet: Limit Fats and Calories
Studies suggest that differences in diet may also play a role in
determining cancer risk. Unlike clear-cut cancer risk factors such as
tobacco, sunlight, and alcohol, dietary components that influence
cancer risk have been difficult to determine. Limiting fat
consumption and calorie intake appears to be one possible strategy
to decrease risk for some cancers, because people who consume
large amounts of meat, which is rich in fat, and large numbers of
calories exhibit an increased cancer risk, especially for colon
cancer.
0
Number of Cases (per 100,000
people)
Grams (per person per day)
Correlation Between Meat Consumption and Colon Cancer Rates in Different Countries
40
30
20
10
300 200 100 80
Diet: Consume Fruits and Vegetables
In contrast to factors such as fat and calories, which appear to
increase cancer risk, other dietary components may decrease cancer
risk. The most compelling evidence has been obtained for fruits and
vegetables, whose consumption has been strongly correlated with a
reduction in cancer risk. Although the exact chemical components in
these foods that are responsible for a protective effect are yet to be
identified, eating five to nine servings of fruits and vegetables each
day is recommended by many groups.
Avoid Cancer Viruses Actions can also be taken to avoid exposure to the small number of
viruses that have been implicated in human cancers. A good
example is the human papillomavirus (HPV). Of the more than 100
types of HPVs, over 30 types can be passed from one person to
another through sexual contact. Among these, there are 13 high-risk
types recognized as the major cause of cervical cancer. Having
many sexual partners is a risk factor for infection with these high-
risk HPVs, which can, in turn, increase the chance that mild cervical
abnormalities will progress to more severe ones or to cervical
cancer.
Noninfected women
HPV Infection Increases Risk for Cervical Cancer
Cervical Cancer
Risk
Low
High
Women infected with
HPV
Because people spend so much time at work, potential
carcinogens in the work environment are studied carefully.
Some occupational carcinogens have been identified
because coworkers exposed to the same substances have
developed a particular kind of cancer at increased
frequency. For example, cancer rates in construction
workers who handle asbestos have been found to be 10
times higher than normal.
Avoid Carcinogens at Work
Avoid Carcinogens at Work
Industrial Pollution
The fact that several environmental chemicals can cause cancer has
fostered the idea that industrial pollution is a frequent cause of
cancer. However, the frequency of most human cancers (adjusted for
age) has remained relatively constant over the past half-century, in
spite of increasing industrial pollution.
So, in spite of evidence that industrial chemicals can cause cancer in
people who work with them or in people who live nearby, industrial
pollution does not appear to be a major cause of most cancers in the
population at large.
1930
Incidence of Most Cancers
Year
1990 1970 1950
Is There a Cancer "Epidemic"?
A common misconception arises from news stories suggesting we are
experiencing a cancer “epidemic.” This only appears to be the case because the
number of new cancer cases reported is rising as the population as a whole is
aging, and older people are more likely to develop cancer. However, this trend is
offset by the number of new births, which is also increasing, and cancer is rare
among the young. So as more and more members of a 75-million-strong “baby-
boomer” cohort begin shifting en masse to older, more cancer-prone ages, the
number of new cancer cases is expected to increase in the next several decades.
But since the birth rate is also expected to increase, the cancer rate may either
stay the same or, perhaps, decline.
1. Progression toward metastatic cancer
2. Role of the circulatory system
3. Soil and seed hypothesis
4. Angiogenesis
Although tumors in situ are usually easily treated with
surgery, Cancer in its metastatic form is often lethal. In
metastasis, cells from the primary tumor break off and
travel to distant parts of the body, including lymph nodes
and other body organs, such as the lung, liver, bone or
brain. In today’s lecture we will discuss mechanisms
tumors use to grow larger and metastasize.
Progression toward metastatic cancer
loosening of intracellular connections
Cell-Cell adhesion mediated by interactions at the surfaces of
cells.
Protein receptors on the surface that interact with similar (homotypic)
or different (heterotypic) receptors on the surface of other cells or
that interact with the extracellular matrix. Act as tumor suppressors
•Integrins
•Cadherins
•Selectins
•Immunoglobulin family
Example:
that mediates communication between a cell
adhesion protein (E-cadherin) and the cytoskeleton
is important for hereditary colon cancer
(adenomatous polyposis coli). May also be a
transcription factor.
Secretion of proteases
Proteases—Enzymes that break down other proteins.
Proteases released by the cell break down proteins that attach cells
together on the outside and on basement membranes, to free cells of
their normal constraints.
Some cells secrete inhibitors (TIMPs=tissue inhibitors of
metalloproteinases); these bind to metalloproteinases and are
associated with decreased metastatic potential.
Extravasion=Escape of cancer cells from the blood vessel.
Involves attachment to the endothelial lining,cancer cell
attachment to and destruction of the basement membrane,
migration into the tissue (often referred to as stroma).
Intravasion=Process of invading blood vessels. Involves attachment
of cancer cells to blood vessel basement membrane, protease
digestion of basement membrane, and migration of cells into blood
stream.
Migration of cancer cells to new site
Requires
1.proteases to digest matrix
2.alternate attachment/detachment of cell
3.signaling from cell surface to trigger
changes in the cytoskeleton
4.“motility factors”
Angiogenesis
Growth and development of blood vessels
Cancer cells need blood vessels in the area or they will starve when the tumor
gets large.
Cancers >1 mm in diameter need blood vessels.
Cancer cells secrete growth factors that attract blood vessels.
+ growth factors for angiogenesis (these help
blood vessels form in tumors)
- growth factors for angiogenesis
(these might serve as anti-tumor drugs)
PDGF
VEGF (vascular endothelial growth factor)
FGF (fibroblast growth factor)
TGF and (transforming growth factor)
angiogenin
thrombospondin (p53 regulates)
angiostatin
endostatin
interferons
TIMPs (inhibitors of metalloproteases)
Genetic instability
Can include:
Loss of chromosomes: visible under microscope
Deletion: loss of some part of a chromosome
Duplications: extra copy of part of the chromosome
Rearrangements and translocations: segments of chromosomes
get moved to another place.
Gene amplification: many copies are made of one region of the
chromosome.
Role of the circulatory system in cancer Circulatory system is a network of blood vessels and the heart,
which acts as pump.
Serves as way of carrying nutrients to all parts of the body and
removing wastes.
Tumors develop blood vessels to provide them with nutrients.
Tumor cells escape their normal tissues and can move in the body
through the blood vessels.
The trip through the circulatory system puts cancer cells in close
range of the immune system; only 1 in 10,000 cells complete the trip.
Secondary tumors often form in the lung or the liver, sites of capillary
beds (small blood vessels). The cancer cells may get stuck in the blood
vessels or may move from the capillaries to surrounding tissues and
start a new growth.
The lymphatic system, which filters the blood, is also often a site of
metastasis as cancer cells can get trapped in the dense lymph nodes
Soil and seed hypothesis
Some primary tumors metastasize often to particular sites.
For example, prostate cancer often metastasizes to bone.
To explain the link between the sites, there is the "soil and seed"
hypothesis.
The idea is that the distant site has a receptor or binding site for a
protein on the surface of the tumor cell. To put it another way, the
distant site provides fertile soil for the growth of the cancer "seed".
. The tumor cell binds to the distant site and begins to grow and
reproduce into a secondary tumor
To further explore this idea, Ruoslahti and others are trying to
identify proteins on the surfaces of cells that specify their "molecular
address", the place in the body they are destined for. Until this is
understood for normal cells, it will be difficult to determine whether
the "soil and seed" hypothesis is a reasonable idea to explain the
behavior of cancer cells.
Process of angiogenesis (blood vessel
development)
1) Proteases enzymes breaks proteins .
2) Angiogenesis is growth and development of blood vessels
specific for cancer cells only.
3) VEGF is a growth factor stimulate angiogenesis.
4) Tumors develop blood vessels to provide them with nutrients.
5) Soil and seed hypothesis isn't able to explain behavior of cancer
cells
1.Cancer treatments.
2.Surgery.
3.Chemotherapy.
4.Radiotherapy.
4
Cancer can be treated by surgery, chemotherapy,
radiation therapy, immunotherapy, monoclonal
antibody therapy or other methods.
The choice of therapy depends upon
1. the location
2. grade of the tumor and the stage of the disease
3. the general state of the patient (performance
status).
5
• Surgery.
• Chemotherapy.
• Radiation therapy Traditional Therapies
• Immune therapy.
• Gene therapy.
• Stem cell therapy.
• Nanotechnology tumor therapy.
New Therapies
6
Prevention
Diagnosis
Treatments
Aims Of Surgery
What is chemotherapy?
Chemotherapy (also called chemo) is a type
of cancer treatment that uses drugs to destroy
cancer cells.
Cancer Chemotherapy
Antineoplastic
Cytotoxic
11
How does chemotherapy work?
Chemotherapy works by stopping or slowing the growth
of cancer cells, which grow and divide quickly. But it can
also harm healthy cells that divide quickly, such as those
that line your mouth and intestines or cause your hair to
grow. Damage to healthy cells may cause side effects.
Often, side effects get better or go away after
chemotherapy is over.
What does chemotherapy do?
Depending on your type of cancer and how advanced it
is, chemotherapy can:
Cure cancer - when chemotherapy destroys cancer cells to the point that
your doctor can no longer detect them in your body and they will not grow
back.
Control cancer - when chemotherapy keeps cancer from spreading, slows
its growth, or destroys cancer cells that have spread to other parts of your
body.
Ease cancer symptoms (also called palliative care) - when chemotherapy
shrinks tumors that are causing pain or pressure.
How is chemotherapy used? Sometimes, chemotherapy is used as the only cancer treatment. But more often,
you will get chemotherapy along with surgery, radiation therapy, or biological
therapy. Chemotherapy can:
1. Make a tumor smaller before surgery or radiation therapy. This is called neo-
adjuvant chemotherapy.
2. Destroy cancer cells that may remain after surgery or radiation therapy. This
is called adjuvant chemotherapy.
3. Help radiation therapy and biological therapy work better.
4. Destroy cancer cells that have come back (recurrent cancer) or spread to other
parts of your body (metastatic cancer).
How is chemotherapy given?
Injection. The chemotherapy is given by a shot in a
muscle in your arm, thigh, or hip or right under the skin in
the fatty part of your arm, leg, or belly.
Chemotherapy may be given in many ways:
Intra-arterial (IA). The chemotherapy
goes directly into the artery that is
feeding the cancer.
Intraperitoneal (IP). The chemotherapy goes directly into the
peritoneal cavity (the area that contains organs such as your
intestines, stomach, liver, and ovaries).
Intravenous (IV). The chemotherapy
goes directly into a vein.
Topically. The chemotherapy comes in a cream that you rub onto
your skin.
Orally. The chemotherapy comes in pills, capsules, or liquids that
you swallow.
What are side effects?
Side effects are problems caused by cancer
treatment. Some common side effects from
chemotherapy are fatigue, nausea, vomiting,
decreased blood cell counts, hair loss, mouth
sores, and pain.
What causes side effects?
Chemotherapy is designed to kill fast-growing cancer
cells. But it can also affect healthy cells that grow
quickly. These include cells that line your mouth and
intestines, cells in your bone marrow that make blood
cells, and cells that make your hair grow. Chemotherapy
causes side effects when it harms these healthy cells.
Side Effects
1. Anemia
2. Appetite changes
3. Bleeding
4. Constipation
5. Diarrhea
6. Fatigue
7. Hair loss
8. Infection
9. Infertility
10. Mouth and throat changes
11. Nausea and vomiting
12. Nervous system changes
13. Pain
14. Sexual changes
15. Skin and nail changes
16. Urinary, kidney, and bladder changes
Chemotherapeutic Drugs Groups
Alkylating Agents:
Nitrosoureasm
Antimetabolites
Anthracyclines and Related Drugs
Topoisomerase Inhibitors
Mitotic Inhibitors
Miscellaneous Chemotherapy Drugs
•Radiation uses high energy x-rays, electron
beams or radioactive isotopes for damaging or
destroying malignant cancer cells.
•The main objective is destroying cancer cells
with minimum injury to normal tissue and
organ.
•There are two types of radio therapy:
External Internal
Internal radiation therapy (also called
brachytherapy)
uses radiation that is placed very close to or inside the
tumor. The radiation source is usually sealed in a small
holder called an implant. Implants may be in the form of
thin wires, plastic tubes called catheters, ribbons, capsules,
or seeds. The implant is put directly into the body. Internal
radiation therapy may require a hospital stay.
External radiation therapy
usually is given on an outpatient basis; most patients do
not need to stay in the hospital. External radiation therapy
is used to treat most types of cancer, including cancer of
the bladder, brain, breast, cervix, larynx, lung, prostate,
and vagina. In addition, external radiation may be used to
relieve pain or ease other problems when cancer spreads
to other parts of the body from the primary site
What are the sources of energy for external
radiation therapy?
X-rays or gamma rays, which are both forms of electromagnetic
radiation. Although they are produced in different ways, both use
photons (packets of energy).
Particle beams use fast-moving subatomic particles instead of
photons. This type of radiation may be called particle beam
radiation therapy or particulate radiation.
Types of Radiation Used to Treat Cancer
Ionizing radiation used in two major
types:
X-rays
Gamma rays
Electrons
Protons
Neutrons
Alpha and Beta
Particles
The most common types of radiation Used
in cancer treatments:
Terminal differentiation
Apoptosis
Necrosis
1) Location isn't play role in determination of treatment of cancer
2) Surgery used in prevention and diagnosis of cancer beside
treatment.
3) Cytotoxic chemotherapeutic drugs used in killing cancer cells.
4) There isn't any effect on blood from chemotherapy.
5) Radiation cause necrosis of cancer cell.