all lecturer of cancer dr faten zahran

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.


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


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


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).


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


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)

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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

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.

all lecturer of cancer dr faten zahran

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