Cancer is the uncontrolled growth of abnormal cells in the body. Cancerous cells are also called malignant cells.

Exposure to Benzene Excessive consumption of alcohol Environmental Toxins Excessive sunlight exposure Genetic problems Obesity Radiation Viruses Unknown Causes

For Men:
Prostate Lung Colon

For Women:
Breast Colon Lung

Brain Cervical Hodgkins Lymphoma Kidney Leukemia Liver Uterine

Non-Hodgkins Lymphoma Ovarian Skin Testicular Thyroid Many more..

 The symptoms of Cancer depends on the type and the location. Example: lung cancer can cause coughing, shortness of breath, or chest pain.

 Cancer grows out of normal cells in the body. Normal cells multiply when the body needs them, and die when the body doesn't need them. Cancer appears to occur when the growth of cells in the body is out of control and cells divide too quickly. Cancer also occurs when cells forget how to die.

 A cell may instruct other cells near it to divide, for

example, by releasing a growth factor.

There are varieties of backup mechanisms to prevent

the cell from dividing uncontrollably.

In order for a cell to become cancerous, every one of

the backup mechanisms should fail.

3-7 different mutations are present for a cell to

become cancerous and may take many years to happen

 When a growth factor message reaches the

cell nucleus, it activates genes called protooncogenes which produces proteins to stimulate the cell to divide.
When a proto-oncogene mutates, it becomes

an oncogene - gene which instructs the cell to grow rapidly and divide repeatedly without instructions from neighboring cells.

 When a runaway cell division occurs, it does not

necessarily lead to cancer. Neighboring cells respond by releasing a growth inhibitor.

This growth inhibitor activates tumor suppresor

genes. When activated, these genes halt the cell cycle, preventing further cell division.
When this gene is mutated, however, the rapidly

dividing cell ignores messages from its neighbors to stop dividing.

 A cell cycle clock is a group of proteins found in the

nucleus. It interprets incoming messages at several checkpoints in the cell division cycle.
If cell conditions are right during the checkpoint,

this clock activates certain proto-oncogenes to continue with the cycle, otherwise, tumor suppresor genes are activated.
If the cell cycle clock detects DNA damage in a cell,

a tumor suppressor gene called p53 prevents the cell from reproducing until the damage is repaired.

 If the cell is unable to repair DNA damage, p53

instructs the cell to undergo programmed cell death, or apoptosis, putting a stop to cell division before is starts.
When mutated, p53 allows a cell to continue to

divide, even with damaged DNA. This, in turn, can further lead to mutations on proto-oncogenes and tumor suppressor genes.

 The life span of a cell is controlled by telomeres -

protective segments at the ends of the cells DNA.

Telomeres shorten with each cell division until they

can no longer protect the DNA. At this point, cell division severely damages the DNA, ultimately killing the cell and ensuring that older cells, which may have had mutations, no longer reproduce.
Cancer cells escape this protective mechanism by

producing a protein called telomerase. Telomerase extends the length of telomeres, rendering the cells immortal and capable of never-ending cell division.

 Normal cells adhere to each other and to a fibrous

meshwork called an extracellular matrix.

While a normal cell will often die if it cannot adhere

to an extracellular matrix, cancer cells survive without this matrix.

A tumor is a mass of cells not dependent upon an

extracellular matrix.
Often a tumor develops its own network of tiny

blood vessels to supply itself with nutrient-rich blood, a process called angiogenesis.

 Two general types of tumors: benign and malignant. Benign tumors do not invade other tissues and are limited

to one site, making surgical removal possible and the odds for a full recovery excellent.
Malignant tumors extend into neighboring tissue or travel

to distant sites, forming secondary growths known as metastases.

To metastasize, tumor cells break through a nearby blood

vessel to enter the circulatory system or through a lymphatic vessel wall to enter the lymphatic system.

 3000 BC Earliest written record about cancer Edwin Smith Papyrus Explained breast cancer Hippocrates (460 BC 370 BC) Explained some kinds of cancer Greek word carcinos (crab or crayfish) Appearance of the cut surface of cancerous tumor- veins stretched on all sides resemble a crab

 Celsus (25 BC 50 AD) Translated carcinos into the Latin cancer (crab) Surgery as treatment for cancer Galen (2nd century AD) Opposed to the use of surgery Purgatives

 15th, 16th, and 17th centuries Bodies were dissected to discover the cause of death Wilhelm Fabry Milk clot in mammary duct was the cause of breast cancer. Francois de la Boe Sylvius Acidic lymph was the cause of cancer.

 Nicolaes Tulp Cancer was a poison that spreads gradually. Contagious John Hill Tobacco snuff was the cause of nose cancer (1761). Percivall Pott Cancer of the scrotum was widespread among chimney sweeps.

 18th Century Campbell De Morgan Determined that cancer spread from the primary tumor to the lymph nodes and to the other sites of the body.

 Mayumi gave birth to Emiko

On December 2005 Normal pregnancy and normal birth

After 36 days of giving birth.....

Heavy vaginal bleeding Blood tested acute lymphoblastic leukemia (ALL)

 Malignant proliferation of lymphoid cells blocked at an early stage of differentiation (Conter et al. 2004)

Originate from mutations in blood-progenitor cells that are destined to differentiate in the Tcell or B-cell pathway (Pui et al. 2008)

 In adults, ALL is usually caused by a chromosomal translocation between 9 and 22, or the Philadelphia chromosome (Pui et al. 2008)

 Emikos DNA was sequenced

Mayumi succumbs to the cancer

January 2006

Hideo takes Emiko back to the hospital

October 2006 Lungs with fluid and large red mass on her right cheeks

 Doctors diagnosed Emiko of having sarcoma

But when the doctors looked at her DNA sequences.......

Philadelphia translocation had occured Conclusion: Emiko and her mother have the same type of cancer

 blood spot card from her birth indicates that Emiko had the cancer already at birth Only the cancer cells had the Philadelphia translocation Emikos cancerous cheek cells came purely from her mother

 The placenta and the babys immune system supposedly counteract all foreign cells. They do this through the MHC (major histocompatibility complex)

A type of cell surface molecule Found in all vertebrates In humans, found in chromosome 6 Has many varieties within every individual and between individuals
Polygenic Polymorphic

 Fights off pathogens

Uniqueness of each MHC protein targets specific pathogens, making them collectively effective

Allows cells to distinguish between the cells of the individual and any foreigners
Reason the body rejects transplanted organs

May also help in sexual selection (GarverAgpar, et.al., 2006)

 It was discovered that Emiko's cancer cells (and perhaps Mayumi's as well) had a shorter chromosome 6 arm. A deletion occurred in the MHC genes! There was no immune barrier for the cancer cells.

 Malignant factor: Philadelphia translocation Invisible factor: MHC mutation

 Previous cases were dismal, but all the research allowed doctors to develop DNAbased treatment for Emiko. As of 2012, Emiko is 7 years old and still alive in Chiba, Japan.

 Kean, Sam (2012). The Violinists Thumb. Hachette Book Group, New York USA. Conter V, Rizzari C, Sala A, Chiesa R, Citterio M and Biondi A. 2004. Acute Lymphoblastic Leukaemia. Orphanet Encyclopedia. Pui CH, Robison LL and Look AT. 2008. Acute lymphoblastic leukaemia. Lancet. 371: 103043.

 Janeway CA Jr, Travers P, Walport M, et. al. (2001). Immuneobiology: The Immune System in Health and Disease. 5th ed. Garland Science, New York USA. Garver-Apgar CE, Gangestad SW, Thornhill R, Miller RD, Olp JJ (2006). Major histocompatibility complex alleles, sexual responsivity and unfaithfulness in romantic couples. Journal of Psychological Science, 17(10): 830-835.