Question

Answer this questions and support you answer by using graphs and diagrams about canser induction :

1- Choose one type of cancer.

2-what are the Statistics of this type of cancer

3-Mutation in proto-oncogene and tumor suppressor gene.

4-How to cure cancer (radiation, surgery, chemotherapy)

Answer 1

BRAIN CANCER

The statistics about brain tumours:

• Brain tumours are the biggest cancer killer of children and adults under 40
• Almost 11,700 people are diagnosed each year with a primary brain tumour, including 500 children and young people – that's 32 people every day
• Over 5,000 people lose their lives to a brain tumour each year
• At least 102,000 children and adults are estimated to be living with a brain tumour in the UK currently
• Brain tumours reduce life expectancy by on average 20 years – the highest of any cancer
• Just 11% of adults survive for five years after diagnosis
• Brain tumours are the largest cause of preventable or treatable blindness in children
• Research offers the only real hope of dramatic improvements in the management and treatment of brain tumours.

From the pie diagram its clear that the majority of cancer in brain is in the neroepithelial region and least is in the sellar region.

Mutation in proto-oncogene and tumor suppressor gene.

Generally speaking, however, mutations in two basic classes of genes—proto-oncogenes and tumor suppressor genes—are what lead to cancer. "Proto-oncogenes" are a group of genes that cause normal cells to become cancerous when they are mutated Mutations in proto-oncogenes are typically dominant in nature, and the mutated version of a proto-oncogene is called an oncogene. Often, proto-oncogenes encode proteins that function to stimulate cell division, inhibit cell differentiation, and halt cell death. All of these processes are important for normal human development and for the maintenance of tissues and organs. Oncogenes, however, typically exhibit increased production of these proteins, thus leading to increased cell division, decreased cell differentiation, and inhibition of cell death; taken together, these phenotypes define cancer cells. Thus, oncogenes are currently a major molecular target for anti-cancer drug design.

The activation of cellular oncogenes represents only one of two distinct types of genetic alterations involved in tumor development; the other is inactivation of " tumor suppressor genes".

The tumor suppressor gene to have been identified is p53, which is frequently inactivated in a wide variety of human cancers, including leukemias, lymphomas, sarcomas, brain tumors, and carcinomas of many tissues, including breast, colon, and lung. In total, mutations of p53 may play a role in up to 50% of all cancers, making it the most common target of genetic alterations in human malignancies. It is also of interest that " inherited mutations of p53 " are responsible for genetic transmission of a rare hereditary cancer syndrome, in which affected individuals develop any of several different types of cancer. In addition, the p53 protein (like Rb) is a target for the oncogene proteins of SV40, adenoviruses, and human papillomaviruses.

Modes of Activation (How Proto-Oncogenes Become Oncogenes)

There are a number of ways in which normal proto-oncogenes can become activated (changed) so that they become oncogenes. The process can begin when carcinogens (cancer-causing agents) in the environment cause a mutation or amplification of a proto-oncogene.Studies on animals have shown that chemical carcinogens can cause the mutations that convert ras proto-oncogenes to oncogenes.DNA damage may occur as an accident during the normal growth of cells; even if we lived in a world free from carcinogens, cancer would occur.

DNA damage can take one of several forms:

• Point mutations: Changes in a single base (nucleotide), as well as insertions or deletions in DNA can result in the substitution of a single amino acid in a protein that changes the function.
• Gene amplifications: Extra copies of the gene result in more of the gene product (proteins that lead to cell growth) being produced or "expressed."
• Translocations/rearrangements: Movement of a portion of DNA from one place to another can occur in a few ways. Sometimes a proto-oncogene is relocated to another site on a chromosome, and because of the location, there is a higher expression (larger amounts of the protein is produced). Other times, a proto-oncogene may become fused with another gene that makes the proto-oncogene (now an oncogene) more active.

Mutations may also occur in a regulatory or promoter region near the proto-oncogene.

Oncogenes Versus Tumor Suppressor Genes

There are two types of genes that when mutated or otherwise changed, can increase the risk that cancer will develop: oncogenes and tumor suppressor genes. A combination of changes in both of these genes is frequently involved in the development of cancer. Even when DNA damage such as point mutations occur to convert a proto-oncogene to an oncogene, many of these cells are repaired. Another type of gene, tumor suppressor genes, code for proteins that function to repair damaged DNA or eliminate damaged cells. These proteins can help reduce the risk of cancer even when an oncogene is present. If mutations in tumor suppressor genes are also present, the likelihood of cancer developing is greater as abnormal cells are not repaired and continue to survive instead of undergoing apoptosis (programmed cell death).

There are several differences between oncogenes and tumor suppressor genes:

Oncogenes

• Most often autosomal dominant, meaning that only one copy of the gene needs to be mutated to elevate cancer risk

• Turned on by a mutation (a gain of function)

• Can be visualized as the accelerator, when viewing a cell as a car

Tumor Suppressor Genes

• Most often (but not always) autosomal recessive, a mutation in both copies must occur before it increases the risk of developing cancer

• Turned off by a mutation

• Can be visualized as the brake pedal, when viewing the cell as a car

Some cells with oncogenes become self-sufficient by making (synthesizing) the growth factors to which they respond. The increase in growth factors alone doesn't lead to cancer but can cause rapid growth of cells that raises the chance of mutations.An example includes the proto-oncogene SIS, that when mutated results in the overproduction of platelet-derived growth factor (PDGF). Increased PDGF is present in many cancers, particularly bone cancer (osteosarcoma) and one type of brain tumor.

Treatment options include surgery, radiation therapy, chemotherapy, targeted biological agents, or a combination of these. Surgical resection (if safe) is generally the first treatment recommendation to reduce pressure in the brain rapidly.

1) Radiation therapy

Types of radiation therapy include:

• Intensity-modulated radiation therapy (IMRT): an advanced mode of high-precision radiotherapy that utilizes computer-controlled x-ray accelerators to deliver precise radiation doses to a malignant tumor or specific areas within the tumor. The radiation dose is designed to conform to the three-dimensional (3-D) shape of the tumor by modulating or controlling the intensity of the radiation beam to focus a higher radiation dose to the tumor while minimizing radiation exposure to healthy cells.
• Stereotactic radiosurgery (SRS): a highly precise form of radiation therapy that directs narrow beams of radiation to the tumor from different angles. For this procedure, the patient may wear a rigid head frame. Computed tomography (CT) or magnetic resonance imaging (MRI) help the doctor identify the tumor's exact location and a computer helps the doctor regulate the dose of radiation. Stereotactic radiotherapy is similar physically to radiosurgery but involves fractionation .This modality would be recommended for tumors within or close to critical structures in the brain that cannot tolerate a large single dose of radiation or for larger tumors.
• Three-dimensional conformal radiation therapy (3D-CRT): a conventional form of radiation treatment delivery that uses a specific arrangement of x-ray beams designed to conform to the shape of the tumor to maximize tumor dose and minimize normal surrounding tissue dose. This form of treatment is tailored to the patient's specific anatomy and tumor location. CT and/or MRI scan is often required for treatment planning.
• Brachytherapy: the temporary placement of radioactive source(s) within the body, usually employed to give an extra dose—or boost—of radiation to the area of the excision site or to any residual tumor.

The external-beam radiation therapy is a superior treatment in some cases. “When patients are treated with modern external-beam radiation therapy, the overall cure rate was 93.3% with a metastasis-free survival rate at 5 years of 96.9%.

2) Chemotherapy treatment

Chemotherapy uses anti cancer (cytotoxic) drugs to destroy brain tumour cells. The drugs circulate throughout your body in the bloodstream. It can be difficult to treat brain tumours with some chemotherapy drugs because the brain is protected by the blood brain barrier. This is a natural filter between the blood and the brain which protects the brain from harmful substances.

Types of chemotherapy

Common types of chemotherapy drugs for brain tumours include:

• temozolamide
• procarbazine
• carmustine (BCNU)
• lomustine (CCNU)
• vincristine
• a combination of drugs called PCV

"Chemotherapy into your brain": Chemotherapy implants (wafers)

Your surgeon might put chemotherapy drugs into the brain tissue as a wafer. The chemotherapy drug is inside a gel wafer, which slowly dissolves over 2 to 3 weeks. As the gel wafer dissolves, the chemotherapy is slowly released into the brain tissue. One example is a Gliadel wafer that contains carmustine (BCNU).

How  chemotherapy is doine?

There are different ways of having chemotherapy for a brain or spinal cord tumour.

• as a drip into your bloodstream (intravenously)
• into your spine (intrathecal chemotherapy)
• directly into your brain
• as tablets or capsules that you swallow (oral chemotherapy)

3) Surgery

Surgery is the removal of the tumor and some surrounding healthy tissue during an operation. It is usually the first treatment used for a brain tumor and is often the only treatment needed for a low-grade brain tumor. Removing the tumor can improve neurological symptoms, provide tissue for diagnosis, help make other brain tumor treatments more effective, and, in many instances, improve the prognosis of a person with a brain tumor.

Surgery to the brain requires the removal of part of the skull, a procedure called a craniotomy. After the surgeon removes the tumor, the patient's own bone will be used to cover the opening in the skull.

There have been rapid advances in surgery for brain tumors, including the use of cortical mapping, enhanced imaging, and fluorescent dyes.

• Cortical mapping allows doctors to identify areas of the brain that control the senses, language, and motor skills.

• Enhanced imaging devices give surgeons more tools to plan and perform surgery. For example, computer-based techniques, such as Image Guided Surgery (IGS), help surgeons map out the location of the tumor very accurately. However, this is a very specialized technique that may not be widely available.

• A fluorescent dye, called 5 aminolevulinic acid, can be given by mouth the morning before surgery. This dye is taken up by tumor cells. Doctors can use a special microscope and light to see the cells that have taken up the dye during the surgery. This helps doctors safely remove as much of the tumor as possible.