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CANCER SALWA HASSAN TEAMA

Cancer

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Page 1: Cancer

CANCERSALWA HASSAN TEAMA

Page 2: Cancer
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SALWA HASSAN TEAMA 2017

CANCER

Cancer is a complex disease,

Result from the same basic process of uncontrolled growth,

Cell proliferation results in a mass that invades neighboring tissues and may metastasize to more distant sites,Fatal, if untreated,

Some cancers, however, such as blood cancers, do not form tumors..

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SALWA HASSAN TEAMA 2017

Tumor formation is a multistep process involving many of genetic changes in the evolving tumor cell population. Tumors are classified by site, tissue type and degree of malignancy.

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SALWA HASSAN TEAMA 2017

CAUSES OF CANCER

Randomly acquired through errors in DNA replication.

Inherited and thus present in all cells from birth.

Carcinogens, such as tobacco smoke, radiation, chemicals, or infectious agents (Viruses are involved in cancers).

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SALWA HASSAN TEAMA 2017

CANCER

Germline mutations Mutation responsible for 5%

to 10% of cancer cases. This is also called familial cancer. These mutations are present in every cell of the body and are passed from parent to

child.

Sporadic cancer or somatic mutation

Mutation caused by tobacco, over-exposure to UV radiation,

and other toxins and chemicals. These mutations are not in every cell of the

body and are not passed from parent to child.

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SALWA HASSAN TEAMA 2017

Cancer is a complex disorder in which the normal control of cell growth is lost.

Cancer is a genetic disorder, nearly all cancers are caused by abnormalities in the genetic material of the transformed cell.

Initiation of cancer; cells undergoing a series of genetic mutation or alteration which result in their instability to respond normally to intracellular/extracellular signals that control proliferation, differentiation and death.New aspects of the genetics of cancer pathogenesis, such as DNA methylation and microRNAs are increasingly recognized.

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Cancer develops when several genes in a cell become mutated in a way that overrides the checks and balances of the cell.

However, many cancers cannot be tied to a specific gene, and some genes may interact in unpredictable ways with other genes or factors in the environment to cause cancer.

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SALWA HASSAN TEAMA 2017

CANCER

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SALWA HASSAN TEAMA 2017

THE CLONAL NATURE OF CANCER

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SALWA HASSAN TEAMA 2017

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SALWA HASSAN TEAMA 2017

CANCER/ GENE INVOLVED

ONCOGENE

TUMOR SUPPRESSOR GENE

DNA REPAIR GENE

……………………

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SALWA HASSAN TEAMA 2017

ONCOGENE

Most oncogenes are mutated forms of normal genes, called proto-oncogenes.

Proto-oncogenes is a normal gene that code for proteins that help to regulate cell growth and differentiation. Proto-oncogenes are often involved in signal transduction and execution of mitogenic signals, usually through its protein product.

Proto-oncogene can become an oncogene due to mutations or increased expression.

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Point mutations Deletions, or insertions that lead to hyperactive gene product. Deletions, or insertions in the promoter region of a proto-oncogene that lead

to increased transcription.

Gene amplification events leading to extra chromosomal copies of a proto-

oncogene lead to normal protein greatly overproduced. Amplified segments of DNA

are often detected as two types of cytogenetic change, double minute and

homogeneously staining regions.

Chromosomal translocation  Relocation of a proto-oncogene to a new chromosomal site that leads to

higher expression Fusion between a proto-oncogene and a second gene, which produces a

fusion protein with oncogenic activity.

Activation of Proto-oncogene

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SALWA HASSAN TEAMA 2017

Activation of Proto-oncogene

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Types of Oncogene

Oncogene can be classified according to their cellular location and function of

their encoded oncoproteins in the signal transduction pathway:Growth factorsGrowth factor receptorsGTP binding proteinsPost receptor tyrosine kinaseCytoplasmic oncogenesNuclear oncogenesApoptotic oncogenes

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CANCER

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SALWA HASSAN TEAMA 2017

Tumor suppressor gene or anti oncogene: Normal genes implicated in the

control of cell cycle, repair DNA mistakes, and tell cells when to die (apoptosis

or programmed cell death).

The product of tumor suppressor genes normally block abnormal growth and

malignant transformation and lead to malignancy when the function of both

alleles is lost. When tumor suppressor genes don’t work properly, cells can

grow out of control, which can lead to cancer.

TUMOR SUPPRESSOR GENE

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p53, located human chromosome 17,

gene with tumor suppressor activities.

p53 protein contains 393 amino acids and

a single amino acid substitution can lead

to loss of function of the gene. Mutations at

amino acids 175, 248, and 273 can lead to

loss of function and changes at 273 (13%)

are the most common.

About 50% of human cancers can be

associated with a p53 mutation including

cancers of the bladder, breast, cervix,

colon, lung, liver, prostate, and skin.

p53 related cancers are also more

aggressive and have a higher degree of

fatalities.

These all act as recessive mutations.

SALWA HASSAN TEAMA 2017

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SALWA HASSAN TEAMA 2017

CANCER

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SALWA HASSAN TEAMA 2017

CANCER

Many viruses infect humans but only a few viruses are known to promote human

cancer. These include both DNA viruses and retroviruses, a type of RNA virus.

Viruses associated with cancer include human papillomavirus (genital

carcinomas), hepatitis B (liver carcinoma), Epstein-Barr virus (Burkitt's

lymphoma and nasopharyngeal carcinoma), human T-cell leukemia virus (T-cell

lymphoma); and, probably, a herpes virus (Kaposi's sarcoma and some B cell

lymphomas).

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CANCER

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