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CANCERSALWA HASSAN TEAMA
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.
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).
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.
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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SALWA HASSAN TEAMA 2017
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.
SALWA HASSAN TEAMA 2017
CANCER
SALWA HASSAN TEAMA 2017
THE CLONAL NATURE OF CANCER
SALWA HASSAN TEAMA 2017
SALWA HASSAN TEAMA 2017
CANCER/ GENE INVOLVED
ONCOGENE
TUMOR SUPPRESSOR GENE
DNA REPAIR GENE
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SALWA HASSAN TEAMA 2017
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.
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
SALWA HASSAN TEAMA 2017
Activation of Proto-oncogene
SALWA HASSAN TEAMA 2017
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
SALWA HASSAN TEAMA 2017
CANCER
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
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
SALWA HASSAN TEAMA 2017
CANCER
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).
SALWA HASSAN TEAMA 2017
CANCER
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SALWA HASSAN TEAMA 2017