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Rx2013
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Neoplasia
- process of altered cell differentiation and growth
- lacks normal regulatory control
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How neoplastic growth differs from normal adaptive changes
- growth is uncoordinated
- growth is autonomous
- growth lacks normal regulatory controls of the cell cycle
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Cancer
disease that results from altered cell dfferentiation
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Cell proliferation
- Cell duplicates contents and divides
- genetic info duplicated and distributed to daughter cells
- checkpoints for pauses or arrests in cell cycle
- Cells become more specialized
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Proliferation Hallmarks of Cancer Cells
- Abnormal and rapid proliferation
- Undifferenciated cells are halmark of cancer cells
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Apoptosis
insufficient apoptosis has been implicated in causing cancer
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Malignant neoplasms
- may grow own blood vessels
- may metastasize to different sites
- invade neighboring tissues
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Benign neoplasms
- localized growth
- doesn't metastasize
- may affect organs that is is near
- better differentiation
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Carcinoma
cover external and internal body surfaces
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Sarcoma
- supporting tissues of the body
- bone
- cartilage
- fat
- connective tissue
- muscle
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Lymphoma
lymph nodes and tissues of the immune system
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Role of Genes in development of neoplasia
- genetic chages in cancer cells alter the normal control of mechanisms of cell physiology
- DNA nucleotide mutations
- DNA strand breakage with loss of genes
- DNA strand breakage with rearrangement of genes
- Amplification of specific genes
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Onccogenes
- enhanced biochemical activity leads to altered cell phenotype
- cell division stimulated w/o growth factor
- activation of proto-oncogenes
- activation of viral oncogene
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Tumor suppressors
- loss of activity leads to altered cell phenotype
- mainly cell cycle regulaters
- tumor necrosis factor
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Genes that control genomic instability
loss of activity leads to many kinds of cell mutations
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Proto-oncogenes
precursors of genes that can gain the ability to be dominant-acting oncogenes
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Viruses
- may induce oncogenes
- 20% of all cancers
- HPV
- HepC
- EBarr Virus
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Viral induced Oncogenes (HPV)
disregulates G1/S checkpoint
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Loss of Tumor suppressor activity
- many tumor suppressor genes encode cell cycle regulatory proteins
- p53 and pRB
- both genes must be inactivated to achieve the "cancer phenotype"
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Epigenetics
- gene expression control
- passed from cell to offspring
- not reflected in changes in DNA sequence
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Examples of epigenetic mechanisms
- DNA methylation
- Histone modification
- Noncoding RNAs
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Carcinogenesis
the process by which carcinogenic agents cause normal cells to become cancer cells
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Steps of Carcinogenesis
- Initiation
- -dose based
- Promotion
- -unregulated and accelerated growth
- Progression
- -gain of malignant characteristics, evasion of immune system
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Clinical manifestations of cancer
- disruption of tissue integrity
- anorexia/cachexia(wasting)
- fatigue and sleep disorders
- anemia
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Goal of cancer therapies
- curative - rid of tumor
- control - stop growth
- palliative - reduce burden
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Methods of treatment
- surgery
- radiation
- chemotherapy
- hormone therapy
- biotherapy
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