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Pathophys 3.2
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Neoplasia
process of altered cell differentiation and growth
lacks normal regulatory control
Neoplasm
new growth
tumor
How neoplastic growth differs from normal adaptive changes
growth is uncoordinated
growth is autonomous
growth lacks normal regulatory controls of the cell cycle
Cancer
disease that results from altered cell dfferentiation
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
Proliferation Hallmarks of Cancer Cells
Abnormal and rapid proliferation
Undifferenciated cells are halmark of cancer cells
Apoptosis
insufficient apoptosis has been implicated in causing cancer
Malignant neoplasms
may grow own blood vessels
may metastasize to different sites
invade neighboring tissues
Benign neoplasms
localized growth
doesn't metastasize
may affect organs that is is near
better differentiation
Carcinoma
cover external and internal body surfaces
Sarcoma
supporting tissues of the body
bone
cartilage
fat
connective tissue
muscle
Lymphoma
lymph nodes and tissues of the immune system
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
Onccogenes
enhanced biochemical activity leads to altered cell phenotype
cell division stimulated w/o growth factor
activation of proto-oncogenes
activation of viral oncogene
Tumor suppressors
loss of activity leads to altered cell phenotype
mainly cell cycle regulaters
tumor necrosis factor
Genes that control genomic instability
loss of activity leads to many kinds of cell mutations
Proto-oncogenes
precursors of genes that can gain the ability to be dominant-acting oncogenes
Viruses
may induce oncogenes
20% of all cancers
HPV
HepC
EBarr Virus
Viral induced Oncogenes (HPV)
disregulates G1/S checkpoint
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"
Epigenetics
gene expression control
passed from cell to offspring
not reflected in changes in DNA sequence
Examples of epigenetic mechanisms
DNA methylation
Histone modification
Noncoding RNAs
Carcinogenesis
the process by which carcinogenic agents cause normal cells to become cancer cells
Steps of Carcinogenesis
Initiation
-dose based
Promotion
-unregulated and accelerated growth
Progression
-gain of malignant characteristics, evasion of immune system
Clinical manifestations of cancer
disruption of tissue integrity
anorexia/cachexia(wasting)
fatigue and sleep disorders
anemia
Goal of cancer therapies
curative - rid of tumor
control - stop growth
palliative - reduce burden
Methods of treatment
surgery
radiation
chemotherapy
hormone therapy
biotherapy
Author
Rx2013
ID
36759
Card Set
Pathophys 3.2
Description
Neoplasia: Dysfunctional Cell Differentiation and Growth
Updated
2010-09-23T02:21:04Z
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