Summary of the entire profession 'mechanisms of human diseases.' Contains comprehensive information on virulence and bacterial infection. A total of seven abstracts covering an around 400 pages substance.
TEST BANK FOR MEDICAL PHYSIOLOGY, UPDATED, 2ND EDITION, WALTER F. BORON, ISBN-10: 1437717535, ISBN-13: 9781437717532
Summary PBC Part 2
8WB00 - Hart en bloed
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Universiteit van Amsterdam (UvA)
Biomedische wetenschappen
Mechanismen van ziekten van de mens
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Metastasis
Before spreading to new organs, cancer cells must chew through the collagen
and other proteins making up the connective tissue that encapsulates organs and
tissues.
It has often been noted that cancer cells are unusual because they are
undifferentiated; that is, they lose functions and, as a result, fail to fully
develop the characteristics and proper activities of mature cells of their type.
MAAR metastatic cancer cells gain new functions
Metastatic cancer cells are altered in such a way that they can break the bonds
that hold cells together.
Further cellular remodeling allows metastatic cells to chew through the
proteinaceous walls that line tissues and blood vessels and quite literally walk
away from their parent organ to invade other tissues and organs.
Metastatic cancer cells crowd out normal cells in the tissue and deprive them of
nutrients. In effect, the metastatic cells starve and displace functional cells.
Carcinogenesis
During this lengthy evolution, cells undergoing cancerous transformation
accumulate genetic abnormalities, one important consequence of which is that
cellular growth becomes deregulated.
Cells that are too old->apoptosis. These cells are replaced by new cells, derived
from primitive precursors, also called stem cells.
Clearly, then, maintaining the proper number of cells in any tissue requires a
delicate balance between cellular production and elimination.
When an excess of cells is produced by unrestrained cell division, or when too
few cells are eliminated by apoptosis, an overabundance of cells accumulates in
the tissue. This basically describes the situation in cancer.
Regulating Proliferation
Majority of cancer cells: one or several of these growth-regulatory genes is either
missing or defective. When functioning properly these genes are crucial in
maintaining the normal growth characteristics for each cell type. These genes
only promote cancer when they become mutated or altered.
1. clusters of genetically identical cells are formed ( each cell dividing with
less restraint than its normal neighbors. This cluster does not at this point
constitute a tumor) 2. Angiogenesis (diameter of about 2 millimeters-> signals
-> blood vessels) -> zuurstof en voedsel + weg om zich te verplaatsen +
omliggend weefsel laat factoren los waardoor de tumor groeit
Celcyclus
Resting cells are in the phase called Gap0 (G0).-> signal-> Gap1 (G1) phase ->
RNA en eiwitproductie -> Synthesis (S) phase -> DNA verdubbelt ->Gap2 (G2) ->
RNA en eiwitten gemaakt -> Mitosis (M)-> 2 cellen.
The p53 protein = checkpoint when the cell enters the S phase. If the DNA is
damaged, the cell cycle is stopped to allow for DNA repair. If the damage is so
severe: apoptosis.
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