In this file of plus minus 150 pages, all lecture notes are merged with notes from the book by chapter. Chapters 7 through 14. very extensive and not really a summary. it's all the material that has been treated. before partial exam 2. also new information is given here that is not given in the lec...
Oncogenic mutations sites in relevant proto and oncogenes
Oncology exam 2 full summary of lectures + practice exam and answers
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Vrije Universiteit Amsterdam (VU)
Gezondheid en Leven: Klinische Wetenschappen
Oncology (AB_1184)
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Lecture: chapter 7 apoptosis
Definition of apoptosis:
= the regulated and orderly destruction of a cell through a genetically encoded process also known as
programmed cell death PCD
= type of cell suicide that is intrinsic to the cell
• Organized, neat and tidy -> leaving behind little evidence of the preexisting cell
• The cell undergoing apoptosis is swept clean during phagocytosis by macrophages,
neighboring cells that recognize molecular flags (phosphatidyl serine)
• Cell shrinkage, membrane blebbing and budding, and chromatin condensation and precise
fragmentation -> neat disposal of the cell
Contrast to necrosis: cells swell, cell membranes become leaky, and cells spill out their contents into
the surrounding tissue and cause inflammation.
• Caspases: catalyze proteolysis -> break down cellular components
25 x 10^6 mitosis per second
25 x 10^6 apoptosis per second
2,2 kg cells per day!
Function of apoptosis:
= Active ATP dependent process
• Developmental morphogenesis
• Controls cell numbers (intestines)
• Removal of damaged cells
• Negative and positive selection of lymphocytes in lymphoid organs (ig spleen)
• Cytotoxic effect of radio-and chemotherapy
,Apoptosis vs necrosis:
Necrosis: external factor induces the process, in heart attacks is necrosis
Differs in morphology! No inflammation vs inflammation!!
A= normal lymphocyte. Small cyptoplasm surrounding the nucleus
B= cell lymhpcote is ….
C= cyoses
D= chromatin is..
E= apoptotic burns
BOEK UITLEG
Leukemia gets drugs MGG or Dapi (fluorescent)
Condensated chromatin is dark purple tov light purple in apoptotic cells
, 7.1 Molecular mechanisms of apoptosis
Apoptosis signalling:
➔ Induction of apoptosis:
- Programmed
- Loss of growth factors, of adhesion
- Death receptors of the TNFR family
- t- and b- cell antigen receptors
- CTLs (cytotoxic t lymphocytes)
- DNA damage (irradiation, chemotherapy)
- Stress conditions
➔ Mitochondrial changes
➔ Activation of the caspase family
➔ Proteolytic cleavage of structural and functional proteins
➔ Induction of apoptosis morphology
Extracellular signals = death factors.
Internal signals= DNA damage, oxidative stress
Caspases:
= specific proteases that act like molecular scissors to cleave intracellular proteins at aspartate
residues.
• Cysteine-rich aspartate proteases, synthesized as zymogens (procaspases)
• Requirement for an aspartic acid at the P1 position
• 14 family members cloned
• Caspases 2,3,6,7,8,9 and 10 are involved in apoptosis
, Cleavage results in activating. But first the pro-domain needs to be removed
QACxG
4 apoptosis pathways:
ER = neurodegenerative diseases (cascades 1,4,5)
Granzyme b= less research
1 and 2 have the most focus!
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