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Summary Subject matter Oncology Ch7/14 $11.28
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Summary Subject matter Oncology Ch7/14

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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...

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  • 7 tot en met 14
  • May 26, 2023
  • 150
  • 2022/2023
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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

Initiators: 2,8,9,10 = up-stream -> activate downstream 3,6,7

Effectors: 3,6,7

Inflammatory: 1,4,5



9= intrinsic

8= extrinsic

, 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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