Onkologie at Medizinische Universität Innsbruck

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Exemplary flashcards for Onkologie at the Medizinische Universität Innsbruck on StudySmarter:

  1. Molecular classifications of ovarian cancer

Exemplary flashcards for Onkologie at the Medizinische Universität Innsbruck on StudySmarter:

  1. What is STIC

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Common features and differences within the p53 family

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Exemplary flashcards for Onkologie at the Medizinische Universität Innsbruck on StudySmarter:

Relevance and features of Gain-of-Function mutations in the p53 family

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Please describe the difference between Typ I and Typ 2 ovarian cancer

Exemplary flashcards for Onkologie at the Medizinische Universität Innsbruck on StudySmarter:

What is the main prognostic marker of advanced ovarian cancer

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  1. Causes of genetic instability and its role in cancerogenesis
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Exemplary flashcards for Onkologie at the Medizinische Universität Innsbruck on StudySmarter:

Cell cycle regulation and cell cycle checkpoints

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DNA damage and DNA damage responses

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Regulation of mitosis and the spindle assembly checkpoint

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Tumor evolution: inter- and intratumor heterogeneity; causes and consequences

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How can caspases be activated?

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Exemplary flashcards for Onkologie at the Medizinische Universität Innsbruck on StudySmarter:

Onkologie

  1. Molecular classifications of ovarian cancer
  • a.       Type I:
    1. Slow growing, early stage
    2. Borderline Tumors
    3. Mutation of K-Ras, B-Raf, PTEN, Beta-catenin
    4. Low Grade Serous
  • b.       Type II:
    1. Highly aggressive, evolves rapidly, high metastatic ability
    2. No precursors
    3. P53-Mutation, genetically instable!
    4. High grade Serous, accounts for 85% of all ovarian cancer deaths! 

Onkologie

  1. What is STIC
  • Serous tubal intraepithelial carcinoma
  • Lesion limited to the fallopian tube epithelium that is a precursor to extrauterine high grade serous carcinoma
  • Confined to epithelium
  • High proliferative index, atypia, architectural alterations, strong p53 staining
  • Most likely in fimbria of the fallopian tube

Onkologie

Common features and differences within the p53 family

  • a.       Common features:
    1. Transcriptional factors
    2. Gain of function mutation (or overexpressing, in the case of p63) is carcinogenic 
    3. Several splice forms known
    4. Help in suppressing tumours
  • b.       P53
    1. Inactivation crucial step in carcinogenesis 
  • c.        P63
    1. Inactivation leads to developmental defects in mouse (limbs, teeth, mammary glands), but no inactivation needed for carcinogenesis
  • d.       P73
    1. No inactivating mutation in malignant transformations

Onkologie

Relevance and features of Gain-of-Function mutations in the p53 family

a.       Relevance: mutp53 Knock-in-Mice show a broader tumour spectrum including adenocarcinomas, higher tumour bulk, grade and invasion, also cells gained metastatic ability, compared to p53 Knockout mice, which got T-lymphomas and never metastasised! 

b.       Features: Mutated p53 gets stabilized and accumulates in the cell. However, mutp53-cells develop an addiction on high levels of mutp53 for survival. Acute withdrawal triggers strong spontaneous cytotoxicity, blocking invasion and metastasis and restoring chemotherapy-induced cell death. 

Onkologie

Please describe the difference between Typ I and Typ 2 ovarian cancer

  • a.       Type I: 
    1. Low-grade serous
    2. Slow growing
    3. All histologies, including:
      • 1.       Low grade serous carcinoma
      • 2.       Lowgrade endometroid carcinoma
      • 3.       Mucinous carcinoma
      • 4.       Some clear cell carcinoma
    4. They likely evolve through a step-wise progress from borderline tumours
    5. Usually chromosomally stable
  • b.       Type II:
    1. High grade
    2. Evolve rapidly
    3. Include
      • 1.       High grade serous carcinoma
      • 2.       High grade endometrioid carcinoma
      • 3.       Carcinosarcoma
      • 4.       Undifferentiated carcinoma
      • 5.       And some clear cell carcinoma
    4. No recognizable precursors in the ovary
    5. Widespread DNA copy number change
    6. Deadly! Early peritoneal dissemination

Onkologie

What is the main prognostic marker of advanced ovarian cancer

  1. Maximale Zytoreduktion! 
    1. Entfernung von minder vaskularisierten Tumorarealen, welche einer zytotoxischen Therapie nicht zugänglich sind.
    2. Kleinere Residuen bedürfen weniger Zyklen Chemotherapie, damit vermindertes Risiko für Resistenzentwicklung
    3. Entfernung potentiell Chemo-resistenter Tumorzellklone durch optimales Debulking

Onkologie

  1. Causes of genetic instability and its role in cancerogenesis
  • Tumourigenesis is a sequential mutagen process that works through the accumulation of mutations. One single mutation is not enough to transform a cell. Carcinogenic mutations can be in morphogens, proliferation control, antiproliferative factors or tumour-suppressors. However, with a mutation rate of 1 in a billion basepairs, which means 6 point mutations per cell division, the probability for two of those mutations is very low. In case of genetic instability, however, mutation rates increase, which makes such a mutation far more likely. A cell like this would then have a growth advantage, which would lead to a selection of cells of this genotype. Further mutagenesis leads to tumour heterogeneity. 
  • Causes: 
    1. P53 mutation: No cell cycle arrest in case of DNA damage; defect cells can divide and multiply
    2. Decreased DNA-repair (miss-match-repair): Raises mutation rates during replication by 10 fold!

Impaired checkpoints: Cell ignores signals that it should not proliferate

Onkologie

Cell cycle regulation and cell cycle checkpoints

  • Checkpoints: 
    1. Restriction point
      • Mitogen -> Ras-cascade -> Myc-expression -> activation of G1-Cdk -> inactivation of Rb-protein through phosphorylation -> release of Transcription factors -> S-phase-gene transcription
      • 2.       Cyclin E (G1/S) and Cyclin A (S-phase) -> active S-Cdk -> S-phase
    2. Exiting S-phase: Licensing factors are degraded, which leads to no more replication
    3. Entering Mitosis
      • Cyclin M is raised throughout the cell cycle, CDK1 is always there, inactivated. CAK phosphorylates CDK1 activatingly, Wee1 inactivates it through phosphorylation.
      • CDC25 removes inactivating phosphate -> active M-Cdk -> Activates phosphatase CDC25 -> positive feedback loop -> Start Mitosis
    4. Anaphase Checkpoints
      • First Spindles have to attach to the kinetochores; when pulling, the anaphase wait signal (Mad2-Csc20) is no longer generated
      • After Spindles attach, APC is activated by CDC20, leads to degradation of securin and activates the separase, which cleaves the cohesines, holding the chromatides together. 

Onkologie

DNA damage and DNA damage responses

  • Damage: 
    1. Chemical changes of bases
    2. Single strand or double strand break
    3. Blockage of DNA replication
  • Recognition:
    1. -> MRN- complex, Localize to site
    2. 53BP1: binds and activates p53
  • Transduction: Double strand breaks, replication block or resected single strand DNA (also open replication origins: no further cell cycle progression until DNA is fully replicated) leads to activation of ATR/ATM (PI3-Kinases)
  • Activates: 
    1. CHK1 and CHK2: G2/M-Arrest
    2. P53: G1/S-Arrest (Activation of p21, which inhibits pRb-Inhibitor E-Cdk!) and Apoptosis (depending on signal amount)
      • P53 is short lived – activation as a pulse
      • Strong ATR/ATM signal: many pulses -> apoptosis (BAX, PUMA, NOXA)
      • Weak signal: less pulses -> arrest (p21)
    3. BRCA1: DNA repair/arrest
  • DSB: Activation of MRN-Complex (Mre11, Rad50, Nbs1): DNA-repair/arrest 
  • In G1: Double strand break: ATM: Fast reaction -> CHK2 -> CDC25A –Cyclin E deactivation, CDK4 deactivation. Afterwards: p53 activation
     single Strand DNA: ATR: Slow reaction: expression of p53 -> p21 -> CDK2 deactivation
  • In G2: ATM and ATR both activate CHK2 and CHK1; both phosphorylate CDC25C

Onkologie

Regulation of mitosis and the spindle assembly checkpoint

  • Cyclin M is raised throughout the cell cycle, CDK1 is always there, inactivated. CAK phosphorylates CDK1 activatingly, Wee1 inactivates it through phosphorylation. 
  • CDC25 removes inactivating phosphate -> active M-Cdk -> Activates phosphatase CDC25 -> positive feedback loop -> Start Mitosis
  • After Mitosis, M-cyclin is ubiquitinated by APC and degraded in the proteasome. 
  • Anaphase Checkpoint: Make sure that all kinetochores are attached to a microtubule, otherwise mitosis can lead to aneuploidy!
    1. First Spindles have to attach to the kinetochores; when pulling, the anaphase wait signal (Mad2-Csc20) is no longer generated
    2. After Spindles attach, APC is activated by CDC20, leads to degradation of securin and activates the separase, which cleaves the cohesines, holding the chromatides together. 
  • Describe horrible effects of mutated spindle check point

Onkologie

Tumor evolution: inter- and intratumor heterogeneity; causes and consequences

  • A random mutation leads to a growth advantage of one cell over others. Naturally, this cell will expand more rapidly. Through rapid growth, the possibility for a second mutation skyrockets (DNA replication is faulty, especially if one of the control mechanisms is out of order, which is often the case here). Again, more growth advantage, faster proliferation, higher mutagenesis. This finally leads to several genetically different cells that have a growth advantage over other cells. Genetic diversity is also increased by aneuploidy! 
  • Intertumour-heterogeneity: Every tumour is different; there are probably not two people in the world with exactly the same genotype in their tumours. 
  • Intratumour-heterogeneity: Cells have different genotypes within a tumour. One cell mutates in the beginning, but from that initiating cell population, several different subpopulations pop up through further mutation. 
  • Consequences: Chemotherapy kills genetic diversity, which means that only resistant cells survive. From those resistant cells, a new tumour arises that is resistant against treatment

Onkologie

How can caspases be activated?

  • After Loss of mitochondrial integrity
  • In response to receptor/ligand interaction
  • Cell-cell contact mediated
    1. Virus-infected target cell
    2. Transformed cell
    3. Graft Versus Host Disease

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