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Pathology of cancer > Oefentoets > Flashcards

Oefentoets Flashcards

1
Q

What is the name of a benign tumor originated from cartilage called?

A

Chondroma

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2
Q

A patient tumor is grading reports states ‘‘Well differentiated, grade 1’’. What does this mean?

A

Tumor cells have an appearance and arranged that is similar to normal cells –> benign

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3
Q

1 theory that is used to explain the formation of metastasis is the ‘‘Seed and Soil’’ theory. What is meant by the Soil?

A

The secundary organ in which the metastasis forms

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4
Q

The sectreted Soluble factors is 1 caterogy comprimising the components of the tumor microenvironment. Which statement is NOT correct regarding this caterogy? Pick 1

  • They are NOT involved in Angiogenesis
  • They ARE involved in Matrix remodelling
  • Proteases are part of this category
  • Cytokines and chemokines are part of this category
A

They are NOT involved in angiogenesis is wrong

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5
Q

Which of the following are hallmarks of cancer?

  • Sustaining proliferative signaling
  • Avoiding immune destruction
  • Enabling replicative immortality
A

All of them are part of the hallmarks of cancer

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6
Q

What is called the ‘‘Gatekeeper’’ to colorectal cancer development?

A

APC/Wnt signaling pathway

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7
Q

What can be present on MHCII in Dendritic Cells?

A

Only peptides from EXTRAcellular matrix

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8
Q

What is NOT a mechanism by which tumor cells can evade the IS?

  • Poor immunogenicity
  • Tolerance of the tumor Ag
  • Down-regulation of MHCII
  • Recruitment/stimulation of Treg
A

Down-regulation of MHCII

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9
Q

In dendritic cell therapy for cancer patients, APC’s (monocytes ex.) are taken out of the circulation of a patient, differentiated to dendritic cells, loaded with Ag ex vivo and injected back into the patient. What is the advantage of this kind of therapy for cancer patiens?

A

It can induce memory

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10
Q

Which of the following protein is defined as a signaling protein?

  • Frizzled
  • Sonic Hedehog SHH
  • Beta catenin
  • Oct4
A

SHH

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11
Q

After EMT, which of these characteristics is not shown?

  • Loss of cell polarity
  • Migration features
  • Acquidition of cell adhesion
  • Loss of cell adhesion
A

Acquisition of cell adhesion

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12
Q

In a Wildtype, NOT transgenic mouse, which is a gene specifically expressed in an intestinal adult stemcell

  • Oct4
    -Wnt 3A
  • GFP
  • Lgr5
A

Lgr5

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13
Q

Which of the DNA repair mechanism uses sequences in the undamaged sister chromatid?

-BER
-HR
-MMR
-NER

A

HR

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14
Q

Benign tumors usually donot have fatal outcome. Give an example in which a benign tumor COULD have a fatal outcome and why it can be fatal

A
  1. Anatomical position: Benign tumor pushing against brain tissue
  2. Systemic effect: Adenoma: insulin producing pancreatic cancer
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15
Q

Why is angiogenesis so important in cancer progression?

A

New bloodvessels help the tumor to grow by feeding the cancer cells with nutrients, oxygen AND it helps by metastase

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16
Q

Explain at molecular level how an APC mutation contributes to colorectal cancer

A

APC is involved in the Wnt signaling cascade. When APC is mutated, it cannot bind beta-catenin and therefore beta-catenin is not in the complex anymore with APC, axin, GSK3 and CK1. So beta-catenin will not be phosphorylated and degraded. It is now present and stable form without the Wnt signal. Stable beta-catenin binds to the transcription factors bound to the DNA (LEF1/TCF). This will lead to uncontrolled transcription of Wnt target genes. Ongoing Wnt signaling because of mutated APC causes more proliferation than differentiation, this imbalance can cause colorectal cancer

17
Q

Name a mechanism how NK-cells can kill a tumor cell

A
  1. Intrinsic mechanism: Perforin-granzyme
  2. Extrinsic mechanism: TNF/TNFR
18
Q

Explain what is meant by ‘‘escape’’ in the immune surveillance hypothesis

A

The IS can no longer kill all carcinogenic cells, causing them to grow into a tumor

19
Q

Name a disadvantage of using Ab’s as tumor immunotherapy

A

Does not provide memory, not patient specific

20
Q

In different tumor types, the mutation of APC causes overactivation of the Wnt signaling pathway. How does the loss of APC activate Wnt signaling?

A

APC is part of the beta-catenin digradation complex. Without APC, beta-catenin is not degraded and is continously going to the nucleus

21
Q

What kind of function do tumor suppressor proteins have

A

They have apoptotic and/or anti-proliferative functions to counterbalance proliferative signals, especially in case of oncogenic stimuli

22
Q

How are phosphotyrosine docking sites for STATS created

A

2 JAKS phosphorylate each other. This increases the activity of the tyrosine kinase domains of the JAKS. Then the JAKS can phosphorylate tyrosines on the cytoplasmic tails of the cytokine receptors. This creates phosphotyrosine docking sites for STATS

23
Q

What is the function of Ksr in the RAS-MAPK signaling pathway

A

Ksr is an important scaffold protein that contains bindngsites for Rad, Mek and Erf. The scaffold protein helps with the transduction of signals and organisation of Rad, Mek and Erf

24
Q

Which kind of stem cells are the cells within the inner cell mass

A

Embryonic stem cells (pluripotent stem cells). This is because each of them can give rise to all the cell types in the body

25
Q

Describe what happens in G1 –> S arrect following DNA damage

A

DNA damage causing activation of protein kinases (ATM/ATR and Chk1/Chk2) that phosphorylates P53, the phosphorylated P53 has now a lower affinity binding to Mdm2. Arf will help removing Mdm2 and now there is a stable P53. Stable and active P53 can bind to the regulatory region of P21 gene as a transcription factor, producing P21 (Cdk inhibitory protein). P21 suppresses G1/S Cdks and S Cdk activities by binding to the Cyclin-Cdk complex

26
Q

What is a Pyrimidine dimer

A

Covalent cross-links between adjacent pyrimidine bases in DNA

27
Q

Why do transplantation patients have a higher risk of developing tumors?

A

They take immunosuppressiva which block the adaptive IS

28
Q

Testis Ag’s are a type of tumor Ag

A

True

29
Q

Which cells can cross present Ag’s

A

Dendritic cells

30
Q

How many signals does a cytotoxic Tcell need to kill a TARGET CELL, and what is the signal

A

1 signal from the MHCI peptide

31
Q

To which cells do tumors become vulnerable after downregulating MHCI

A

NK cells. They will still kill them. Tumors will be invivable for cytotoxic Tcells

32
Q

What is a neo-epitode

A

Newly immunogenetic version of protein evoking Tcell response

Pathology of cancer (7 decks)

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