Neoplasia 2 Flashcards

1
Q

Two enabling factors of malignancy

A

Tumor promoting inflammation and genomic instability (mutator phenotype)

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2
Q

Examples of tumor suppressor genes

A

Rb, p52, TGF β, APC

These send proliferating cells to enter G0

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3
Q

How do tumors evade apoptosis?

A

Usually by the lost of p53 function that cause over expression of MDM2 which is a p53 inhibitor

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4
Q

What is BCL2?

A

Anti-apoptotic member

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5
Q

Explain the mechanism of how tumor cells have limitless replciative potential (telomeres)

A

Tumor cells deactivate telomerase and thus telomeres do not shorten after replication and thus allowing for limitless replicative potential

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6
Q

Metabolism of cancer cells

A

Warburg metabolism where they favor glycolysis over oxidative phosphorylation

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7
Q
Some ocoproteins (products of mutated oncogenes) causes formation of high levels of abonromal metabolites that leads to \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_? 
Give an example of a metabolite
A

Epigenetic changes and oncogenic gene expression

Ex. Mutated isocitrate dehydrogenase (IDH)

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8
Q

Tumor cells can activate and influence stromal cells.

How are stromal cells changed to allow for tumor cell invasion and metastasis?

A

Proteases remodel the ECM and TGF β promotes epithelial mesenchymal transition (EMT)

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9
Q

Genetic component of HNPCC

A

Micro satellite instability characterized by changes in length of short tandem repeating sequences

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10
Q

Xeroderma pigmentosum have a defect in ____________ (genetics)

A

Nucleotide excision repair pathway

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11
Q

Tumors with high/low growth fractions are susceptible to chemotherapy

A

High;

Growth fraction: # of cycling cells / # of total cells

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12
Q

In tumor cells there is more cells in the proliferative/nonproliferative pool in the cell cycle

A

Proliferative;

Normal cells you will see more of them in the non proliferative pool

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13
Q

Sub populations of tumors may vary in:

A

Antigenicity, invasiveness, metastatic potential, and growth factor requirement

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14
Q

Phases of metastasis

A
  1. Invasion of ECM
  2. Spread into the interstitial tissue
  3. Hematogenous spread and tumor homing
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15
Q

How do tumor cells detach and degrade ECM proteins

A

Detach Bria ↓ Catherine’s

Degrade via colagenase and Cathepsin B

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16
Q

The homing (metastatic site) of tumors is related to:

A
  • presence of absence of specific molecules
  • chemokines
  • unfavorable environment like the muscle
17
Q

Examples of tumor antigens for tumor immunity

A
  • Products of mutated oncogenes and tumor suppressor genes such as RAS, BCR-ABL
  • overexpressed cellular proteins such as PSA
  • antigens produced by viruses
  • oncofetal antigens such as CEA
  • ## altered cell surface protein CA125, CA19.0
18
Q

Tumors with high/low infiltrating lymphotes (CTL and TH1 cells) have a better prognosis

A

High

19
Q

How do tumor cells breakdown the immulogical barrier?

A

Production of proteins that inhibit CTL’s, antigenic modulation and outgrowth of antigen negative clones

20
Q

Therapy involving CLTA4

A

Using an inhibitor antibody for CLTA4 allows CD8 T cells to engage B7 coreceptors and thus activate T cells

21
Q

Immunotherapy involving program cell death ligand

A

Using an anti-PD1 ligand can lead to activation of CTL which kill the tumor cells

22
Q

Describe grade of a tumor

A

Level of differentiation and is particular tot he tumor

Based on differentiation, mitosis and necrosis

23
Q

What is the stage of a tumor

A

Extent of spread

Usually more important than grade

24
Q

Explain the TNM categories in staging a tumor

A

T: size of tumor
N: extent of spread to regional lymph nodes
M: metastases (presence or absence)