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CMB > Oncogenesis and metabolism in cancer self study flashcards > Flashcards

Oncogenesis and metabolism in cancer self study flashcards

1
Q

bcr-abl

A

Fusion oncogene. Example of uninhibited tyrosine kinase activity. Activates all downstream signals.

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2
Q

Is carcinogenesis usually somatic or germ line?

A

Usually somatic (nonheritable)

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3
Q

What are germ line mutations?

A

Present in egg or sperm, heritable

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4
Q

What are somatic mutations?

A

Occur in nongermline tissues, nonheritable. May be caused by intefections, toxins.

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5
Q

Early onset bilateral cancers are associated with what?

A

Germline mutations

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6
Q

Knudson 2 hit hypothesis

A

Usually underlying germline mutation (1st hit) and later onset somatic mutation (2nd hit)

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7
Q

What happens if you give an identical twin a stem cell transplant?

A

Perfect match but more risk of relapse because immune systems identical

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8
Q

T-cell depletion in donor bone marrow

A

Cause more relapses, suggesting donor t-cells help eradicate cancer cells

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9
Q

Tumor vaccines

A

Use patient’s own cells to prevent cancer recurrence

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10
Q

6 hallmarks of cancer

A
  1. Sustaining proliferative signaling 2. Resisting cell death 3. Inducing angiogenesis 4. Enabling replicative immortality 5. Evading growth suppressors 6. Activating invasion and metastasis
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11
Q

2 emerging hallmarks of cancer

A
  1. Deregulating cellular energetics 2. Genome instability and mutation
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12
Q

2 enabling characteristics of cancer

A
  1. Avoiding immune destruction 2. Tumor-promoting inflammation
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13
Q

Immune system and cancer

A

Plays critical role in suveillance of, prevention of, and elimination of cancer and pre-cancerous cells. More profound immune dyfunction means higher cancer risk.

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14
Q

What are the 2 most common cancers associated with immunodeficiency?

A
  1. Leukemias 2. Lymphomas
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15
Q

What predisposes someone to leukemia?

A

Damage to bone marrow

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16
Q

Chromosome instability and cancer

A

Fragile chromosomes greatly increase chromosomal mutations and DNA damage. In damaged DNA failure to undergo apoptosis allows persistence of mutations which can lead to cancer.

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17
Q

p53

A

Guardian of the genome. Arrests cell in G1 and G2 when DNA damage is detected to give cell time to repair or die

18
Q

p53 in cancer

A

If mutation in p53 the probability of survival for more than a few years is extremely low.

19
Q

BRCA1 and NBS in breast cancer

A

Participate in DNA repair

20
Q

ATM

A

Mediates response to DNA damage and cell cycle progression. Detects the DNA damage so p53 can drive cell to repair or apoptosis.

21
Q

2 things oncogenes control

A
  1. Cell proliferation 2. Apoptosis (or both)
22
Q

Oncogene product 3 categories

A
  1. Transcription factors 2. Tyrosine Kinase activity (often growth factor receptors and activate downstream targets) 3. Chromatin remodelers “Imprinting”
23
Q

Transcription activators

A

Potent for very active genes (like Immunoglobin genes). Can inappropriately activate oncogenes that can lead to cancer.

24
Q

Philadelphia chromosome

A

Discovered by Janet Rowley. Chromosome 9 and chromosome 22 switched places which is called chronic myelogenous leukemia (CML). This started to convice scientific community that cancer is genetic.

25
Q

Imatinib AKA “Gleevec” AKA STI

A

Drug which has lock and key fit for abnormal Bcr-abl protein. Had 40-50% cure rate and turned it into a 98% cure rate.

26
Q

Imprinting

A

Example of chromatin remodeling. Methylation which changes transcription of a gene, turning off the promoter.

27
Q

Uninhibited activity of growth factors

A

Can happen through imprinting and loss of heterozygosity

28
Q

Loss of heterozygousity

A

One allele vanishes and only one parent’s allele is expressed—uniparental disomy

29
Q

Unilateral disomy

A

Two copies from the SAME parent instead of one copy from each parent

30
Q

Is suppressing the suppressor (p53 and Rb) or activating the activator worse for cancer?

A

Suppressing the supressor (taking away the defense) because the tumor suppressor gene can fix the problems caused by the activator

31
Q

What does loss of tumor suppressors do?

A

Leads to overexpression of oncogenes

32
Q

Vascular endothelial growth factor (VEGF)

A

Stimulates formation of vasculature for new tumor site (there is a drug that targets this)

33
Q

Angiogenesis

A

New blood vessels (does NOT happen normally)

34
Q

Wrong number of chromosomes and embryologic defects

A

Increased risk of cancer

35
Q

What is the difference between embryology and cancer?

A

Embryology is “regulated” growth vs cancer is dysregulated

36
Q

Malignant tumors are characterized by what 4 things?

A
  1. Upregulated cell division 2. Immortality, resistance to apoptosis 3. Ability to metastasize 4. Induce angiogenesis (make new blood vessels)
37
Q

Tumor cells and energy needs

A

Main energy source is glucose-will take it under any conditions. Tumor cells are not responsive to insulin or glucagon. Tumor cells also have high AA requirements for building proteins.

38
Q

Source of glucose for tumor cells

A

Blood (glycogen breakdown oe glucose synthesis in liver). Glycolysis highly upregulated; some glycolytic enzymes become much more efficient variants.

39
Q

Source of amino acids for tumor cells

A

Skeletal muscle

40
Q

Cancer cachexia and 4 causes

A

Unexplained weight loss in cancer patients possibly caused by: 1. Decreased appetite 2. Increased energy need of cancer cells 3. Secretion of factors that stimulate skeletal muscle/fat tissue wasting 4. Endocrine imbalance (insulin resistance, higher cortisol, higher BMR)

41
Q

5 factors released by cancer cells which moderate metabolism

A
  1. ACTH 2. Nerve growth factor 3. Insulin-like growth factor 4. Proteolysis inducing factor 5. Lipid mobilizing factor
42
Q

Host response to tumor

A

Release of IL-1, IL-6, interferon-gamma, tumor necrosis factor-alpha by immune cells which cause fever, proteolysis (breakdown of proteins), lipolysis

CMB (34 decks)

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