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Genetics > Cancer Genetics > Flashcards

Cancer Genetics Flashcards

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1
Q

What are the hallmarks of cancer?

A
  1. Resist cell death
  2. Sustain proliferative signaling
  3. Evading growth suppressors
  4. Activate invasion and metastasis
  5. Enable replication immortality
  6. Induce angiogenesis
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2
Q

Neoplasm

A

Abnormal new growth of cells

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3
Q

Malignant

A

Tumor that invades and metastasizes

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4
Q

Benign

A

Tumor that grows locally

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5
Q

Metastasis

A

Spread to new sites

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6
Q

Why are benign tumors not always harmless?

A

Can cause localized damage

  • ex: broken spine, passing on tissues
  • hormones
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7
Q

Major classifications of cancer (4)

A
  1. Carcinoma
  2. Sarcoma
  3. Leukemia and lymphoma
  4. Neuroectodermal tumors: glioblastoma, Schwanoma
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8
Q

Minor classifications of cancer (4)

A
  1. Melanomas
  2. Small cell lung carcinomas
  3. Teratomas
  4. Anaplastic
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9
Q

What are some environmental risk factors?

A
  1. Smoking
  2. Obesity
  3. Tumor viruses
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10
Q

Ames test

A
  • Looks for reversion mutations
  • salmonella needs histidine
  • put Salmonella in non histidine plate to see if something grows (means there’s a mutation)
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11
Q

Germline cancers are what percent of all cancers?

A

5-10%

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12
Q

Features of heritable cancers in individual patient

A
  • Bilateral primary tumors in paired organs

- Younger than usual age at tumor diagnosis

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13
Q

Features of heritable cancers in patients’ family

A

One first degree relative with the same or a related tumor and one of the individual features listed.
Two or more first degree relatives with tumors of same site.
Two or more first degree relatives with tumor types belonging to a known familial cancer

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14
Q

What is a susceptibility loci?

A

Lock that only increases chance of cancer if combined with another genetic/environmental change

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15
Q

Susceptibility loci are an example of what genetic principle?

A

Gene by environment

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16
Q

Changes that allow metastasis (2)

A
  1. Changes in the genome of cancerous cells

2. Signaling from normal supportive cells (stroma)

17
Q

What is a proto-oncogene?

A

A gene that drives cancer progression when mutated

18
Q

What is a tumor suppressor gene?

A
  • cause loss of expression in proteins necessary to control cancer development when mutated
  • need mutation in 2 copies
19
Q

Caretaker tumor suppressors

A

Involved in DNA repair

20
Q

Broken brake

A

Tumor suppressor-need mutation in 2 copies

21
Q

Stuck gas pedal

A

Oncogenes-only need mutation in 1 copy

22
Q

Describe matrix metalloproteases

A

Proteins on cancer cell that allow breaking down basement membrane of stroma cell. (Clears itself a path to invade healthy cell) (Chew through basement membrane)

23
Q

Major points of determining how to treat a specific cancer

A
  • We now know that the genomic profile is not exactly the same in a specific type of cancer
  • treat by genomic profile?
  • treat by primary tumor location?
24
Q

What is the two hit theory of tumor suppressor gene inactivation?

A
  • An individual is heterozygous for a germline mutation in TSG
  • A second, somatic event inactivates the other normal alleles
25
Q

Examples of two hit theory of TSG

A

Retinoblastoma

26
Q

What causes the second hit in TSG? (3)

A
  1. Mutations
  2. Epigenetic silencing
  3. Loss of heterozygosity
27
Q

What is loss of heterozygosity?

A

Loss of good chromosome or duplication of bad chromosome

28
Q

Familial adenomatous polyposis is an example of what type of cancer?

A
  • Inherited
  • autosomal dominant
  • loss of function of TSG Adenomatous Polyposis Coli affects cell adhesion,cell division, and chromosome copy number
29
Q

DNA repair disorders….tell me about it

A
  • autosomal recessive DNA repair mutations can increase cancer risk
  • if you get mutations in TSG that can’t be repaired, you get cancer
30
Q

Example of DNA repair disorder

A
  • Xeroderma pigmentosum
  • Extremely sensitive to UV rays
  • Minutes in sun cause severe blistering, freckling, dry skin, skin discoloration
  • Half of children with the have skin cancer by age 10
31
Q

Why do we usually not see inherited oncogenes mutations?

A
  • They’re lethal alleles

- Only need one mutated copy, that’s enough to kill you

32
Q

How do you activate an oncogene?

A
  1. Point mutation from proto-oncogene to oncogene
  2. Chromosomal translocations
  3. Chromosomal shattering/chromothripsis (complex rearrangements)
33
Q

Example of chromosomal translocation in activation of oncogenes

A

Philadelphia chromosome

34
Q

What is p53 and what does it do?

A

Tumor suppressor involved in

  • cell cycle regulation
  • DNA repair
  • apoptosis
35
Q

How to use genomics to individualize treatment

A

-Use gene expression profiling (mRNA expression using microarray)

36
Q

Example of targeted drug therapy

A
  • Imatinib/Gleevec for CML
  • active tyrosine kinase leads to unregulated cell division
  • Imatinib is a tyrosine kinase inhibitor
37
Q

Cancer therapy: increase local immune response

A
  • Aldara/Imiquimod
  • topical cream
  • inflammatory response which induces immune response
  • tx for basal cell carcinoma, skin neoplasms, melanomas, genital warts
38
Q

Cancer therapy: CAR T-cell therapy

A
  • approved for children with acute lymphoblastic leukemia and adults with lymphomas
  • T-cells from patient extracted and engineered to make specific antigen receptor
  • T-cell when reintroduced recognizes specific antigens on T cells

Genetics (13 decks)

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