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Pathology Summer 2020 > Cancer > Flashcards

Cancer Flashcards

1
Q

Neoplasm

A

“new growth” or “tumor”
An uncontrolled growth of new cells.
May be benign or malignant

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2
Q

Benign

A

A neoplasm not capable of metastiasizing
usually not capable of causing death
“bulk effect” may compress tissues around it

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3
Q

Malignant

A

“Cancer”
Neoplasm capable of metastasizing
Capable of causing death- various ways it can do this.

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4
Q

Men and women risk of cancer

A

Men 1:2

Women 1:3

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5
Q

How can some cancer types be preventable?

A

30% of cancer death caused by tobacco use

30% related to obesity, physical inactivity, and poor nutrition.

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6
Q

Preventable causes of cancer

A

HPV vaccine
HBP vaccine
HIV safe practices, PREP prophylactic med.
Heliobacter pylori (can treat with antibiotics)
Skin cancer

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7
Q

Of cancers that affect the eye:
Only ____% of cancers are primary to the eye
___ of cancers metazoic to the eye

A

5-10% primary

90-95% metastatic to the eye.

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8
Q

Where do cancer typically spread to in the eye?

A

Uvea. Highly vascularized.

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9
Q

Most common cancers that spread to the eye

A

Breast and lung cancer

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10
Q

Transofmration

A

Normal cells become cancer cells. This is a long process.

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11
Q

How can cancer cells gain autonomy through mutation?

A

They gain independence from normal cellular controls.

They become anchorage independent (do not need to be anchored in order to divide)
Immortal (telomerase activity)
Evade/avoid apoptosis (telomerase activity)
Angiogenic
Self-stimulating
Insensitive to anti-growth signals
Invasive

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12
Q

Loss of telomeres in a normal cell=

A

Apoptosis

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13
Q

What does it mean that cancer cells are anchorage independent?

A

They do not exhibit contact inhibition and continue to divide, piling up on top of each other. They can proliferate suspended in a soft agar- normal cells cannot and need to be anchored.

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14
Q

How can chronic inflammation lead to cancer?

A

Creates a hyper proliferative environment via cytokines and free radicals. Cytokines signal for cell proliferation and angiogenesis. Free radicals cause DNA damage and can lead to mutation.

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15
Q

Tumor is a wound that

A

Fails to heal. Cancer cells avoid/evade immune system.

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16
Q

Cancer causes: 3 mechanisms

A
  1. Chronic inflammation without infection
  2. Chronic infection with inflammation
  3. Genetic mutations (inherited or environmental)
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17
Q

External causes of cancer

A

Toxins (workplace, cigarette smoke) causes DNA damage or inflammation.

Infections (bacteria, virus, fungus, parasite) cause DNA damage and/or chronic inflammation.

Radiation causes DNA damage

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18
Q

Internal causes of cancer

A

Hormonal imbalance- breast, ovarian, and colon cancer (maybe due to insulin resistance in obesity)

Autoimmune diseases- chronic inflammation

Metabolic disorders: Metabolic byproducts may have toxic effects.

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19
Q

Mutagens

A

Chemical or physical agent that causes a change in the DNA of a cell.

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20
Q

Carcinogen

A

A type of mutagen that contributes to the development of cancer. Changes DNA or metabolic processes.
Causes non-lethal genetic damage

Two types: Initator, promotor

21
Q

Two types of carcinogens

A

Initiator: Causes genetic damage
Promotor: promotes tumor growth

22
Q

Factors that might be carcinogenic

A 
Insecticides
Nitrates
Cisplatin 
Haridresser inhalants 
Very hot beverages
23
Q

Factors that are definitely carcinogenic

A 
Plutonium (radioactive) 
Benzene (oxidation) 
HPV
Alcoholic beverages
Tobacco smoke 
Tanning beds
24
Q

How can viruses cause cancer?

A

Inserting genetic material into infected cells.

Initiating a chronic inflammatory response.

25
Q

Viruses associated with cancers

A 
Hepatitis B and C
Epstein Barr 
Herpes virus 
Human papilloma virus 100% causes cervical cancer
Lymphoma virus
26
Q

How can bacteria cause cancer?

A

Chronic infection= chronic inflammatory response = cancer
More likely with high concentration of bacteria

Helicobacter pylori associated with peptic ulcer disease, stomach carcinoma, and MALT lymphomas.

27
Q

Cancer tends to involve multiple mutations

A

Mutation inactivates suppressor gene
Cells proliferate
Mutations inactivate DNA repair genes
Proto-oncogenes mutate to oncogenes

28
Q

Proto-oncogenes

A

Code for proteins that regulate cell growth and proliferation.
Normal and necessary
Capable of becoming an oncogene with one mutation.

29
Q

Oncogene

A

Can cause a cell to become a cancer cell.
Come from mutated proto-oncogene.
Growth and proliferation are no longer regulated.
Over-active growth signals. More receptors = more activity.

30
Q

Tumor suppressor genes

A

Act like a break pedal. Slow down cell proliferation or induce apoptosis when cell damage is present. Same as anti-oncogenes.

31
Q

Anti-oncogenes

A

Tumor suppressor genes. Act like a brake pedal.

32
Q

What happens if there is a mutation in a tumor suppressor gene?

A

Mutation allows for unregulated growth. Both copies must be inactivated for progression of cancer

33
Q

How many copies of the tumor suppressor gene must be inactivated for progression of cancer?

A

2

34
Q

p53 (a tumor supressor gene)

A

P53 is activated if there is DNA damage. It will be made into a protein that can stall division until the DNA is fixed. High levels of P53 protein in the cell will initiate apoptosis.

35
Q

Most common tumor suppressor gene defect

A

P53.

Greater than 1/2 of all types of tumors lack functional p53.

36
Q

What is the goal of chemotherapy/radiation?

A

Will hopefully cause DNA damage, activating p53 to be made.

This will only work if there is a functioning P53 allele in the cell. Cell with 2 mutated alleles will not respond to chemo.

37
Q

Point mutation

A

Changes in 1 base pair. Ex: Sickle cell anemia

Can be mutated or inherited

38
Q

Gene amplification mutation

A

Duplication of a small piece of chromosome over and over. Can result in an increased expression of an oncogene. Greater likelihood it could mutate into protoncogene.

39
Q

Chromosome translocation in somatic cell mutation

A

Piece of one chromosome is transferred to another. Leads to excess production of abnormal protein or novel protein that may have new role.

Ex: Chronic myeloid leukemia and philadelphia chr (9 +22 translocation)

40
Q

What happens if there a mutation to a caretaker gene?

A

Loss of these genes lead to increased mutation.

Normal role is to help with gene repair.

41
Q

Chromosome instability (increased in malignant cells after continuous replication) occurs during mitosis and can lead to:

A

Chromosome loss
Loss of heterozygosity
Chromosome amplification (duplication of small piece of Chr over and over)

42
Q

How could an epigenetic mutation lead to cancer?

A

Abnormal silencing of tumor suppressor genes could lead to cancer. By methylation or histone modification.

Or loss of silencing for oncogenes. (Taking foot off break -tumor suppressor gene, and putting it on the gas- oncogene)

43
Q

Hereditary cancers are largely associated with

A

Tumor suppressor genes and rarely associated with oncogenes.
Usually heterozygous initially, then at risk for loss of heterozygosity.

44
Q

How many cases of retinoblastoma are inherited

A

1/2 due to mutated/deleted Rb1 gene that should suppress cell growth.

45
Q

What does RB1 code for in retinoblastoma

A

Proteins, pRB, that suppress growth. Regulates cell cycle.

46
Q

Clinical signs of retinoblastoma

A

Leukocoria
Strabismus
Loss of vision

47
Q

Is retinoblastoma unilateral or bilateral

A

75% are unilateral.

All bilateral cases are inherited.

48
Q

Hereditary of retinoblastoma

A

Autosomal dominant with incomplete penetrance

49
Q

How can you lose heterozygosity

A

Child must be born heterozygous for the allele- one normal and one mutant. Occurs when eyes are developing, during on-going cell division.

  1. Messegregation
  2. Mitotic recombination

Pathology Summer 2020 (19 decks)

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