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Patho > Topic 6 - Neoplasia > Flashcards

Topic 6 - Neoplasia Flashcards

1
Q

What is Neoplasia?

A

Abnormal Cell growth
–> Can be Benign or malignant

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2
Q

What are carcinomas?

A

Cancer of epithelial cells

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3
Q

What is the most common kind of cancer?

A

Carcinoma (>90% of cancers, accounts for 80% of deaths)

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4
Q

What are adenocarcinomas?

A

Cancer of secretory epithelia
e.g., lung, colon, breast, pancreas, stomach, esophagus, prostate, endometrium, ovary

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5
Q

What is squamous cell carcinoma?

A

Cancer of protective cell layers
–> e.g., skin, nasal cavity, oropharynx, lung, esophagus, cervix

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6
Q

What are sarcomas?

A

Cancer in bone, connective tissue, and muscle

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7
Q

How common are sarcomas?

A

They account for 1% of tumors

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8
Q

What is leiomyosarcoma?

A

Cancer of smooth muscle

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9
Q

What is Rhabdomyosarcoma?

A

Cancer of skeletal muscle

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10
Q

What is angiosarcoma?

A

Cancer of the lymph lining of vessels

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11
Q

What are neuroectodermal malignancies?

A

Cancer that originates in neuroectoderm tissue

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12
Q

What is the most common form of neuroectodermal malignancy?

A

Glioblastoma - cancer of glial cells

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13
Q

What is leukemia?

A

Cancer present in bone marrow, circulates in blood

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14
Q

What is lymphoma?

A

Cancer that originates in lymph tissue and is confined to lymph nodes + tissue

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15
Q

What are myelogenous leukemias?

A

Cancers from the myeloid progenitor branch that originate in bone marrow

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16
Q

What are lymphocytic leukemias?

A

Cancers from the lymphoid progenitor branch that originate in lymph.

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17
Q

Where do chronic leukemias arise from?

A

Mature cells, and they therefore have a slow progression

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18
Q

What is CML?

A

Chronic myelogenous leukemia

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19
Q

When is the onset typical onset of CML? What at typical common characteristics of it?

A

Onset around 40-50 years
–> Typically granulocytic leukemia containing the Philedelphia chromosome

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20
Q

What is the Philadelphia chromosome?

A

A change in the BCR gene to produce BCR-ABL
–> BCR is expressed in high levels in most cells
–> ABL modulates cell growth

When expressed together, this fusion produces a powerful oncogene: cells with high expression of a gene that codes for cell growth (very fast growing cells)
Associated with CML

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21
Q

How is CML treated?

A

Chronic myelogenous leukemia is treated with imatinib, a tyrosine kinase inhibitor.
Bone marrow transplant, and limited use of standard chemotherapy.

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22
Q

From where do most acute leukemias arise? At what age is their onset?

A

Arises early in immature cells
–> 80% are acute myeloid leukemias
–> Mostly onset before 60 years

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23
Q

What is M2/M3 leukemia?

A

Acute promyelocytic leukemia

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24
Q

How is acute leukemia treated?

A

Chemotherapy

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25
Q

Which kind of leukemia can be successfully treated with retinoic acid?

A

M2/M3 - Acute promyelocytic Leukemia

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26
Q

What is the prognosis for M0/M1 Leukemia?

A

The prognosis for undifferentiated acute myeloblastic leukemia is poor due due rapid disease progression.

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27
Q

Chronic Lymphoid Leukemia (CLL)
–> What kind of cell causes most cases?
–> When is onset and how does it progress?
–> Symptoms?

A

Causes most frequently by B cells

Onset 60-70 years, with slow progression.

Patients often present with fatigue and weight loss, with eventual lymphadenopathy.

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28
Q

Acute Lymphoblastic Leukemia/Lymphoma (ALL)
–> What kinds of cells usually cause it?
–> What age does it usually affect and what is the prognosis?
–> Symptoms?

A

80% B cell and 20% T cell

It is the most common malignancy in children 3-7, and has a good prognosis with treatment, especially the pre-B cell subtypes.
It also occurs in those 40-50 years, with a worse prognosis.

Rapid onset of symptoms: Bone pain, bruising, fever, infection.

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29
Q

What is lymphedenopathy?

A

Swelling of the lymph nodes

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30
Q

Hodgkin’s Lymphoma is accounts by what percent of lymphoma?

A

30%

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31
Q

What is characteristic of Hodgkin’s Lymphoma? How is it treated? What is the prognosis?

A

Characterized by Reed-Sternberg cell, derived from B cells.
This kind of cancer metastasizes along continuous lymph nodes - but is usually first evident in cervical lymph nodes.

Treated with localized radiation/chemotherapy.

If caught early, 90% of patients survive 10 more years

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32
Q

What are Reed-Sternberg cells?

A

A type of multinucleated cells derived from B cells. Associated with Hodgkin’s lymphoma.

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33
Q

Hodgkin’s lymphoma can be organized into how many subgroups?

A

Four subtypes - depending on numbers of different inflammatory cells present.

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34
Q

How many subgroups can Non-Hodgkin’s lymphoma be sorted into?

A

15-20, depending on characteristics

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35
Q

Non-Hodgkin’s Lymphoma:
Involves which kind of cells?
When is onset and what is the prognosis?

A

Involved B, T and NK cells with no evidence of Reed-Sternberg cells

Adult onset with variable prognosis and treatment because many patients present with advanced disease

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36
Q

Genetics play a role in cancer, but what is the biggest factor impacting cause of cancer for most individuals?

A

Modifiable risk factors - such a diet and lifestyle

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37
Q

What kind of cancer can tobacco use be related to?

A

Lung, bladder, and kidney

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38
Q

What kind of cancers are high-fat, low fiber, and broiled/fried foods related to?

A

Bowel, pancreas, prostate and breast cancers.

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39
Q

What are the basic building blocks of DNA?

A

Cytosine, Thymine, Adenine, and Guanine.

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40
Q

What are codons? What identifiable pattern is present for most of them?

A

Codons are triplets of DNA bases that code for amino acids.

The first 1-2 bases on most codons are the same - this provides some leeway for mutations

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41
Q

What is a point mutation?

A

Occurs in a genome when a single base pair is added, deleted or changed.

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42
Q

What kind of mutation is a base deamiantion?

A

A point mutation

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43
Q

What happens when cytosine undergoes base deamination?

A

It becomes Uracil.

Uracil is not part of DNA, so the DNA must be repaired if it is present. The process of replacing damaged bases repeatedly can overwhelm the system designed to fix it, which can result in the wrong base being placed instead of the uracil.

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44
Q

What are ROS?

A

Reactive Oxygen Species
Independent molecules containing an oxygen that are capable of causing direct damage to bases and DNA.
e.g., hydroxyl radical (OH-), superoxide anion (O2-)

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45
Q

What produces ROS?

A

Radiation, UV, and metabolic cellular stresses.

46
Q

Why are antioxidants important?

A

They can reduce the amount of reactive oxygen species present in the body

47
Q

How does UV radiation impact DNA?

A

It causes cross linking of pyrimidines, which causes pyrimidine dimers.

These dimers have to be removed and replaced, which predisposes the repair mechanism to make a mistake –> Mutation

48
Q

How does BPDE (a carcinogen) impact DNA? Who does this impact most commonly?

A

Can form adducts - large molecules attached to bases, must be replaced in order to replicate.

Adducts often result in replacing Guanine with Thymidine.
–> Very common with smokers.

49
Q

What is an insertion mutation?

A

A mutation where a new base is introduced where is does not belong. Results in Frameshift.

50
Q

What is a deletion mutation?

A

A mutation where a base is removed from where it should be. Results in

51
Q

What is frameshift?

A

Occurs in a deletion or insertion mutation - results in a string of incorrect bases that code for a mutant or shortened protein.

52
Q

What is a nonreciprocal intrachromosomal translocation?

A

When part of a chromosome is shifted to a different part of the same chromosome.

53
Q

What is a Nonreciprocal Interchromosomal translocation?

A

When part of a chromosome is shifted onto another chromosome.

54
Q

What is a Reciprocal Interchromosomal translocation?

A

When two chromosomes trade part of a piece of information.

55
Q

What is gene amplification?

A

The increase in the number of copies of a gene sequence.

For example, an amplification where multiple HER2 genes are overexpressed results in a cell with many HER@ receptors. As a results, the cell with more of a receptor that signals for cell growth with proliferate faster.

56
Q

What is a HER2+ cell?

A

HER2 is a receptor that signals for cell growth.

Cells that are HER2+ have multiple HER2 gene overexpressions, and therefore too many receptors that code for growth

57
Q

There are two kinds of genes involved in the development of cancer. What are they?

A

Tumor suppressor genes and oncogenes.

58
Q

What are tumor suppressor genes?

A

Normal cells that slow down cell growth and screen for DNA damage.

59
Q

List Three Important tumour supressors

A

–> Rb
–> BRCA1/2
–> P53

60
Q

What are the phases of the cell growth cycle?

A

G1
–> Growth (gap) phase 1. Cell grows and duplicates organelles.
S
–> DNA replication and synthesis
G2
–> Secondary growth period

61
Q

Some tumor suppressor genes are known as “gatekeepers.” What is the role of these genes?

A

To prevent entry into the cell cycle or induce cell death. Their role is to prevent or enable to cell to enter different phases.

62
Q

Some tumor suppressor genes are known as “caretakers.” What is the role of these genes?

A

To repair DNA and maintain its integrity.

63
Q

What is the role of the retinoblastoma (Rb) gene?

A

To prevent the cell from entering G1.

64
Q

What kind of cancer is retinoblastoma? Who does it usually affect?

A

A rare type of retina cancer that usually develops before the age of 5.

65
Q

What is hereditary retinoblastoma? How many eyes are usually affected?

A

When a child is born with one defective copy of the gene, so only one needs to mutate for the cancer to develop.
Additionally, having lost one gene predisposes you to losing the other.

Usually affects both eyes.

66
Q

What is Non-hereditary retinoblastoma?

A

When a person is born with normal Rb genes, but during childhood they both mutate.
Because having only one gene predisposes you to losing the other, usually only one eye experiences the first somatic mutation, and it usually only affects one eye.

67
Q

How many copies of Rb have to become mutated to result in cancer?

A

Both of them.

68
Q

What is p53?

A

An important tumor suppressor that acts as both a gatekeeper and a caretaker.

69
Q

What are the two roles of p53?

A

To induce apoptosis and activate checkpoints to stop the cell cycle in response to stress and DNA damage.

Evidence shows that mice missing both copies of the gene die have dramatically shortened lifespans.

70
Q

Almost all types of cancer are associated at least in some part to a mutation of which gene?

A

p53

71
Q

Does the Rb gene only impact the retina?

A

No. People with a mutated Rb likely will likely develop other cancers, and not just retinosarcomas.

72
Q

What is Li Fraumeni Syndrome?

A

When a person is a heterozygous mutation of the p53 gene. This person an incredibly high risk of developing cancer in their lifespan - especially sarcomas, breast cancer, lymph/leukemias, and adrenal cancers.

73
Q

Why is it so important that young people are vaccinated for HPV?

A

HPV is associated with cervical cancer.
HPV produces a protein that binds to and degrades p53 - cells are then therefore subject to genomic instability and will result in cancer.

74
Q

What are the roles of BRCA1/2?

A

They are tumor suppressors that act as caretakers in the S phase. Mutations in these genes are associated with familial breast cancer.

75
Q

Which gene is responsible for responding to both internal and external stresses of the cell and generating stop check points to prevent it from progressing further into the cell cycle?

A

p53

76
Q

What is senescence?

A

The cessation of cell division.

77
Q

What are oncogenes?

A

Mutations of genes that promote cellular processes necessary for cancer cell proliferation and survival - they maintain viability in addition to promoting multiplication, but can be coopted for cancerous growth

78
Q

There are typically two kinds of oncogenes, what are they? Give an example of both.

A

Growth factors receptors and proteins that help growth factor receptors to function
e.g., HER2/neu, EGF, Ras

Proteins that are involved in the transcription of genes involved in cell proliferation.
e.g., myc

79
Q

Many treatments for cancer aim to inhibit which proteins?

A

Oncogenes - help cancerous cells with proliferation and viability.

80
Q

What is a pro/proto-oncogene?

A

A normal protein that we need to survive that can be co-opted to be overexpressed if there is a mutation. Once mutated, they have the capacity to become oncogenes.

81
Q

What is Myc?

A

A transcription factor for D cyclin, which is responsible for activating genes in G1.

82
Q

What is the R point in G1?

A

The point where all necessary organelles and RNA has been synthesized - the cell no longer requires signaling from growth factors to progress into S phase.

83
Q

What is Ras? Why is it so good at this?

A

Ras is an oncogene
–> Growth factors involved in inhibiting apoptosis, and stimulation of protein synthesis
–> Involved in the signaling for cell movement (metastasis)

84
Q

What is HER2/neu?

A

Oncogene - A growth factors receptor.

85
Q

What is Herceptin (trastuzumab)?

A

An antibody used to kill cells expressing HER2/neu on their surface.
Has been very successful therapy for this kind of breast cancer.

86
Q

Why is is possible to target HER2/neu expressing cells with an antibody drug, when this is not possible with Ras?

A

Because HER2/neu is a surface receptors, whereas Ras is expressed internally and reacts more downstream than HER2/neu.

87
Q

Which system s used to stage tumors?

A

The TNM system.
T - extent of tumor
N - spread to lymph nodes
M - A number indicating the size of extent of metastasis.

88
Q

What is Carcinoma in Situ? What stage is this cancer?

A

Stage 0 - an early cancer that is only present in the layer of cells in which it began. Currently non-invasive.

89
Q

What is stage I, II, and III cancer?

A

Higher numbers in this range indicate more extensive disorder.
e.g., greater size, spread to nearby lymph nodes, or adjacent organs.

90
Q

What is stage IV cancer?

A

The cancer has spread to another organ - clear, distant, metastasis.

91
Q

What is hyperplasia?

A

Abnormal cell growth that has not yet invaded the basement membrane, the amount of mutations if still relatively small.

92
Q

A a cancerous cell’s phenotype transforms, it produces enzymes that break down the basement membrane. How does it do this?

A

It produces enzymes that cleave collagen, making it easier for the cell to move into the basement membrane.
At this point, laminin and fibronectin receptors gain more access to the basement membrane and the cell pulls our of its normal position.
After punching through the stroma, they begin producing autocrine motility factor, which allows the cell the finish the job and escape the basement membrane.

93
Q

How does stroma affect cancers?

A

Fibroblasts and other cells in stroma can help cancer cells to grow.

94
Q

Does hyperproliferation indicate cancer?

A

Not necessarily, it must be atypical and cells must have hits to many oncogenes/tumor suppressors for it to progress into cancer.

95
Q

In order for a ras mutation to cause cancer, the cells still need to get rid of ___ to become cancerous.

A

p53 tumor suppressor.

96
Q

Cells require repeated exposure to a promotor in for a tumor to grow before an initiator mutates to alter a tumor suppressor, why is this?

A

Because even cells with an oncogene like ras mutated, with no p53 mutation a promotor is still needed to induce cell proliferation.

Once p53 has mutated the cells can expand independent of the promotor - only at this point are they considered cancerous.

97
Q

_____ can act as a tumor promotor is Breast Cancer. How can this receptor be blocked?

A

Estrogen
–> Receptors can be blocked by tamoxifen

98
Q

Breast cancers are subdivided into three main subtypes. What are they?

A
  1. Estrogen+/progesterone receptor+
  2. HER2/neu +
  3. Triple negative
    –> No presence of overexpression of hormone/growth factor receptors.
99
Q

Where are estrogen receptors located?

A

Within the cytoplasm - move into the nucleus in the presence of estrogen and act as a transcription factor.

100
Q

How is triple negative breast cancer treated?

A

Must be treated with chemotherapy.

101
Q

What is an adenoma?

A

A benign tumor.

102
Q

In a PET scan, areas of high metabolic activity glow yellow. Why is this?

A

Areas of high metabolic activity include cancerous cells and the brain.
PET scans with radioactive dye (F18 (Fluorodeoxyglucose) allow for imaging and identification or metastases

103
Q

Which dye is used in PET scans to identify metastases?

A

F18, Fluorodeoxyglucose
–> Cancer cells are dependent on and use a lot of glucose
–> So does the brain

104
Q

What kind of imaging can be used to identify metastases?

A

MRI, PET & CT scan.

105
Q

What is intravasion?

A

When cancer cells squeeze into blood vessels and interact with normal blood and the immune system.
This allows them to metastasize and camouflage from the immune system.

106
Q

What kinds of cancer like to metastasize to the bone, liver, and lung?

A

Bladder, breast, kidney, lung, melanoma, prostate, thyroid, and uterus.

107
Q

What kinds of cancer like to metastasize to the liver, lung and peritoneum?

A

Colorectal, ovary, pancreas, stomach, uterus.

108
Q

What kind of cancer likes to metastasize to the adrenals?

A

Kidney, lung, prostate

109
Q

What is the biggest risk factor in increasing risk for cancer?

A

Aging
–> Aging is associated with the production of inflammatory factors, which contribute to initiation, promotion, and progression of cancer.

110
Q

What are the systemic effects of cancer?

A

Cachexia
–> Reduced appetite
–> Strongly increased metabolism
–> Production of tumor necrosis factor

+ Leukopenia

111
Q

What is leukopenia?

A

Decreased WBC count

112
Q

How does tumor necrosis factor impact body cells?

A

It causes harm and death to normal body cells.

Patho (14 decks)

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