Chapter 10: biology of cancer Flashcards

1
Q

_____ tumor: grow slowly with a well defined capsule

A

Benign

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2
Q

_____ tumor: grow rapidly and not encapsulated

A

Malignant

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3
Q

____ tumor: well differentiated and low mitotic index

A

Benign

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4
Q

____ tumor: poorly differentiated and high mitotic index

A

Malignant

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5
Q

Do benign tumors metastasize?

A

No. Malignant do.

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6
Q

Lipoma, Leiomyoma, and Meningioma are examples of which type of tumor?

A

Benign

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7
Q

Can benign tumors progress to cancer?

A

Yes

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8
Q

Which -oma cancers are malignant? (usually only benign tumors end in -oma)

A

Carcinoma, adenocarcinoma, sarcoma, and lymphoma

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9
Q

Carcinoma arises from

A

Epithelial tissue

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10
Q

Adenocarcinoma cancer arises from

A

ductal or glandular tissue

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11
Q

Sarcoma arises from

A

Mesenchymal tissue

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12
Q

Lymphoma arises from

A

Lymphatic tissue

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13
Q

Sarcoma. B or M?

A

Malignant

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14
Q

Carcinoma, B or M?

A

Malignant

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15
Q

Carcinoma in situ (CIS)

A

Pre-invasive epithelial malignant tumors of glandular or epithelial origin that have not broken through basement membrane or invaded the surrounding stoma

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16
Q

When is an epithelial malignant tumor considered in situ?

A

When the tumor has not broken through the basement membrane or invaded the surrounding stroma

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17
Q

What are possible outcomes of CIS?

A
  1. Remain stable
  2. Regress and disappear
  3. Become cancer
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18
Q

is CIS often treated?

A

Yes

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19
Q

What are the two foundational concepts for understanding biology of cancer cells?

A
  1. Cancer is a very complex genetic disease

2. Tumors exist in a complex microenvironment that contains both benign and cancerous cells.

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20
Q

The microenvironment affects tumors in what three ways?

A
  1. Tumor initiation
  2. Tumor promotion
  3. Tumor progression
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21
Q

Are multiple mutations required before oncogenes are activated?

A

Yes

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22
Q

Name three multiple mutations that are required before onco-genes are activated

A
  1. Small-scale DNA changes
  2. Large changes in chromosomes
  3. Epigenetic changes
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23
Q

After enough mutations, a normal cell transforms into a cancer cell. T or F

A

True

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24
Q

____ _____ means cancer cells accumulate faster than noncancer cells

A

Clonal proliferation

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25
Q

The cell acquires characteristics that allow it to have what over its neighbors?

A

Selective advantage

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26
Q

Increased growth rate or _____ apoptosis increases chances of survival for cancer cell

A

decreased

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27
Q

Hallmark of cancer: ________ immune destruction

A

avoiding

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28
Q

Hallmark of cancer: ______ growth suppressors

A

evading

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29
Q

Hallmark of cancer: ______ replicative immortality

A

Enabling

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30
Q

Hallmark of cancer: Inflammation that…

A

promotes tumors

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31
Q

Hallmark of cancer: Activating invasion and ______

A

metastasis

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32
Q

Hallmark of cancer: ________ ______ (mutator phenotype)

A

Genomic instability

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33
Q

Hallmark of cancer: inducing ______

A

angiogenesis

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34
Q

Hallmark of cancer: _____ cell death

A

resisting

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35
Q

Hallmark of cancer: ______ cellular genetics

A

de-regulating

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36
Q

Hallmark of cancer: ______ proliferative signaling

A

sustaining

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37
Q

What is tumor initiation when considering the complex microenvironment?

A

Produces an initial abnormal cancer cell

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38
Q

What is tumor promotion when considering the complex microenvironment that contains both benign and cancerous cells?

A

Cancer cells multiply and expand

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39
Q

What is tumor progression when considering the complex microenvironment that contains both benign and cancerous cells?

A

Tumor is spreading to local, regional, and distant sites (mets)

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40
Q

Cancer is predominantly a disease of ____ ____ ___ during aging

A

disease of cumulative genetic changes during aging

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41
Q

Which mutation refers to silencing or expression of genes?

A

Epigenetic changes

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42
Q

Cellular genes may become cancerous oncogenes as a result of _____ _____

A

epigenetic changes

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43
Q

Explain how inflammatory and immune cells help tumor growth

A
  1. non-malignant cells nearby release pro-inflammatory mediators.
  2. the i and i cells infiltrate and form the stroma (microenvironment) which helps the cancer suppress the immune system and evade
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44
Q

Stomal cells evolve to phenotypes that promote CA progression and ______

A

metastasis

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45
Q

Can cancer cells proliferate without growth factors?

A

Yes

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46
Q

______ ______: can grow without adhering to normal extracellular matrix (ECM)

A

Anchorage independence

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47
Q

What’s important to remember about anchorage independence?

A

Cancer cells can be grown outside the body/independence for the need of anchorage

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48
Q

_____ also known as cancer cells

A

oncogenes

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49
Q

_____: mutant proto-oncogenes or over-expressed p-o’s; always proliferating/uncontrolled cell death

A

Oncogenes

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50
Q

What genes encode proteins that, in their normal state, negatively regulate proliferation; independent of normal growth factors

A

Tumor-suppressor genes

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51
Q

Example of point mutations

A

in lung cancer, RAS gene converts from regulated to unregulated

52
Q

_______: burkitt lymphomas. Chronic myeloid leukemia: results in an abnormal chromosome called the Philadelphia chromosome. Resulting in the uncontrolled growth of the myeloid

A

Translocations

53
Q

What results in the inactivation of tumor-suppressor genes?

A

Mutations

54
Q

Is Retinoblastoma gene a tumor supressor gene?

A

yes

55
Q

Mutated RB leads to what?

A

Leads to persistent cell growth

56
Q

What is the “guardian of the genome”?

A

Tumor protein p53

57
Q

What does TP53 do?

A

Activates caretaker genes to repair damaged DNA and initiate apoptosis

58
Q

_____ ______ may result from epigenetic silencing, or modulation of gene functioning

A

genomic instability

59
Q

____ _______ leads to an increase in malignant cells

A

chromosome instability

60
Q

______ cells are not _____, and can only divide a limited number of times before senescence or apoptosis

A

Somatic; immortal

61
Q

______ are protective caps on each chromosome that germ and cancer cells target

A

Telomeres

62
Q

In _____ cells, telomeres are held in place by telomerase which allows for longer cell division

A

germ

63
Q

90% of what can activate telomerase?

A

cancer cells (unlimited division and proliferation)

64
Q

______: growth of new vessels

A

angiogenesis

65
Q

Advanced cancers activate this which leads to secretion of angiogenic factors

A

HIF-1alpha

66
Q

Name the highlighted angiogenic factor from the powerpoints

A

Vascular endothelial GF

67
Q

Normal cells generate ATP via oxphos, whereas cancer cells use _____ even under normal oxygen conditions

A

glycolysis

68
Q

Why do some cancer cells also use oxphos along with CAF to under aerobic glycolysis?

A

To secrete usable metabolites, which allow cancer cells to replicate quickly

69
Q

Apoptosis is controlled by the balance of pro-apoptotic and anti-poptotic members of what family?

A

Bcl-2 family

70
Q

What two pathways trigger apoptosis?

A
  1. Intrinsic in response to cellular stress; especially if the DNA is damaged
  2. Extrinsic, via activation of death receptor
71
Q

Dysregulation of intrinsic or extrinsic pathways in most cancers provide resistance to ______

A

apoptotic cell death

72
Q

Is chronic inflammation an important factor in the development of cancer?

A

yes

73
Q

Example of chronic inflammation and its association of cancer?

A

Helicobacter pylori: peptic ulcer disease, stomach carcinoma, and mucosa-asociated lymphoid tissue lymphomas

74
Q

Name three viruses associated with cancers

A

Epstein-Barr virus, Kaposi sarcoma, and HPC (cervical cancer)

75
Q

Cancer cells recruit _____ cells to decrease host immune response

A

immune

76
Q

Treg cell function is manipulated in tumors and used to produce high levels of which immunosuppressive cytokine?

A

Interleukin-10

77
Q

Tumors using interleukin 10 suppresses what two things?

A

Antigen recognition, and the ability of CD8+ T cells to recognize and kill tumor cells

78
Q

Increased treg cells and decreased T cells in the tumor microenvironment also makes the tumor more resistant to what?

A

Chemo treatment and xrt

79
Q

Once cells become malignant, they enhance _______

A

inflammation

80
Q

what is TAM?

A

Tumor associated macrophage

81
Q

_____ cells turn acute inflammatory response on its head from “rejection” to “regeneration” respons

A

cancer

82
Q

the presence of tumor-associated macrophages frequently…

A

frequently correlates with a worse prognosis

83
Q

TAM mimic M1 phenotype of _____, a phenotype that induces cellular proliferation

A

macrophages

84
Q

TAM have a diminished ____ response

A

cytotoxic

85
Q

TAM block T-cytotoxic cells and NK cell functions, and produce cytokines that are advantageous for….

A

tumor growth and spread

86
Q

Direct invasion of contiguous organs is known as ____ ____

A

local spread

87
Q

Metastases to distant organs…cancer is traveling through the _____ and ____

A

Lymphatics and blood

88
Q

Activation and metastasis requires great _____ and occurs late

A

efficiency

89
Q

Epithelial mesenchymal transition is the mode that changes fixed cancer cells to

A

metastatic cancer cells

90
Q

Initially, tumors spread locally through “direct extension” t or f

A

True

91
Q

After growing, tumors spread by invasion into surrounding tissues through the release of _____ ____

A

lytic enzymes

92
Q

Concerning metastases, some cancer cells bind to _____

A

platelets

93
Q

Breast cancer goes into the _____ and lymphomas migrate to the _____

A

bone; spleen

94
Q

Can metastatic cancer cells enter dormancy?

A

Yes

95
Q

Early signs of cancer?

A

Unexplained weight loss. Skin changes, nagging cough, indigestion, and change in bowel habits

96
Q

New growth is called ________ syndromes

A

Paraneoplastic syndromes

97
Q

Paraneoplastic syndromes are commonly caused by ______ and _____.

A

Serotonin and bradykinin.

98
Q

Serotonin and bradykinin are released from _______ tumors

A

carcinoid

99
Q

Hypoxia

A

No oxygen

100
Q

Hypoxemia (like anemia)

A

No oxygen in the blood (is a type of hypoxia)

101
Q

Are paraneoplastic syndromes common? Arise late or early?

A

Not common. arise late.

102
Q

Malignancy has little or no pain during what stage

A

early

103
Q

What is pain from cancer influenced by?

A

Fear, anxiety, sleep loss, fatigue, and overall physical deterioration

104
Q

Name the mechanisms of pain from cancer

A
  • pressure
  • obstruction
  • invasion of sensitive structures
  • tissue destruction
  • inflammation/infection
105
Q

What is the most frequently reported symptom of cancer?

A

Fatigue

106
Q

What is syndrome of cachexia?

A

Most severe form of malnutrition

107
Q

What do you treat anemia with?

A

Exogenous erythropoietin

108
Q

Mechanism of anemia

A

Chronic bleeding resulting from iron deficiency

109
Q

Direct tumor invasion to the bone marrow causes ______ and ______

A

leukopenia and thrombocytopenia

110
Q

Chemotherapy drugs are toxic to the _____ ____

A

bone marrow

111
Q

Risk of infection increases when the absolute _____ and ______ count falls

A

neutrophil and lymphocyte

112
Q

How do they test for cancer

A

Biopsy, aspiration collection, and exfoliative cytology (i.e pap smear)

113
Q

Microscopic analysis for staging cancers is based on presence of _________

A

metastasis

114
Q

Stage I

A

no metastasis

115
Q

Stage II

A

Local invasion

116
Q

Stage III

A

Spread to regional structures

117
Q

Stave IV

A

Distant metastasis

118
Q

Tumor cell markers are substances produced by ____ ___

A

cancer cells

119
Q

Tumor cell markers are found on or in tumor cells, in the ____, ____, or ____

A

blood, CSF, or urine

120
Q

What are tumor markers used to do?

A

Screen and identify individuals at high risk for cancer

121
Q

Tumors are classified based on __________ analysis of protein expression for improved treatment

A

Immunohistochemical

122
Q

_____ chemotherapy is for shrinkage or disapperance of tumors

A

induction

123
Q

______ chemotherapy : eliminate micrometastasis after surgery

A

adjuvant

124
Q

______ therapy: given before localized treatment to shrink tumor

A

Neoadjuvant

125
Q

Cancer tx: gene therapy

A

Patients own T-cells are genetically modified with a new gene for a protein that directs T-cells to target and kill leukemia cells