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AU17: Gen Pathology > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

Define neoplasia.

A

New growth - lack of responsiveness to normal growth controls

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2
Q

What is the study of neoplasms called?

A

Oncology

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3
Q

T/F: Benign neoplasms are often localized, slow growth.

A

TRUE

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4
Q

T/F: Benign tumors can move to other sites in the body.

A

FALSE

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5
Q

How can benign tumors cause serious problems for patients?

A

Can grow and put pressure on vital areas (ex. Major artery)

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6
Q

What is the most important differentiation between a benign and malignant cancer?

A

Malignant cancers can undergo METASTASIS

Can invade and destroy adjacent tissue

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7
Q

What is the difference between the parenchyma and the stroma?

A

Parenchyma: actual cancer cells making the tumor

Stroma: supporting connective tissue for the tumor

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8
Q

How are benign tumors named?

A

Type of parenchymal cell followed by -oma.

Ex. Fibroma, osteoma, etc.

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9
Q

What is a papilloma?

A

Benign tumor on surface epithelium with numerous finger-like projections

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10
Q

How are malignant tumors of mesenchymal tissue named?

A

Parenchymal tissue plus -sarcoma.

Ex. Fibrosarcoma, osteosarcoma, etc.

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11
Q

Describe the differences between a hamartoma and a choristoma?

A

Hamartoma: tissue normally found at the site

Choristoma: tissue not normally found at the anatomic site

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12
Q

A ____________ is a neoplasm derived from more than one germ layer.

A

Teratoma

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13
Q

What is the term for an epithelial malignant tumor?

A

Carcinoma

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14
Q

What are some various exceptions to nomenclature in malignant neoplasms?

A
  1. Lymphoma - lymph tissue
  2. Melanoma - melanocytes
  3. Mesothelioma - pleural
  4. Seminoma - testicular
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15
Q

T/F: Benign tumors have often lost their differentiation and do not resemble their tissue of origin.

A

FALSE

Benign are well-differentiated

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16
Q

T/F: Malignant tumors may have a wide range of differentiation.

A

TRUE

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17
Q

What is the term for a poorly-differentiated malignancy?

A

Anaplastic malignancy (high-grade)

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18
Q

What are some characteristics of anaplasia?

A
  1. Pleomorphism (odd size and shape)
  2. Nuclear hyperchromatism
  3. Atypical nuclei
  4. Odd mitotic patterns
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19
Q

__________ describes a tissue with disorderly growth, that although not cancerous, has the potential to become neoplastic.

A

Dysplasia

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20
Q

What is the most severe form of epithelial dysplasia?

A

Carcinoma-in-situ

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21
Q

T/F: If the cells of a tumor continue to show functional ability of the original cell-type, the cancer is more likely to be very severe.

A

FALSE

Functional ability means the cell is still well-differentiated.

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22
Q

Why might there be areas of necrosis in the center of a large malignancy?

A

It is growing so fast that it outgrows its blood supply

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23
Q

Many benign tumors have a __________, a compressed layer of connective tissue enclosing the tumor.

A

Capsule

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24
Q

What are two common benign neoplasms that do not have a capsule?

A

Hemangioma and neurofibroma

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25
Q

What is the most reliable feature in distinguishing malignant from benign tumors?

A

LOCAL INVASIVENESS

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26
Q

What is considered the hallmark of malignancy?

A

Metastasis

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27
Q

The process where malignancies invade nearby surrounding tissue is ___________; while the development of secondary deposits of a tumor at a distant site is __________.

A

Local invasions; metastasis

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28
Q

T/F: Basal cell carcinoma will rarely metastasize.

A

True

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29
Q

Approximately ___% of newly diagnosed patients with solid tumors will have metastases.

A

30%

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30
Q

What makes a tumor more likely to metastasize?

A

The larger and more anaplastic it is

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31
Q

What are the three ways which a neoplasm can metastasize?

A
  1. Seeding within body cavities
  2. Lymphatic spread
  3. Hematogenous spread
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32
Q

Which type of cancer spreads through both the blood and lymphatics?

A

Melanoma

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33
Q

Which types of cancers typically spread via the lymphatics? Via blood?

A 
Lymphatics = carcinomas
Blood = sarcomas
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34
Q

In 2017 there was how many deaths due to cancer?

A

600,000

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35
Q

What have been the trends of incidence in males and females over the last 50 years?

A

Increase in males but decrease in females. Most likely due to pap smears

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36
Q

Women have seen in increase in ______ cancer, but a decrease in _______ cancer over the last 40 years.

A

Lung; uterine

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37
Q

Approximately what proportion of cancer risk can be attributed to environmental factors?

A

2/3

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38
Q

Stomach cancer is much more common in Japan, while breast and prostate cancer is much more common in the U.S. What would the incidence trend be over several generations after a Japanese immigrant comes to the United States?

A

The incidence of stomach cancer would decrease, while the incidence of breast and prostate cancer would increase.

Because environment plays greater role than genetics

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39
Q

Between what ages does most cancer mortality occur?

A

Between 55-75

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40
Q

Cancer accounts for what percentage of deaths among children under 15 years of age?

A

10%

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41
Q

T/F: Cancer occurs in 1 out of every 5 people.

A

True

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42
Q

What are the three broad categories of genetic predisposition to cancer?

A
  1. Inherited cancer syndromes
  2. Familial cancers
  3. Defective DNA repair
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43
Q

What are some common inherited cancer syndromes?

A
  1. Retinoblastoma
  2. Familial adenomatous polyposis
  3. Multiple endocrine neoplasia
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44
Q

Inherited cancer syndromes are usually due to a ________ _____ mutation and generally show autosomal __________ transmission.

A

Single gene; dominant

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45
Q

T/F: Breast, colon, and ovarian cancers commonly run in families.

A

True

46
Q

What percentage of all human cancers have an identifiable heritable basis?

A

5-10%

47
Q

What is an acquired preneoplastic disorder?

A

A setup for cancer that is characterized by persistent regenerative cell replication.

48
Q

What is the central molecular basis of all cancers?

A

Nonlethal genetic damage

49
Q

What are the three classes of genes (and their functions) that are often affected in cancer cells?

A
  1. Protooncogenes: promote growth
  2. Cancer suppressor genes: inhibit growth
  3. Apoptosis genes: promote cell death
50
Q

T/F: Most cancers are a result of a few genetically altered cells.

A

False

Most come from just one altered cell

51
Q

What type of genes play an indirect role in the onset of carcinogenesis?

A

DNA repair genes

52
Q

Carcinogenesis is a multi-step process both _________ and _________.

A

Phenotypically and genetically

53
Q

What is the difference between a protooncogene and an oncogene?

A

Protooncogenes and oncogenes produce identical proteins except oncoproteins are NOT regulated

54
Q

T/F: In carcinogenesis, protooncogenes are transformed to oncogenes.

A

TRUE

55
Q

What are the two ways that oncogenes are activated?

A
  1. Structural mutation of the gene -> abnormal product

2. Altered regulation of gene expression -> increased production of normal product

56
Q

What is the most commonly mutated proto-oncogene?

A

RAS

57
Q

How does the mutant RAS differ from the normal RAS?

A

Cell continues to recieves signals to divide due to the inability for RAS to be deactivated properly

58
Q

What is the most commonly affected nuclear transcription factor leading to carcinogenesis?

A

MYC gene

59
Q

How does MYC mutation lead to carcinogenesis?

A

MYC gene is constantly overexpressed -> cell continuously dividing

60
Q

What role do CDKs play in carcinogenesis?

A

CDKs play important role in determining if a cell will enter the cell cycle. Over-expression is seen in a variety of tumors.

61
Q

While protooncogenes __________ cell growth, suppressor genes ________ cell proliferation.

A

stimulate; inhibit

62
Q

What was the first tumor suppressor gene to be discovered?

A

Retinoblastoma (Rb)

63
Q

Describe Knudson’s two-hit hypothesis for retinoblastoma.

A

For someone to develop Rb they inherit one mutated Rb allele, then the second must be mutated somatically.

Either way BOTH alleles must be mutated

64
Q

T/F: The products of tumor suppressor genes are more well understood than those of protooncogenes.

A

False

65
Q

T/F: Many of the tumor suppressor gene products regulate the cell cycle, cell adhesion, and signal transduction.

A

True

66
Q

What is pRb’s role in regulating growth?

A

Binds transcription factors to regulate the cell-cycle

67
Q

What gene is the single most common target for genetic alteration in human tumors?

A

TP53

68
Q

T/F: The homozygous loss of TP53 is found in virtually every type of cancer.

A

True

69
Q

What is Li-Fraumeni syndrome?

A

Being born with one mutated TP53 gene - higher risk of cancer

70
Q

What is the role of normal TP53 products in the nucleus?

A

Slows the cell cycle during to allow time for the repair of DNA damage. If repair fails TP53 will trigger apoptosis

71
Q

What would happen to a cell if TP53 was not functioning?

A

DNA damage would be incorporated into the DNA and the cell would continue to divide without undergoing apoptosis

72
Q

What is the prototypic anti-apoptosis gene?

A

BCL2

73
Q

The (over or under)expression of BCL2 protects cells from apoptosis?

A

Over-expression

74
Q

T/F: A mutation in BCL2 will normally result in “high-grade” lymphomas.

A

FALSE

Slow growing so “low-grade”

75
Q

What are the two major phases of metastasis?

A
  1. Invasion of extracellular matrix

2. Vascular dissemination and adhesion/homing of tumor cells

76
Q

What is the process for tumor cells to invade the extracellular matrix?

A
  1. Tumor cells detach from each other
  2. Attach to ECM components
  3. Degradation of ECM components
  4. Migration
77
Q

T/F: Tumor cells are in danger of being destroyed by host immune cells in the blood stream?

A

TRUE

78
Q

How can one predict possible metasteses sites?

A

Follow the lymphatic and venous drainage from the original tumor site

79
Q

What is organ tropism?

A

Tumor cells can only bind to specific sites when metastesizing

80
Q

What is a familial disease that can lead to cancer of the colon that results from a defect in DNA mismatch repair and MSI?

A

Hereditary nonpolyposis colon cancer syndrome

81
Q

__________ ___________ puts patients at higher risk for skin cancers due to an inability to repair UV damage.

A

Xeroderma pigmentosum

82
Q

Bloom syndrome, ataxia telangiectasia, Fanconi anemia, and BRCA 1 & 2 breast cancers all cause _________ DNA.

A

fragile

83
Q

T/F: Most cancers are the result of a single DNA mutation.

A

FALSE

Combo of several genetic alterations

84
Q

What happens to the tumor cells as they continuously divide that could cause newer tumor cells to be more resistant to therapies?

A

As they divide they continue to develop more and more mutations

These severely mutated “subclones” are often selected for survival

85
Q

Give an example of a balanced translocation that commonly leads to cancer.

A

Translocation between chromosome 22 and 9 - chronic myelogenous leukemia

86
Q

What type of karyotypic changes often result Rb, colon, and oral cancer?

A

Deletions

87
Q

Neuroblastomas and some breast cancers can be caused by this type of karyotypic change.

A

Gene amplifications

88
Q

What are the three major classes of carcinogenic agents?

A
  1. Chemicals
  2. Radiation
  3. Virus
89
Q

What was the first link between chemical carcinogens and cancer?

A

Sir Percival Pott linked chimney soot to scrotal skin cancer

90
Q

T/F: Only synthetic compounds are capable of causing cancer.

A

FALSE

Both natural and synthetic chemical carcinogens

91
Q

T/F: Most chemical carcinogens directly react with the nuclear DNA.

A

FALSE

Most are indirect - become active after metabolic conversion

92
Q

In indirect chemical carcinogens, the ___________ is the original chemical, while the __________ is the active metabolite.

A

Procarcinogen; ultimate carcinogen

93
Q

T/F: All chemical carcinogens are highly reactive electrophiles.

A

True

94
Q

How long are latent periods between radiation exposure and cancer development?

A

7-12 years

95
Q

Which RNA oncogenic virus is indemic in parts of Japan and the Caribbean basin?

A

Human T-cell Leukemia Virus Type I

96
Q

How long is the latent period for T-cell Leukemia Virus Type I?

A

20-50 years

97
Q

What are three common DNA oncogenic viruses?

A

HPV, EBV, and Hep B

98
Q

What is the difference between tumor-specific antigens and tumor-associated antigens?

A

Specific: only associated with tumor cells

Associated: found on normal cells, but may be over-expressed in neoplastic cell

99
Q

What are four antitumor effector mechanisms?

A
  1. Cytotoxic T cells: virus induced cancer
  2. NK cells: first line of defense
  3. Macrophages
  4. Humoral factors
100
Q

What is the strongest evidence to show that the immune system plays a role in seeking out and destroying cancer cells?

A

Immunocompromised patients have a large increase in risk of developing cancer

101
Q

How do tumors evade the immune system?

A
  1. Selection of antigen-negative subclones
  2. Reduced expression of histocombatible cells
  3. Lack of T-cell costimulation
  4. Immunosuppression
102
Q

Adenomas and carcinomas arising from beta cells in the pancreatic islets may be fatal in what way?

A

Can cause altered hormone production and produce too much insulin

103
Q

What needs to be worried about if a tumor expands to break through an epithelial surface?

A

Ulceration: bleeding and secondary infection

104
Q

What is cachexia?

A

Progressive wasting involved with cancer

105
Q

How many cancer patients will develop paraneoplastic syndromes?

A

10-15%

106
Q

Hypercalcemia, Cushing’s syndrome, and paraneoplastic pemphigus are all examples of what?

A

Paraneoplastic disease

107
Q

Grading attempts to assess the _____________ of cancer; staging describes the ____________ of cancer.

A

Aggressiveness; size and extent

108
Q

T/F: Grade 1 cancer cells are more differentiated than grade 4.

A

True

109
Q

Which is more important: staging or grading?

A

Staging

110
Q

What is the TNM method for diagnosing squamous cell carcinoma?

A

T: primary tumor diameter
N: regional lymph node involvement
M: metastases

111
Q

Which is quicker: frozen section biopsy or electron microscopy?

A

Frozen section biopsy

AU17: Gen Pathology (22 decks)

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