Chapter 5: Neoplasia Flashcards

1
Q

What are the two structural components of a tumor?

A

Parenchyma and stroma

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2
Q

This component of a tumor is composed of transformed cells that are neoplastic and clonal. This components also determines the biological nature (aggressiveness) of the cancer.

A

Parenchyma

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3
Q

This component of a tumor is composed of supportive tissue and is non-neoplastic. This component is involved in long-term tumor survival.

A

Stroma

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4
Q

These are benign epithelial neoplasms producing or derived from glandular tissue.

A

Adenoma

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5
Q

These are benign epithelial neoplasms which have finger-like fronds.

A

Papilloma

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6
Q

These are benign tumors of capillary endothelial cells.

A

Hemangioma

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7
Q

These are benign tumors of adipose tissue.

A

Lipoma

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8
Q

These are benign tumors of smooth muscle (“fibroid”).

A

Leiomyoma

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9
Q

These types of malignant tumors are formed from mesenchyme (mesoderm) and can develop at any age. Examples include bone, muscle, vasculature.

A

Sarcomas

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10
Q

These types of malignant tumors are formed from epithelia (ectoderm, endoderm) and most commonly occur in mid to late adulthood. Examples include lung, breast, and colon.

A

Carcinoma (>90% of cancers)

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11
Q

These types of malignant tumors are formed from multiple germ cell layers.

A

Teratomas

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12
Q

This is the most common benign tumor of the female breast. It contains two tissue types and is only fibrous neoplasia.

A

Fibroadenoma

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13
Q

This is a benign tumor of tissue native to a particular site. It is well-differentiated.

A

Hamartoma

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14
Q

This is a mass that projects from a mucosal surface.

A

Polyp

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15
Q

This is the first phase of carcinoma progression and is characterized by disorderly proliferation, cells are irregular, and non-neoplastic.

A

Dysplasia

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16
Q

This is the second phase of carcinoma progression and is characterized by dysplasia throughout the epithelia. It is well-localized and has no penetration of the basement membrane.

A

Carcinoma in situ: early neoplasm

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17
Q

This is the third phase of carcinoma and involves local destruction of cells, penetration of the basement membrane, and the most likely to metastasize.

A

Invasive carcinoma: more aggressive

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18
Q

What are the four characteristics of neoplasia?

A
  • Differentiation and anaplasia
  • Rate of growth
  • Local invasiveness
  • Metastasis
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19
Q

This characteristic of neoplasia is used to describe how closely cells resemble their precursors both structurally and functionally.

A

Differentiation

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20
Q

This characteristic of neoplasia is used to describe a loss of differentiation.

A

Anaplasia

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21
Q

What is the rate of growth of a benign tumor? Malignant?

A

Benign: slow and controlled
Malignant: fast and uncontrolled

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22
Q

In terms of local invasion, how would benign and malignant tumors be described?

A

Benign: well-localized, isolated, non-invasive, and likely to be encapsulated
Malignancy: is destructive, has progressive invasion (local and distant), and is less likely to be encapsulated

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23
Q

This characteristic of neoplasia is used to describe secondary implantation into remote tissue and is the most reliable indicator of malignancy.

A

Metastasis (mets)

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24
Q

This method of metastasis is characterized by the invasion of natural body caivites by cancer cells.

A

Seeding within body cavities (ovaries, CNS, ventricular system)

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25
Q

This method of metastasis is the most common mode of cacinoma metastasis and is determined by site and tumor parenchyma.

A

Lymphatic spread

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26
Q

In lymphatic spread of cancer, what is typically the first area to be affected by?

A

Sentinel lymph node

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27
Q

This method of metastasis is very rapid and is the most common mode of sarcoma metastasis.

A

Hematogeneous spread

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28
Q

In hematogeneous spread of cancer, what is typically the first area to be affected?

A

Capillary beds

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29
Q

This is the study of health/disease in populations.

A

Epidemiology

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30
Q

Overall cancer rates increase with age. When do they typically occur?

A

At the age extremes

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31
Q

What are the three categories of hereditary cancer?

A
  • Autosomal dominant cancer syndromes
  • Autosomal recessive syndrome
  • Familial cancer of uncertain inheritance
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32
Q

This type of hereditary cancer is due to a single gene mutation that is inherited. It is usually named by its marker phenotype (BRCA1).

A

Autosomal dominant cancer syndromes

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33
Q

This type of hereditary cancer is due to two altered alleles leading to genomic instability. Defective DNA repair enzymes are present and the best example of this is Xeroderma pigmentosa (sensitivity to UV light).

A

Autosomal recessive syndrome

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34
Q

This type of hereditary cancer is the most sporadic cancer and has some familial association. There is no marker phenotype and has multifactorial inheritance.

A

Familial cancer of uncertain inheritance

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35
Q

This is the formation of cancer.

A

Carcinogenesis

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36
Q

What are the primary targets of genetic damage related to carcinogenesis?

A

Regulatory genes

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37
Q

What are the four types of regulatory genes that could be involved in carcinogenesis?

A
  • Proto-oncogenes
  • Tumor suppressor genes (TSGs)
  • Apoptosis genes
  • DNA repair genes
38
Q

This regulatory gene is a normal gene that regulates cellular growth. When genetically altered, they become oncogenes.

A

Proto-oncogene

39
Q

This gene is associated with a gain of function and the alteration of 1 allele (dominant).

A

Oncogenes

40
Q

This gene is associated with a loss of function and the loss of 2 alleles (recessive).

A

Tumor suppressor genes

41
Q

This term is used to describe the number and appearance of chromosomes in the nucleus.

A

Karyotype

42
Q

This term is used to describe an abnormal number of chromosomes.

A

Aneuploidy

43
Q

What are the three types of structural abnormalities?

A
  • Balanced translocations
  • Deletions
  • Gene amplification
44
Q

These are non-coding RNA molecules that function to inhibit gene expression. They also suppress translation.

A

MicroRNAs

45
Q

These are heritable changes of gene expression. They are not mutations.

A

Epigenetics

46
Q

Genes are “silenced” by what?

A
  • DNA methylation

- Histone modification

47
Q

What are the hallmarks of cancer?

A
  • Evading apoptosis
  • Self-sufficiency in growth signals
  • Insensitivity to anti-growth signals
  • Tissue invasion and metastasis
  • Limitless replicative potential
  • Sustained angiogenesis
48
Q

What are some emerging features of cancer that could be added to the original hallmarks?

A
  • Change in energy metabolism (aerobic glycolysis)
  • Evasion of the immune system
  • Genomic instability
  • Tumor-promoting inflammation
49
Q

How do cancer cells express self-sufficiency in growth signals?

A
  • Produce own GFs
  • Stimulate stromal GFs
  • Altered GF receptors
50
Q

This is a good example of an overexpressed growth receptor. It is overexpressed in many cancers, but the most common is breast cancer.

A

HER2 (Human epidermal GF receptor 2)

51
Q

What are some common signal transduction mutations?

A
  • RAS: mutated in 30% of all tumors

- ABL: mutated in many leukemias

52
Q

What is a common nuclear transciption factor? CDK activation and aerobic glycolysis are charateristic.

A

MYC gene

53
Q

What controls the restiction point G1-S phase transition in the cell cycle?

A

Cyclin proteins (CDKs and CDKIs)

54
Q

These genes encode inhibitory proteins, normally decrease cellular proliferation, and regulates growth (“apply brakes”).

A

Tumor suppressor genes (TSGs)

55
Q

What is the “two-hit hypothesis”?

A

Both alleles must be inactivated (hit)

-There is a change in phenotype

56
Q

This tumor suppressor gene is the “governor of the cell cycle”. It governs the G1-to-S checkpoint. It is dysfunctional in many cancers and viruses may inactivate it.

A

RB gene

57
Q

This tumor suppressor gene is the “guardian of the genome”. It is commonly altered in all cancers and it maintains DNA integrity.

A

TP53 gene

58
Q

This term is used to describe reversible cell cycle arrest (G1). There is minor DNA damage and an increase in repair genes.

A

Quiescence

59
Q

This term is used to describe a permanent cell cycle arrest. There is major DNA damage and has failed repair.

A

Senescence

60
Q

This is programmed cell death.

A

Apoptosis

61
Q

This condition is characterized by a mutation in the TP53 gene and results in multiple tumors.

A

Li-Fraumeni syndrome

62
Q

This apoptotic pathway is characterized by death receptors, TNF, and caspase-8.

A

Extrinsic apoptosis pathway

63
Q

This apoptotic pathway is charcterized by DNA damage and caspase-9.

A

Intrinsic apoptosis pathway

64
Q

Both extrinsic and intrinsic apoptotic pathways stimulate what caspase?

A

Caspase-3 (executioner)

65
Q

When angiogenesis occurs in tumor cells, what do the blood vessels typically look like?

A

Poorly organized: leaky, dilated, and tortuous

66
Q

What are the steps of the invasion-metastasis cascade?

A
  • Invasion of ECM
  • Vascular spread: dissemination and homing
  • Micrometastases grow and invade
67
Q

What are the steps involved with invasion of the ECM by cancer cells?

A
  • Loosening of tumor cells
  • Breakdown of ECM
  • Changes in ECM attachment
  • Migration of tumor cells
68
Q

What is the “glue” that holds cells together?

A

E-cadherin

69
Q

What is the most common site of vascular metastasis for cancer?

A

1st capillary bed

70
Q

What are three DNA repair systems?

A
  • Mismatch repair
  • Nucleotide excision repair
  • Homolgous recombination repair
71
Q

What condition is characterized by a defective nucleotide excision repair system?

A

Xeroderma pigmentosum

72
Q

What are some general categories of carcinogenic agents?

A
  • Chemical
  • Radiant energy (irradiation)
  • Microbial (Helicobacter pylori)
73
Q

What are the two types of chemical carcinogens and what are some examples of each?

A
  • Direct-acting: no metabolic conversion (chemotherapy meds)

- Indirect-acting: require metabolic conversion (tobacco smoke, fossil fuel exhaust, smoked or broiled meats)

74
Q

What are the mechanisms of chemical carcinogens?

A
  • Cause genetic alterations
  • Specific target genes
  • Augmented by non-carcinogenic promoters
75
Q

What is radiation carcinogenesis characterized by?

A

Formation of pyrimidine dimers

76
Q

What is the most common form of cancer in the US?

A

Skin cancer

77
Q

This is an oncogenic RNA virus that is transmitted by sex, blood, and breast feeding. The TAX gene, which increases cyclins and decreases TP53, is involved.

A

Human T cell lymphotropic virus-1 (HTLV-1)

78
Q

What are some examples of oncogenic DNA viruses?

A
  • Human papillomaivrus (HPV)
  • Epstein-Barr virus (EBV)
  • Hepatitis B and C viruses (HBV, HCV)
  • Kaposi sarcoma herpesvirus (KSHV) a.k.a. human herpesvirus-8 (HHV-8)
79
Q

This oncogenic virus causes genital warts, squamous cell carcinomas, and influence many hallmarks of cancer (activation of cyclins to increase growth, decrease apoptosis, resist cellular senescence, and degrades p53).

A

Human papillomavirus (HPV)

80
Q

This oncogenic DNA virus causes infectious mononucleosis and its genes stimulate B cell proliferation, which inhibits apoptosis by decreasing macrophage and T cell activity.

A

Epstein-Barr virus

81
Q

This oncogenic DNA virus has a strong association with liver cancer. Infection leads to the inhibition of apoptosis.

A

Hepatitis B and C viruses

82
Q

This was the first “cancer bacteria” to be discovered (Gastric adenocarcinomas, gastric lymphomas).

A

Helicobacter pylori

83
Q

What are some antitumor effector mechanisms?

A
  • Cytotoxic T cells (CD8+ T cells)
  • Natural killer cells
  • Macrophages
84
Q

Cancer is the most common among the immunocompromised. True or False?

A

True

85
Q

This is unexplained weight loss, weakness, and anorexia due to cancer. It is irreversible with nutrition and indicates end-stage cancer.

A

Cancer cachexia (wasting syndrome)

86
Q

These are features associated with cancer development. They are not associated with invasion and some examples include hypercalcemia, cushing syndrome, polycthemia, and hypertrophic osteoarthropathy.

A

Paraneoplastic syndromes

87
Q

Grading (I-IV) and staging of cancers are based on what?

A

The degree of cellular differentiation

88
Q

How many stages of cancer are there and how are they determined?

A
  • Stage 0-IV

- Determined by the size of the primary tumor, lymph node involvement, and presence of metastasis.

89
Q

What are three laboratory methods of cancer diagnosis?

A
  • Biopsy
  • Fine-needle aspiration
  • Cytologic smear (Pap smear)
90
Q

What are tumor markers?

A

Enzymes or hormones associated with tumor growth

91
Q

What substance indicates problems with the prostate gland when found in high amounts?

A

Prostate-specific antigen