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MOD Midterm > Neoplasia: General Approach > Flashcards

Neoplasia: General Approach Flashcards

1
Q

What makes neoplasia benign or malignant?

A

benign tumors are localized; malignant tumors invade and metastasize

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2
Q

What does a circumscribed tumor mean?

A

benign; smooth and encapsulated edge

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3
Q

Why can you not discriminate between benign and cancerous tumors based on their ability to cause harm?

A

even benign tumors can cause harm- spinal cord compression, airway compression, hemorrhage, and hormone secretion

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4
Q

All tumors are composed of two components. What are these?

A

neoplastic cells that constitute the tumor parenchyma and reactive stroma made up of connective tissue, blood vessels, and cells of the adaptive and innate immune system

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5
Q

the classification of tumors and their biologic behavior are based primarily on?

A

the parenchymal component

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6
Q

what is the growth and spread of tumors critically dependent on?

A

their stroma

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7
Q

Why is induction of scar-like tissue around a tumor helpful for us?

A

it gives us a hard detectable lump (scirrhous)

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8
Q

what is an invasive cervical carcinoma surrounded by?

A

dense lymphatic infiltrate

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9
Q

What are malignant tumors arising in solid mesenchymal tissues called?

A

sarcomas

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10
Q

what are some mesenchymal tissues that come off the mesoderm?

A

supportive tissues: fibrous tissue, fat, bone, cartilage, muscle (smooth muscle)

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11
Q

Where does our epithelium come from?

A

endoderm or ectoderm

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12
Q

What might be considered epithelium?

A

lining of all of our visceral organs or lining of our glands, or skin surface

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13
Q

What are malignant tumors arising from blood-forming cells?

A

leukemias or lymphomas

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14
Q

what are malignant neoplasms of epithelial cell origin called?

A

carcinomas

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15
Q

What is a teratoma from? and how is it defined?

A

totipotent stem cells; defined on the basis of more than one germ cell layer

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16
Q

What are hamartomas?

A

overgrowth of mature tissue that normally occur in that area, but they are disorganized

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17
Q

what are choristomas?

A

mass of tissue histologically normal, but in the wrong location (heterotopic or ectopic)

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18
Q

What is the effect of metaplasia?

A

the new cell type is prone to acquisition of genetic damage

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19
Q

what does metaplasia that acquires additional genetic damage become?

A

dysplasia

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20
Q

how can dysplasia be defined?

A

dysplasia is the first step on the route to cancer; it is disorder growth

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21
Q

what is carcinoma in situ?

A

severe dysplasia; something is malignant but incapable of spreading (because it has to go through that basement membrane in order to invade and metastasize)

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22
Q

how would you define a neoplasm that resembles the cells of origin a lot?

A

well-differentiated

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23
Q

how would you define a neoplasm that does not resemble the cells of origin at all?

A

poorly differentiated: anaplasia

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24
Q

What is one of the most common areas where metaplasia occurs and one of the most common places that gives us disease?

A

Respiratory epithelium (columnar–> squamous)

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25
Q

What do you call a malignant tumor of the gastric epithelium?

A

gastric adenocarcinoma

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26
Q

What morphologic feature (microscopically viewable) can reflect that tumor’s rate of growth?

A

mitotic figures

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27
Q

What are 5 telltale morphology features of malignancy?

A

anaplasia, pleomorphism, abnormal nuclear morphology, increased or abnormal mitosis, loss of polarity

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28
Q

what is pleomorphism?

A

variability of cell size/shape

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29
Q

How can we use techniques of staining/immunostaining to diagnose tumors?

A

the way a tumor stains for something will help you identify differentiation; you can use what a tumor produces (eg. mucin or keratin) to identify what kind of differentiation it has

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30
Q

what if you find mucin in a tumor?

A

it means that it is a glandular epithelial neoplasm

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31
Q

How might you prove that a tumor was of thyroid origin?

A

we could do a special immunostain for thyroglobulin

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32
Q

What are endocrine tumors often associated with?

A

they are usually well-differentiated and are often associated with hormone secretion (they can produce excess amounts of different hormones)

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33
Q

What are the tumor markers for the breast in females?

A

CA 15-3

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34
Q

what are the tumor markers for the Liver/bile duct in females and males?

A

CEA, AFP, CA19-9

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35
Q

what are the tumor markers for the ovaries?

A

CA-125

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36
Q

what are the tumor markers for the stomach/pancreas in females/males?

A

CEA, CA19-9

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37
Q

what is the tumor markers for the colorectal in males and females?

A

CEA, CA19-9

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38
Q

what is the tumor marker for the prostate?

A

PSA

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39
Q

what is the tumor marker for the testicle?

A

AFP and BHCG

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40
Q

What are the different types of leukemia differentiation?

A

acute vs chronic

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41
Q

in acute leukemias, where have the cancerous cells halted maturation?

A

at the blast stage

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42
Q

in chronic leukemias, what do the cancer cells look like?

A

more mature cells (chronic leukemias show full maturation)

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43
Q

What separates the two different types of leukemias from a biological standpoint?

A

where the arrest occurs

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44
Q

What is one of the most common benign breast tumors?

A

fibroadenoma

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45
Q

What are the three different types of metastasis?

A

lymphatic spread, hematogenous spread, trans-coelomic spread (direct seeding of body cavities)

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46
Q

what occurs during trans-coelomic spread (direct seeding)?

A

gain of entry into a free compartment (like the peritoneal space)

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47
Q

What organ uses all three modes of metastasis?

A

the bowel

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48
Q

What is the most common route of spread for carcinomas?

A

lymphatic spread (however they are not restricted to just lymph spread)

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49
Q

what is lymphatic spread dependent on?

A

regional drainage

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50
Q

What is a sentinel lymph node biopsy?

A

at the time of surgery, a tracer dye is injected into the tumor; the first node to take up the dye are the “sentinel nodes” and these nodes are removed

51
Q

what does a sentinel lymph node biopsy prevent?

A

more extensive lymphadenectomy

52
Q

Where is virchow’s node located?

A

supraclavicular area (usually left)

53
Q

what is typically associated with supraclavicular lymphadenopathy (virchow node)?

A

any thoracic or abdominal carcinoma

54
Q

How do cancers way below the clavicle get all the way up to virchow node?

A

the thoracic duct is responsible for the end lymphatic drainage for everything below the diaphragm, the entire left hemithorax, and the entire left head, neck, and arm

55
Q

Where does the thoracic duct eventually drain into?

A

the left subclavian vein (in that site is virchow’s node)

56
Q

What is the classic mechanism for metastasis for sarcomas?

A

hematogenous route

57
Q

what organs are the primary targets for hematogenous mets coming from the original site?

A

lung, liver, and bone

58
Q

How do you stage tumors?

A

TNM staging

59
Q

what does the T indicate in TNM staging?

A

tumor size, and the extent of invasion (primary tumor)

60
Q

what does the N stand for in TNM staging?

A

Degree of lymph node involvement

61
Q

what does the M stand for in TNM staging?

A

presence/absence of distant mets

62
Q

What is the leading site of new cancer in males in the US?

A

prostate

63
Q

what is the leading site of new cancer in females in the US?

A

breast

64
Q

What is the leading cause of death from cancer in males in the US?

A

lung and bronchus

65
Q

what is the leading cause of death from cancer in females in the US?

A

lung and bronchus

66
Q

Why is liver cancer high in some countries?

A

viral hepatitis

67
Q

why is non-hodkin’s lymphoma high in some countries?

A

Epstein-barre virus

68
Q

What causes Kaposi sarcoma?

A

HIV

69
Q

What does exposure to asbestos lead to?

A

mesothelioma

70
Q

what does exposure of benzene lead to?

A

acute myeloid leukemia

71
Q

what is the typical use or occurrence of benzene?

A

dry cleaning; adhesives, coatings, and detergents

72
Q

what does exposure to radon and its decay products lead to?

A

lung carcinoma

73
Q

what is the typical use or occurrence of radon?

A

from decay of materials containing uranium; underground mines

74
Q

what does exposure to vinyl chloride lead to?

A

hepatic angiosarcoma

75
Q

what is the typical use or occurrence of vinyl chloride?

A

it is a refrigerant

76
Q

What sets many childhood cancers apart from adult cancers?

A

germline mutations

77
Q

What are some acquired predisposing conditions for cancer?

A

chronic inflammation; precursor lesions; immunodeficiency

78
Q

Why does screening work?

A

it identifies cancer early; it identifies cancers before they are cancers

79
Q

What is an example of something used to identify cancer before its cancer?

A

colon polyps–> they are the adenoma to carcinoma sequence

80
Q

benign neoplasms are not typically the precursor to their malignant counterparts; what is the exception to this?

A

the colon adenoma–> carcinoma sequence

81
Q

What may offer protection to certain individuals to lung cancer (even though they have an extensive history of smoking)?

A

P450 halotypes may offer protection

82
Q

What else may play a role in a BRCA1 mutated patients getting breast cancer?

A

diet and reproductive history

83
Q

What is a paraneoplastic syndrome?

A

when the tumor secretes substances such as PTH-rP and ACTH; and the tumor also evokes the elaboration of other factors such as autoantibodies and cytokines

84
Q

What are two lung cancers with typical paraneoplastic syndromes?

A

squamous carcinoma and small cell neuroendocrine carcinoma

85
Q

what paraneoplastic syndrome does squamous carcinoma cause?

A

humoral hypercalcemia of malignancy

86
Q

what occurs during humoral hypercalcemia of malignancy?

A

there is elaboration of PTHrP secretion; this works on PTH receptors to give patients hypercalcemia

87
Q

what paraneoplastic syndrome is associated with small cell neuroendocrine carcinoma?

A

cushing syndrome

88
Q

what occurs during the paraneoplastic syndrome of cushing syndrome?

A

Hypercortisolism due to excessive ACTH secretion by tumor cells

89
Q

What is Trousseau syndrome?

A

a paraneoplastic thrombophilia classically associated with pancreatic carcinoma

90
Q

When might you suspect Trousseau syndrome?

A

if someone comes in with a thrombosis and you can’t explain it, you may want to start looking for cancer

91
Q

What is another example of a vascular and hematologic manifestation that could occur in some cancers besides Trousseau syndrome?

A

Disseminated intravascular coagulation

92
Q

what cancer might cause DIC?

A

acute promyelocytic leukemia

93
Q

what occurs in acute promyelocytic leukemia to cause DIC?

A

the leukemic cells express tissue factor which activates factor X, high levels of Annexin II receptors on plasma cells convert plasminogen into plasmin; both TF and Annexin II are highly expressed by APL cells

94
Q

What is the philadelphia chromosome?

A

When you combine the ABL from chromosome 9 and the BCR from chromosome 22, to give you a changed chromosome 22: BCR-ABL

95
Q

what is the protein that results from the philadelphia chromosome?

A

a constitutively active tyrosine kinase; creates a perpetually diving cell clone

96
Q

When you see a BCR-ABL chromosome, what can you do?

A

diagnose the patient with CML, treat, and monitor

97
Q

how do you treat a patient with a philadelphia chromosome?

A

give them Imatinib (a tyrosine kinase inhibitor); this is extremely effective at controlling this cancer clone

98
Q

how can you test for the philadelphia chromosome?

A

we can use a BCR-ABL PCR test to look for even tiny amounts of this transcript–> so you can tell if your therapy is working or not

99
Q

What defines a successful treatment of CML with a tyrosine kinase inhibitor?

A

molecular response (a negative BCR-ABL PCR)

100
Q

What are the two different categories of carcinogens and what is the difference between them?

A

direct vs indirect; direct carcinogens are carcinogenic right away (there is no need for conversion); indirect carcinogens require a metabolic process to take place for the substance to become an active (ultimate) carcinogen

101
Q

what is responsible for converting most indirect carcinogens to their active forms?

A

cytochrome p450

102
Q

What effect does an increased amount of thymine dimers have?

A

these dimers distort the DNA, which blocks the progress of DNA and RNA polymerase

103
Q

Removal of thymine dimers is primarily accomplished utilizing what?

A

nucleotide excision repair

104
Q

what happens if you don’t have nucleotide excision repair?

A

it is a hereditary disorder: Xeroderma pigmentosum

105
Q

what happens if you overwhelm your nucleotide excision repair (especially by excess exposure to UV light)?

A

sporadic melanomas and other skin cancers

106
Q

what cancers resulted after the atomic bombs were dropped in Hiroshima and Nagasaki?

A

there was an increase in leukemias within 5-7 years; solid tumors increased such as colon carcinoma, breast carcinoma, and lung carcinoma

107
Q

What was the Chernobyl accident in 1986?

A

exposure to radioactive iodine, which caused a sharp increase in thyroid carcinoma

108
Q

What is Human T cell Leukemia Virus (HTLV-1) associated with?

A

endemic T cell leukemias/lymphomas

109
Q

What is hepatitis B and C viruses associated with?

A

hepatocellular carcinomas

110
Q

what is helicobacter pylori bacterium associated with?

A

B cell lymphomas of the stomach

111
Q

what is Human papillomavirus associated with?

A

squamous carcinoma of the cervix, anogenital region, and pharynx/larynx

112
Q

What are the viral proteins of human papillomavirus associated with oncogenesis?

A

E6 and E7

113
Q

What occurs as progressive integration of E6/E7 proteins occurs?

A

there is inactivation of tumor suppressor genes and upregulation of oncogenic pathways

114
Q

What is epstein Barr virus implicated in oncogenesis of?

A

in B-cell lymphomas as well as certain carcinomas

115
Q

What was the first virus associated with cancer and what was this cancer?

A

Epstein Barr Virus; associated with endemic Burkitt lymphoma

116
Q

what does EBV result in?

A

immortalization and increased replication of B lymphocytes

117
Q

What is the role of EBNA 2?

A

it upregulates oncogenes

118
Q

what is the role of LMP?

A

it induces cell proliferation

119
Q

What causes Burkitt Lymphoma?

A

the IgH/MYC translocation

120
Q

What benign sounding designations are always always always malignant?

A

lymphoma, melanoma, mesothelioma, and seminoma

121
Q

What are some epithelial tissues?

A

surface epithelium (skin, mucosa), glandular epithelium, “specialized” epithelium

122
Q

What is a benign uterine smooth muscle tumor called?

A

leiomyomata

123
Q

what is a malignant uterine smooth muscle tumor called?

A

leiomyosarcoma

MOD Midterm (22 decks)

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