Gen Path Exam 2 - Neoplasia Flashcards

1
Q

New growth

A

Neoplasia

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2
Q

Loss of normal growth control; cells start doing their own thing, “transformed”

A

Neoplasia

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3
Q

Parasitic and autonomous qualities

A

Neoplasia

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4
Q

Study of neoplasms (tumors)

A

Oncology

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5
Q

What is the spectrum of neoplasia?

A

Benign -> locally aggressive -> intermediate malignant -> malignant

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6
Q

What are the 2 anatomic components of tumors?

A

Parenchyma
Stroma

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7
Q

Neoplastic cells; determines how a tumor is named

A

Parenchyma

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8
Q

Supporting CT and vasculature

A

Stroma

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9
Q

Degree of resemblance of tumor cells to parent cells

A

Differentiation

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10
Q

More resemblance between tumor cells and parent cells

A

Well differentiated (“low grade”)

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11
Q

Little resemblance between tumor cells and parent cells

A

Poorly differentiated (“high grade”)

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12
Q

Dedifferentiated or undifferentiated

A

Anaplasia

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13
Q

What does increased/abnormal DNA replication lead to (“poorly differentiated”)? (6)

A

Pleomorphism
Nuclear hyperchromatism
Increased nuclear/cytoplasmic ratio
Atypical nuclei
Numerous and atypical mitoses
Prominent nucleoli

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14
Q

A microscopic, potentially reversible, altered growth or maturation pattern

A

Dysplasia

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15
Q

In epithelial tissues (cervix, oral mucosa), it is precancerous and may progress to malignancy

A

Dysplasia

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16
Q

What is seen under the microscope in precancerous epithelial tissues undergoing dysplasia?

A

Disorderly:
Maturation
Pleomorphism
Mitotic activity

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17
Q

In bone lesions, it does NOT imply a precancerous state, just altered growth

A

Dysplasia

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18
Q

Dysplastic changes involving the full-
thickness of the epithelium

A

Carcinoma in-situ

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19
Q

Known as the most advanced stage of dysplasia

A

Carcinoma in-situ

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20
Q

Still a pre-invasive (precancerous) state, so
not cancer

A

Carcinoma in-situ

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21
Q

Clinical appearance, anatomic site, or
cell type (root word) + “oma”

A

Benign epithelial tumors

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22
Q

Named for appearance- finger-like epithelial
projections overlying cores of vascular fibrous CT

A

Papilloma

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23
Q

Arises from surface epithelium (Squamous-
skin, larynx, tongue; Transitional- bladder,
ureter, renal pelvis)

A

Papilloma

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24
Q

Benign tumor of glandular epithelium; can have many variants

A

Adenoma

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25
Q

Characterized by adenomatous papillary processes that extend into cystic spaces, as in cystadenoma of the ovary

A

Papillary cystadenoma

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26
Q

Most often named by tissue of origin

A

Benign mesenchymal

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27
Q

Fibrous tissue (benign mesenchymal)

A

Fibroma

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28
Q

Cartilaginous (benign mesenchymal)

A

Chondroma

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29
Q

Smooth muscle (benign mesenchymal)

A

Leiomyoma

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30
Q

Skeletal muscle (benign mesenchymal)

A

Rhabdomyoma

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31
Q

Fat (benign mesenchymal)

A

Lipoma

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32
Q

Bone (benign mesenchymal)

A

Osteoma

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33
Q

Vessels (benign mesenchymal)

A

Angioma

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34
Q

Pleomorphic adenoma (salivary), fibroadenoma (breast)- only fibrous portion is neoplastic

A

Benign mixed tumors

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35
Q

Neoplasm with cells derived from more than 1 germ layer, totipotent cells

A

Teratoma

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36
Q

Disorganized tissue native to the site (non-neoplastic generally)

A

Hamartoma

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37
Q

Disorganized tissue at unexpected site (non-neoplastic)

A

Choristoma

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38
Q

A mass that projects above a mucosal surface

A

Polyp

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39
Q

What are the notable malignant -oma exceptions? (6)

A

Lymphoma
Melanoma
Mesothelioma
Seminoma
Glioblastoma
Hepatoma

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40
Q

What are the notable non-neoplastic -oma exceptions?

A

Granuloma (group of macrophages)
Hematoma (bruise)

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41
Q

Root word anatomically or cellularly + “Carcinoma”

A

Malignant epithelial

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42
Q

Synonym of malignant

A

Cancer

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43
Q

From squamous epithelium (skin, mouth, esophagus, vagina) or areas of squamous metaplasia (bronchi or cervix)

A

Squamous cell carcinoma

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44
Q

Marked by production of keratin

A

Squamous cell carcinoma

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45
Q

From urinary tract epithelium

A

Transitional cell carcinoma

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46
Q

Glandular origin; includes tumors of GI, mucosa, endometrium, pancreas

A

Adenocarcinoma

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47
Q

Often shows desmoplasia

A

Adenocarcinoma

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48
Q

The root word anatomically/cellularly +
“Sarcoma

A

Malignant mesenchymal

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49
Q

Fibrous (malignant mesenchymal)

A

Fibrosarcoma

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50
Q

Cartilaginous (malignant mesenchymal)

A

Chondrosarcoma

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51
Q

Bone (malignant mesenchymal)

A

Osteosarcoma

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52
Q

Skeletal muscle (malignant mesenchymal)

A

Rhabdomyosarcoma

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53
Q

Smooth muscle (malignant mesenchymal)

A

Leiomyosarcoma

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54
Q

Fat (malignant mesenchymal)

A

Liposarcoma

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55
Q

Vessels (malignant mesenchymal)

A

Angiosarcoma

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56
Q

Burkitt lymphoma
Hodgkin disease/lymphoma
Wilm’s tumor

A

Eponyms

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57
Q

Which one is correctly matched?

a. chondroma, non-neoplastic collection of tissue not native to the site
b. angioma, malignant tumor of blood vessels
c. pleomorphic adenoma, a high-grade malignancy of glandular epithelium
d. rhabdomyoma, benign tumor of skeletal muscle

A

d. rhabdomyoma, benign tumor of skeletal muscle

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58
Q

Name some words often added to describe variants of a tumor’s appearance under the microscope

A

Cystic, papillary, tubular, solid, etc

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59
Q

Benign or malignant?

Clinical presentation:

Non-cancerous
Slow growing
Local, does not spread, may cause local damage
Surgically removable
Survivable - good prognosis

A

Benign

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60
Q

Benign or malignant?

Clinical presentation:

Cancerous
Rapid growth
Invade and destroy adjacent tissue
Metastasis = defining feature
Can cause death - poor prognosis

A

Malignant

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61
Q

Benign or malignant?

Microscopic:

Well-differentiated
Normal mitoses
Encapsulation

A

Benign

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62
Q

Benign or malignant?

Microscopic:

Well to poorly differentiated (or anaplastic)
Atypical mitoses
Non-encapsulated

A

Malignant

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63
Q

Benign or malignant?

Rate of growth is slow (months to years)

A

Benign

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64
Q

Benign or malignant?

Rate of growth affected by hormones, blood supply, pressure constraints

A

Benign

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65
Q

Benign or malignant?

Rate of growth is variable, may be rapid

A

Malignant

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66
Q

Benign or malignant?

Rate of growth may outgrow blood supply, leading to necrosis

A

Malignant

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67
Q

Benign or malignant?

Local invasion capsule at periphery

A

Benign

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68
Q

Benign or malignant?

Local invasion beyond anatomic tissue boundaries

A

Malignant

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69
Q

Benign or malignant?

Local invasion is destructive and no capsule

A

Malignant

70
Q

Benign or malignant?

Crosses over anatomical boundaries (ex: nose up to brain)

A

Malignant

71
Q

What is the hallmark of malignancy?

A

Metastasis

72
Q

What does the capacity of metastasis depend on?

A

Tumor type

73
Q

What percentage of newly diagnosed malignant tumors have clinically evident
metastases?

A

30% (early detection is important!)

74
Q

More anaplastic, larger tumor = _______ likely to spread

A

more

75
Q

In what ways does malignancy spread?

A

Seeding in body cavities
Lymphatic spread
Hematogenous (blood) spread
Paths of least resistance

76
Q

What type of malignancy spread?

Ovarian cancer

A

Seeding in body cavities

77
Q

What type of malignancy spread?

Carcinomas

A

Lymphatic spread

78
Q

What type of malignancy spread?

Sarcomas

A

Hematogenous (blood) spread

79
Q

What type of malignancy spread?

Lung and liver are common vsecondary sites

A

Hematogenous (blood) spread

80
Q

What type of malignancy spread?

Neural spread

A

Path of least resistance

81
Q

What type of malignancy spread?

Batson’s venous plexus - along vertebral column, potential spread to jaw

A

Path of least resistance

82
Q

Cancer is a _________ disorder- mostly from acquired random mutations during regular ______ ___________ (Bad luck!) or from environmental exposure

A

genetic; cell division

83
Q

Genetic changes are heritable with the
accumulation of mutations leading to
characteristic features of cancer; however,
actual inherited cancers are ____________

A

infrequent

84
Q

Cancer is a _____________ process. It does not just happen from one time of “bad luck”

A

multi-step

85
Q

What are the steps of neoplasm formation?

A

Initiation
Promotion
Progression

86
Q

What step of neoplasm formation?

Carcinogen exposure causing genetic damage and single cell (“monoclonal”) growth

A

Initiation

87
Q

What step of neoplasm formation?

Additional genetic damage over time leads to heterogenous population of cells (visible clinically)

A

Promotion

88
Q

What step of neoplasm formation?

Evolution and selection of more aggressive tumors capable of metastasis that are less responsive to treatment

A

Progression

89
Q

Name 3 carcinogens that can cause a neoplasm to form

A

Chemicals
Radiant energy
Microbial agents (ex: viruses like HPV, EBV)

90
Q

What are the 4 major classes of cancer genes that control growth?

A

Proto-oncogenes
Tumor suppressor genes
Apoptosis regulation genes
Tumor cell/host cell interaction genes

91
Q

Which major class of cancer genes that control growth?

Increase growth

A

Proto-oncogenes

92
Q

Which major class of cancer genes that control growth?

Stop cell growth and help in DNA repair

A

Tumor suppressor genes

93
Q

What is the classic example of a tumor suppressor gene?

A

TP53 (aka p53)

94
Q

Which major class of cancer genes that control growth?

Determine cell death

A

Apoptosis regulation genes

95
Q

Which major class of cancer genes that control growth?

Cytotoxic T lymphocytes kill cells with unrepaired genetic damage

A

Tumor cell/host cell interaction genes

96
Q

Name the 4 hallmarks of cancer highlighted in class

A
  1. Self-sufficiency in growth signals (oncogenes)
  2. Insensitivity to growth inhibition (tumor suppressor genes)
  3. Evasion of apoptosis (apoptosis regulation genes)
  4. Evasion of immune system (tumor cell/host interaction genes)
97
Q

The immune system (cell-mediated) helps prevent what?

A

Tumor formation/progression

98
Q

What is the evidence that the immune system helps prevent tumor formation and progression?

A

Increased frequency of cancer in immunocompromised (ex: congenital, transplant, AIDS)

99
Q

Uses endogenous or synthetic substances to improve or restore immune system function to fight cancer

A

Immunotherapy

100
Q

What is the target and indication of Rituximab?

A

Target = CD20
Indication = B-NHL

101
Q

What is the target and indication of Herceptin?

A

Target = HER2/neu
Indication = breast cancer

102
Q

What is the target and indication of Certuximab?

A

Target = EGFR
Indication = Head, neck, oral cancer

103
Q

The majority of cancers are inherited.

About 1/3 of newly diagnosed malignancies have already metastasized.

a. Both statements are true
b. Both statements are false
c. The first statement is true, the second statement is false
d. The first statement is false, the second statement is true

A

d. The first statement is false, the second statement is true

104
Q

The branch of medicine which deals with the incidence, distribution, and possible control of diseases and other factors relating to health

A

Epidemiology

105
Q

Studying who (Age, gender) gets a tumor,
where they live (environmental risk
factors) and their family (genetic factors,
acquired predisposing conditions) helps identify etiology and pathogenesis

A

Epidemiology

106
Q

What helps with the following?

Preventing and reducing disease burden
Improving tx
Reducing cost
Predicting needs for resource allocation

A

Epidemiology

107
Q

Has the overall death rate increased or decreased?

A

Decreased (less smoking, earlier detection, better tx)

108
Q

Has the overall incidence rate increased or decreased for women and men?

A

Increased for women
Stable for men

109
Q

Which state has the highest incidence of new cancer cases and deaths in the US?

A

KY

110
Q

Name environmental exposures that are associated with increased cancer risk

A

Occupational
Chronic sun exposure
Smoking
Alcohol
Obesity
Oncogenic viruses (HPV)

111
Q

T/F: Older people are more likely to get cancer

A

True

112
Q

What kind of cancers do children usually get?

A

Leukemia, lymphoma, sarcoma, CNS tumor

113
Q

What should you closely follow for early cancer detection?

A

Precursor (precancer/premalignant) lesions

114
Q

Risk for?

Smoking induced squamous metaplasia
Dysplasia of bronchial mucosa

A

Bronchogenic carcinoma

115
Q

Risk for?

Endometrial hyperplasia and dysplasia

A

Endometrial carcinoma

116
Q

Risk for?

Oral, vulvar, and penile leukoplakia

A

Squamous cell carcinoma

117
Q

Risk for?

Villous adenoma of colon

A

Colorectal carcinoma

118
Q

Are benign tumors premalignant?

A

Generally no

119
Q

Name the tumor effects on host

A

Location is crucial
Hormone production
Bleeding + infedction
Intestinal complications

120
Q

Symptoms not related to tumor spread or hormone production

A

Paraneoplastic syndromes

121
Q

Affects 10-15% of cancer patients

A

Paraneoplastic syndromes

122
Q

May indicate underlying neoplasm

A

Paraneoplastic syndromes

123
Q

Can be lethal and can mimic metastatic disease

A

Paraneoplastic syndromes

124
Q

Diverse and associated with many tumors

A

Paraneoplastic syndromes

125
Q

Name the 4 Paraneoplastic syndromes

A

Cachexia
Hypercalcemia
Cushing syndrome
Hypercoagulability

126
Q

Which Paraneoplastic syndrome?

Progressive loss of body fat and lead body mass with weakness, anorexia, and anemia

A

Cachexia

127
Q

Which Paraneoplastic syndrome?

High metabolic rate

A

Cachexia

128
Q

Which Paraneoplastic syndrome?

Caused by tumor and host cytokines, not due to tumor’s nutritional demands

A

Cachexia

129
Q

Which Paraneoplastic syndrome?

Due to release of PTHrP, TGF-a (activates osteoclasts and active vitamin D)

A

Hypercalcemia

130
Q

Which Paraneoplastic syndrome?

Ectopic ACTH production

A

Cushing syndrome

131
Q

Which Paraneoplastic syndrome?

Venous thrombosis and nonbacterial thrombotic endocarditis

A

Hypercoagulability

132
Q

Estimates aggressiveness based on cytologic differentiation

A

Grading

133
Q

Goes from I - IV in order of increasing anaplasia

A

Grading

134
Q

Which has greater clinical value, grading or staging?

A

Staging

135
Q

Size of primary tumor and extent of regional and distant spread

A

Staging

136
Q

TNM system

A

Staging

137
Q

What does TNM system measure/stand for?

A

T = tumor size (1-4)
N = regional nodal involvement (0-3)
M = metastasis (0,1)

138
Q

AJC system (0-IV)

A

Staging

139
Q

What is required for a lab diagnosis of cancer?

A

Detailed clinical findings
Adequate, representative, properly preserved biopsy

140
Q

What do you put biopsied samples in?

A

Formalin

141
Q

What are the sampling approaches?

A

Cytologic smear
Biopsy

142
Q

What are the 2 types of cytologic smears?

A

Direct scraping
Fine needle aspiration

143
Q

Which type of cytologic smear?

Good for superficial fungal and herpes infections

A

Direct scraping

144
Q

Which type of cytologic smear?

Good for readily palpable lesions (breast, thyroid, lymph node, salivary gland)

A

Fine needle aspiration

145
Q

Which sampling approach?

Incisional (part of the tissue) or excisional (all abnormal tissue)

A

Biopsy

146
Q

____________ assistance ensures accurate sampling for internal lesions. Name a few examples

A

Radiologic

Ex: mammogram-guided, CT-guided, ultrasound-guided

147
Q

Routine samples are _________ fixed and embedded in paraffin wax (FFPE) for routine H&E staining.

This same tissue block can later be used for additional ______-based molecular tests (FISH, IHC, PCR etc.)

A

formalin; DNA

148
Q

Useful to determine the cellular differentiation of poorly differentiated tumor cells

A

Immunohistochemistry

149
Q

Useful in diagnosis of lymphomas to determine lineage (B or T cell) and differentiation stage and in treatment of B-cell lymphomas

A

Immunohistochemistry

150
Q

Requires fresh tissue (no formalin!)

A

Flow cytometry

151
Q

Helps classify leukemia and lymphoma

A

Flow cytometry

152
Q

What are the serologic markers for tumors?

A

PSA
Carcinoembryonic antigen (CEA)
Alpha-fetoprotein

153
Q

Which serologic marker for tumors?

Low sensitivity and low specificity

A

PSA

154
Q

Which serologic marker for tumors?

Cancers of colon, pancreas, stomach, and breast

A

Carcinoembryonic antigen (CEA)

155
Q

Which serologic marker for tumors?

Hepatocellular carcinomas, yolk sac remnants

A

Alpha-fetoprotein

156
Q

Which serologic marker for tumors?

Not good for early detection, but GREAT for detecting reccurrences

A

PSA, CEA, and alpha-fetoprotein

157
Q

Uses body fluids that contain tumor cells or their products for screening, detecting, and monitoring cancer

A

Liquid biopsy

158
Q

Can detect monoclonality in lymphoid malignancies

A

PCR

159
Q

Translocations and gene amplification

A

FISH/PCR

160
Q

Which molecular technique?

Tumors from different sites with similar mutations can be given similar drugs

A

Targeted therapy

161
Q

Rapid sequencing on entire genome

A

Genomics

162
Q

Can identify driver and passenger mutations that help target treatment

A

Genomics

163
Q

Epigenetic modifications genome-wide

A

Epigenomics

164
Q

Microarray quantifies all RNAs expressed

A

Transcriptomics

165
Q

Measure all proteins simultaneously

A

Proteomics

166
Q

Test all of the cell’s metabolites

A

Metabolomics

167
Q

T/F: RNA is easier to work with than DNA

A

FALSE, DNA is easier to work with

168
Q

Currently developing methods to sequence several hundred _____ _________ to detect mutations in as few as 5% of tumor cells

A

key genes

169
Q

Used to identify changes in DNA copy number

A

DNA arrays

170
Q

In the future, may be used to predict drug efficacy

A

Epigenomics

171
Q

In the future of cancer diagnostics, there will be a paradigm shift to classify tumors based on _____________ and associated therapeutic _________, rather than on morphology or cell origin

A

mutation; targets

172
Q

Optimal diagnosis and management combines what?

A

Histopathology + molecular diagnostic techniques