Chapter 7 (Neoplasia) Pathophysiology

Front 1

Five phases of the cell cycle

Back 1

G0, G1, G2, M, S

Front 2

The first gap of the cell cycle.
Where RNA and protein synthesis occurs.
The end of this phase marks a critical event that occurs that commits the cell to continue through all phases of the gap cycle.

Back 2

G1

Front 3

The resting stage. Cells can leave G1 and enter this stage.
Time spent in this stage varies and not all cells enter this stage.

Back 3

G0

Front 4

DNA synthesis occurs here.

Back 4

S

Front 5

Premitotic phase.
Cell engages in RNA and protein synthesis again.

Back 5

G2

Front 6

Mitosis where cell divides

Back 6

M

Front 7

Cell that cannot enter cell cycle. Permanently differentiated.

Back 7

Permanent cells (Amitotic Cells)

Front 8

Examples of permanent cells

Back 8

Neurons, striated muscle cells (skeletal and cardiac muscle)

Front 9

Cells usually in G0 (resting) phase.
Cells can still divide, but can only give rise to daughter cells of the same cell type.

Cellular injury stimulates to enter G1 phase.

Back 9

Stable Cells

Front 10

Examples of Stable Cells

Back 10

Hormones (estrogen), Growth factors (epidermal derived growth factor), Progenitor blood cells, skin cells, liver cells, smooth muscle, and most other cells.

Front 11

Cells constantly making new cells.

Back 11

Labile Cells

Front 12

Examples of labile cells

Back 12

Stem cells, cancer or tumor cells

Front 13

The act or process in development in which unspecialized cells or tissues acquire more specialized characteristics.

Back 13

Cell differentiation

Front 14

The reproduction or multiplication of similar forms, especially cells.

Back 14

Proliferation

Front 15

Tissue name + -oma

Back 15

Benign tumor

Front 16

Any cancer that arises from epithelial cells (90%)

Based on appearance
Based on putative cell of origin

Back 16

Carcinoma

Front 17

A cancer that arises from mesenchymal tissue, the connective or supportive tissue (bone, cartilage, fat, muscle, blood vessels)

Back 17

Sarcoma

Front 18

Adenoma

Back 18

Benign epithelial neoplasm of glandular tissue

Front 19

Osteoma

Back 19

Benign bone tumor

Front 20

Chondoma

Back 20

Benign cartilage tumor

Front 21

Lipoma

Back 21

Benign adipose tumor

Front 22

Melanoma

Back 22

Skin cancer

Front 23

Adenocarcinoma

Back 23

Malignancies that originate from glandlike structures

Front 24

Fibrosarcoma

Back 24

Cancer of fibrous tissue

Front 25

Chondrosarcoma

Back 25

Malignant tumor composed of chondrocytes

Front 26

Myeloma

Back 26

Cancer of plasma cells

Front 27

Lymphoma

Back 27

Cancer of the lymphocytes

Front 28

Hepatoma

Back 28

Liver cancer

Front 29

Osteosarcoma

Back 29

Malignant Bone Tumor

Front 30

Liposarcoma

Back 30

Malignant Adipose Tumor

Front 31

Angiosarcoma

Back 31

Cancer of the vessel walls

Front 32

Leiomyosarcoma

Back 32

Smooth muscle cancer

Front 33

A variety of cancer that originates in lymphocytes, originate in lymph nodes

Back 33

Lymphoma

Front 34

A cancer of the blood or bone marrow characterized by an abnormal proliferation of blood cells, usually WBCs

Back 34

Leukemia

Front 35

Well-differentiated cells that resemble cells in the tissue of origin

Back 35

Benign Tumor Cells

Front 36

Undifferentiated cells, do not resemble cells in the tissue of origin

Back 36

Malignant Tumor Cells

Front 37

Slow growth

Back 37

Benign Tumor Cells

Front 38

Expansion and not invasion, usually encapsulated

Back 38

Benign Tumor Cells

Front 39

Grows at periphery and invades

Back 39

Malignant Tumor Cells

Front 40

Involves metastasis

Back 40

Malignant Tumor Cells (via blood and lymph)

Front 41

Small size
Slow growing
Encapsulated or well demacrated borders
Well differentiated
Non-invasive
Never metastasize

Back 41

Benign Tumor Cell

Front 42

Larger in size
Rapid growth
Necrosis and hemorrhage common
Poorly demacated borders
Anaplastic
Vary in size and shape (Pleomorphism)
Increased nuclear/cytoplasmic ratios
Nuclear hyperchromasia (dark) and prominent nucleoli
High mitotic activity
Invasive growth
Metastasizes

Back 42

Malignant Tumor Cells

Front 43

A multistep process
Requires the accumulation of multiple genetic changes (inherited or aquired)

Back 43

Cancer

Front 44

Cancer mutations (genes)

Back 44

Growth promoting
Growth inhibiting
Apoptosis regulating

Front 45

Normal cellular genes involved with growth and cellular differentiation

Back 45

Protooncogenes (growth promoting oncogenes)

Front 46

Mechanisms of oncogene activation

Back 46

Point mutations
Chromosomal translocations
Gene amplification
Insertional mutagenesis

Front 47

__________ oncogenes lack regulatory control and are _____________, resulting in ______________ ____________ ___________.

Back 47

Activated;
overexpressed;
unregulated cellular proliferation.

Front 48

A multistep process
Requires the accumulation of multiple genetic changes (inherited or aquired)

Back 48

Cancer

Front 49

Encode proteins that regulate and supress cell proliferation by inhibiting progression of the cell through the cell cycle

Back 49

Tumor suppressor genes

Front 50

Cancer mutations (genes)

Back 50

Growth promoting
Growth inhibiting
Apoptosis regulating

Front 51

Mechanisms of tumor suppressor genes

Back 51

p53 prevents a cell with damaged DNA from entering S-phase
Rb prevents the cell from entering S-phase until the appropriate growth signals are present

Front 52

Normal cellular genes involved with growth and cellular differentiation

Back 52

Protooncogenes (growth promoting oncogenes)

Front 53

Prevents a cell with damaged DNA from entering S-phase

Back 53

p53

Front 54

Mechanisms of oncogene activation

Back 54

Point mutations
Chromosomal translocations
Gene amplification
Insertional mutagenesis

Front 55

Prevents the cell from entering S-phase until the appropriate growth signals are present

Back 55

Rb

Front 56

__________ oncogenes lack regulatory control and are _____________, resulting in ______________ ____________ ___________.

Back 56

Activated;
overexpressed;
unregulated cellular proliferation.

Front 57

Both genes must be inactivated for oncogenesis

Back 57

Two hit hypothesis

Front 58

Encode proteins that regulate and supress cell proliferation by inhibiting progression of the cell through the cell cycle

Back 58

Tumor suppressor genes

Front 59

Mechanisms of tumor suppressor genes

Back 59

p53 prevents a cell with damaged DNA from entering S-phase
Rb prevents the cell from entering S-phase until the appropriate growth signals are present

Front 60

Prevents a cell with damaged DNA from entering S-phase

Back 60

p53

Front 61

Prevents the cell from entering S-phase until the appropriate growth signals are present

Back 61

Rb

Front 62

Both genes must be inactivated for oncogenesis

Back 62

Two hit hypothesis

Front 63

A multistep process
Requires the accumulation of multiple genetic changes (inherited or aquired)

Back 63

Cancer

Front 64

Cancer mutations (genes)

Back 64

Growth promoting
Growth inhibiting
Apoptosis regulating

Front 65

Normal cellular genes involved with growth and cellular differentiation

Back 65

Protooncogenes (growth promoting oncogenes)

Front 66

Mechanisms of oncogene activation

Back 66

Point mutations
Chromosomal translocations
Gene amplification
Insertional mutagenesis

Front 67

__________ oncogenes lack regulatory control and are _____________, resulting in ______________ ____________ ___________.

Back 67

Activated;
overexpressed;
unregulated cellular proliferation.

Front 68

Encode proteins that regulate and supress cell proliferation by inhibiting progression of the cell through the cell cycle

Back 68

Tumor suppressor genes

Front 69

Mechanisms of tumor suppressor genes

Back 69

p53 prevents a cell with damaged DNA from entering S-phase
Rb prevents the cell from entering S-phase until the appropriate growth signals are present

Front 70

Prevents a cell with damaged DNA from entering S-phase

Back 70

p53

Front 71

Prevents the cell from entering S-phase until the appropriate growth signals are present

Back 71

Rb

Front 72

Both genes must be inactivated for oncogenesis

Back 72

Two hit hypothesis

Front 73

A multistep process
Requires the accumulation of multiple genetic changes (inherited or aquired)

Back 73

Cancer

Front 74

Cancer mutations (genes)

Back 74

Growth promoting
Growth inhibiting
Apoptosis regulating

Front 75

Normal cellular genes involved with growth and cellular differentiation

Back 75

Protooncogenes (growth promoting oncogenes)

Front 76

Mechanisms of oncogene activation

Back 76

Point mutations
Chromosomal translocations
Gene amplification
Insertional mutagenesis

Front 77

__________ oncogenes lack regulatory control and are _____________, resulting in ______________ ____________ ___________.

Back 77

Activated;
overexpressed;
unregulated cellular proliferation.

Front 78

Encode proteins that regulate and supress cell proliferation by inhibiting progression of the cell through the cell cycle

Back 78

Tumor suppressor genes

Front 79

Mechanisms of tumor suppressor genes

Back 79

p53 prevents a cell with damaged DNA from entering S-phase
Rb prevents the cell from entering S-phase until the appropriate growth signals are present

Front 80

Prevents a cell with damaged DNA from entering S-phase

Back 80

p53

Front 81

Prevents the cell from entering S-phase until the appropriate growth signals are present

Back 81

Rb

Front 82

Both genes must be inactivated for oncogenesis

Back 82

Two hit hypothesis

Front 83

Inherited germ-line mutation

Back 83

First hit (two hit hypothesis)

Front 84

Acquired somatic mutation

Back 84

Second hit (two hit hypothesis)

Front 85

Germ-line mutation of Rb on chromosome 13

High rate of retinoblastoma and osteosarcoma

Back 85

Familial retinoblastoma

Front 86

Germ-line mutation of p53 on chromosome 17

High rate of many types of tumors

Back 86

La-Fraumeni syndrome

Front 87

Top 3 incidences of cancer (male)

Back 87

Prostate
Lung
Colon & rectum

Front 88

Top 3 incidences of cancer (female)

Back 88

Breast
Lung
Colon & rectum

Front 89

Top 3 mortalities of cancer (male)

Back 89

Lung
Prostate
Colon & rectum

Front 90

Top 3 mortalities of cancer (female)

Back 90

Lung
Breast
Colon & rectum

Front 91

Top 3 causes of death in U.S.

Back 91

Heart disease
Cancer
Cerebrovascular disease

Front 92

Stomach cancer

Japan or US?

Back 92

Japan

Front 93

Breast cancer

US or Japan

Back 93

US

Front 94

Liver hepatoma

Asia or US

Back 94

Asia (Hep B)

Front 95

Prostate Cancer

African American or Caucasian

Back 95

African American
(higher androgen)

Front 96

Predispositions to cancer

Back 96

Age
Heredity
Acquired preneoplastic disorders

Front 97

Rb gene mutation

Back 97

Familial retinoblastoma

Front 98

MEN gene mutation

Back 98

Multiple endocrine neoplasia => thyroid cancer

Front 99

Familial adenomatous polyps (FAP)

Back 99

Colon cancer

Front 100

Cervical dysplasia =>

Back 100

Cervical cancer

Front 101

Endometrial hyperplasia =>

Back 101

Endometrial carcinoma

Front 102

Cirrhosis =>

Back 102

Liver cancer

Front 103

Ulcerative colitis =>

Back 103

Colon cancer

Front 104

Chronic atrophic gastritis =>

Back 104

Gastric cancer

Front 105

Most common carcinogen

Back 105

Chemical carcinogens

Front 106

Multi-step process involving a sequence of mutation (initiation) followed by proliferation (promotion)

Back 106

Carcinogenesis

Front 107

Mutations that cause cancer directly or indirectly by modifying DNA

Back 107

Indicators

Front 108

Cause cellular proliferation of mutated (initiated) cells

Proliferation of a mutated cell may lead to accumulation of additional mutations

Back 108

Promoters

Front 109

Most common carcinogenic agent

Back 109

Cigarette smoke

Front 110

Asbestos
Radiation
Oncogenic bacteria and viruses

Back 110

Carcinogenic agents

Front 111

Ultraviolet radiation _____________ and ionizing radiation ____________ damage DNA.

Back 111

UVB sunlight; x-rays

Front 112

Helicobacter Pylori => Peptic Ulcer =>

Back 112

Gastric carcinoma

Front 113

Human T-cell leukemia virus (HTLV-1) =>

Back 113

Adult T-cell leukemia/lymphoma

Front 114

DNA oncogenic viruses

Back 114

Hep B
Epstein-Barr virus
Human papilloma virus (HPV)
Kaposi-sarcoma-associated herpesvirus (HHV8)

Front 115

Epstein-Barr virus =>

Back 115

Burkitt lymphoma (African)
B-cell lymphoma (Immunosuppressed patients)
Nasopharyngeal carcinoma (S. China)

Front 116

Hep B virus =>

Back 116

Hepatocellular carcinoma

Front 117

Human papilloma virus (HPV) =>

Back 117

Cervical cancer

Front 118

Kaposi-sarcoma-associated herpesvirus (HH8V) =>

Back 118

Kaposi sarcoma (skin cancer)

Front 119

bcl-2

Back 119

Prevents apoptosis;
Overexpressed in follicular B-cell lymphomas

Front 120

Human T-cell leukemia virus (HTLV-1) =>

Back 120

Adult T-cell leukemia/lymphoma

Front 121

Genes promoting apoptosis

Back 121

bax; bad; bcl-xS; bid; p53

Front 122

DNA oncogenic viruses

Back 122

Hep B
Epstein-Barr virus
Human papilloma virus (HPV)
Kaposi-sarcoma-associated herpesvirus (HHV8)

Front 123

p53

Back 123

Promotes apoptosis in mutated cells by stimulating bax synthesis

Front 124

Epstein-Barr virus =>

Back 124

Burkitt lymphoma (African)
B-cell lymphoma (Immunosuppressed patients)
Nasopharyngeal carcinoma (S. China)

Front 125

c-myc

Back 125

Causes Burkitt lymphoma;
Promotes cellular proliferation;
With p53 leads to apoptosis;
With bcl-2 inhibits apoptosis

Front 126

Hep B virus =>

Back 126

Hepatocellular carcinoma

Front 127

Human papilloma virus (HPV) =>

Back 127

Cervical cancer

Front 128

Kaposi-sarcoma-associated herpesvirus (HH8V) =>

Back 128

Kaposi sarcoma (skin cancer)

Front 129

bcl-2

Back 129

Prevents apoptosis;
Overexpressed in follicular B-cell lymphomas

Front 130

Genes promoting apoptosis

Back 130

bax; bad; bcl-xS; bid; p53

Front 131

p53

Back 131

Promotes apoptosis in mutated cells by stimulating bax synthesis

Front 132

c-myc

Back 132

Causes Burkitt lymphoma;
Promotes cellular proliferation;
With p53 leads to apoptosis;
With bcl-2 inhibits apoptosis

Front 133

Human T-cell leukemia virus (HTLV-1) =>

Back 133

Adult T-cell leukemia/lymphoma

Front 134

DNA oncogenic viruses

Back 134

Hep B
Epstein-Barr virus
Human papilloma virus (HPV)
Kaposi-sarcoma-associated herpesvirus (HHV8)

Front 135

Epstein-Barr virus =>

Back 135

Burkitt lymphoma (African)
B-cell lymphoma (Immunosuppressed patients)
Nasopharyngeal carcinoma (S. China)

Front 136

Hep B virus =>

Back 136

Hepatocellular carcinoma

Front 137

Human papilloma virus (HPV) =>

Back 137

Cervical cancer

Front 138

Kaposi-sarcoma-associated herpesvirus (HH8V) =>

Back 138

Kaposi sarcoma (skin cancer)

Front 139

bcl-2

Back 139

Prevents apoptosis;
Overexpressed in follicular B-cell lymphomas

Front 140

Genes promoting apoptosis

Back 140

bax; bad; bcl-xS; bid; p53

Front 141

p53

Back 141

Promotes apoptosis in mutated cells by stimulating bax synthesis

Front 142

c-myc

Back 142

Causes Burkitt lymphoma;
Promotes cellular proliferation;
With p53 leads to apoptosis;
With bcl-2 inhibits apoptosis

Front 143

c-myc + p53 =

Back 143

apoptosis

Front 144

c-myc + bcl-2 =

Back 144

inhibited apoptosis

Front 145

New growth, non-adaptive, uncoordinated, autonomous, proliferation and differentiation out of control, competitive and parasitic

Back 145

Neoplasm

Front 146

Hallmark of malignant transformation

Back 146

Anaplasia

Front 147

Histologic estimate of the malignancy of a tumor (I-IV)

Back 147

Grade of tumor

Front 148

Criteria of tumor grade

Back 148

Degree of differentiation
Number of mitosis

Front 149

Clinical estimate of the extent of tumor spread

Back 149

Stage of tumor

Front 150

TNM staging system

Back 150

T= Tumor size (0-4)
N= Node of involvement (0-3)
M= Metastasis (0/1)

Front 151

Better predictor of tumor prognosis?

Back 151

Staging

Front 152

Key distinction between benign and malignant tumors

Back 152

Capacity of malignant tumors to invade and metastasize (except basal cells of carcinoma do not metastasize)

Front 153

In situ

Back 153

Original site

Front 154

Tx

Back 154

Tumor removed

Front 155

Use of tumor markers

Back 155

Screening
Monitoring
Detecting recurrance

Front 156

Common tumor marker

Back 156

Prostate specific antigen (PSA)

Front 157

True or False;
Tumor markers, usually proteins can not tell if cells are cancerous or not and should not be used as the primary diagnostic tool.

Back 157

True

Front 158

The spread of cancer from its primary site to other places in the body

Back 158

Metastasis

Front 159

Cancer cells use these enzymes to invade the basement membrane

Back 159

Type IV collagenases. hydrolases, and protease

Front 160

Transforming growth factors (TGF) that promote angiogenesis

Back 160

a (alpha) and B (beta)

Front 161

When cancer cells spread to form a new tumor, it is called a ___________, or __________ tumor.

Back 161

Secondary; Metastatic

Front 162

Types of Metastasis

Back 162

Lymphatic
Hematogenous
Seeding

Front 163

Cancer cells break away from a primary tumor and penetrate into lymphatic vessels

Back 163

Lymphatic Metastasis

Front 164

Cancer cells break away from a primary tumor and penetrate into blood vessels.

Back 164

Hematogenous Metastasis

Front 165

Malignant cells exfoliate and implant/invade tissue

Back 165

Seeding Metastasis

Front 166

Most common route of spread for epithelial carcinomas

Back 166

Lymphatic Metastasis

Front 167

Most common sites for hematogenous metastatsis

Back 167

Lung and brain

Front 168

Certain tumors seed in particular organs:

Prostate cancer =>
Colon cancer =>
Stomach cancer =>

Back 168

Bones
Liver
Ovary in women (Krukenberg tumor)

Front 169

Local symptoms of cancer

Back 169

Lumps or swelling
Hemorrhage
Necrosis
Pain
Ulceration
Jaundice (compression of surrounding tissues)

Front 170

Systems of metastasis

Back 170

Enlarged lymph nodes
Cough
Hemoptysis
Hepatomegaly (enlarged liver)
Bone pain
Fracture of affected bones
Neurological symptoms

Front 171

Systematic symptoms of cancer

Back 171

Weightloss and cachexia
Paraneoplastic syndromes
Fatigue
Anorexia
Low-grade fever
Excessive sweating
Anemia

Front 172

Factors (cytokines) released directly effect satiety centers in hypothalamus or indirectly by injuring tissues

Back 172

Cachexia

Front 173

Occur when a neoplasm elaborates a substance that results in an effect that is not directly related to growth, invasion, or metastasis

Most result from elaboration or hormone-like substances

Back 173

Paraneoplastic syndromes

Front 174

PTH control Ca 2+ concentration =>

Back 174

Too much Ca 2+ => Stone formation

Front 175

ADH => decrease urination => H20 => dilute plasma =>

Back 175

Decrease sodium

Front 176

Insulin =>

Back 176

Lowers blood sugar

Front 177

Erthroprotein-like substance =>

Back 177

Polycythemia

Front 178

Cytotoxic drugs used to treat cancer

Back 178

Chemotherapy

Front 179

Chemotherapy drugs:

a. Alkylating agents
b. Anti-metabolites
c. Anti-tumor antibiotics
.d. Plant alkaloids
e. Topoisomerase inhibitors
f. Monoclonal antibodies
g. Anti-tumor agents

Back 179

a. Cyclophosphamide
b. Methotrexate, 5-fluorouracil
c. Dactinomycin
d. vinca alkaloids, Taxanes
e. flouroquinolones
f. Rituximab
g. a-interferon, IL-2

Front 180

Drugs that affect cell division or DNA synthesis and function in some way

Back 180

Chemotherapy

Front 181

Tamoxifen

Back 181

Selective estrogen receptor modulator, reduces the risk of breast cancer

Front 182

Finasteride

Back 182

5-a reductase inhibitor, lowers risk of prostate cancer

Front 183

Aspirin

Back 183

Reduces the incidence of stomach, esophogeal, colorectal cancers

Front 184

Types of cells mostly affected by anti-cancer drug

Back 184

Bone marrow
Mucosal cells of GI tract
Gonadal cells

Front 185

Cancer is a disorder of altered cell ___________ and ___________.

Back 185

Differentiation; growth

Front 186

The process of cell division results in cellular _________.

Back 186

Proliferation

Front 187

__________ is the process of specialization whereby new cells acquire the structure and function of the cells they replace.

Back 187

Differentiation

Front 188

Proteins called _________ control entry and progression of cells through the cell cycle.

Back 188

Kinases

Front 189

Kinases are enzymes that __________ proteins.

Back 189

phosphorylate

Front 190

Continually renewing cell populations rely on __________ cells of the same lineage that have not yet differentiated to the extent that they have lost their ability to divide.

Back 190

progenitor

Front 191

__________ cells remain incompletely undifferentiated throughout life.

Back 191

Stem

Front 192

____________ stem cells are pluripotent cells derived from the inner cell mass of the blastocyst stage of the embryo.

Back 192

Embryonic

Front 193

The term _________ refers to an abnormal mass of tissue in which the regrowth exceeds and is uncoordinated with that of the normal tissues.

Back 193

neoplasm

Front 194

__________ do not usually cause death unless the location interferes with a vital organ's function.

Back 194

Benign tumors

Front 195

Malignant neoplasms are less well __________ and have the ability to break loose, enter the circulatory or lymphatic systems, and form secondary malignant tumors at other sites.

Back 195

differentiated

Front 196

Tumors usually are named by adding the suffix -____ to the parenchymal tissue type from which the growth originated.

Back 196

-oma

Front 197

A ________ is a growth that protects from a mucosal surface.

Back 197

polyp

Front 198

The term __________ is used to designate malignant tumor of epithelial tissue organ.

Back 198

carcinoma

Front 199

There are two categories of malignant neoplasms, _________ and _______ cancers.

Back 199

solid tumors; hematological

Front 200

The term ________ is used to describe the loss of cell differentiation in cancerous tissue.

Back 200

anaplasia

Front 201

A characteristic of of cancer cells is the ability to proliferate even in the absence of _________.

Back 201

growth factors

Front 202

With homologous loss of _________ gene activity, DNA damage goes unrepaired and mutations occur in dividing cells, leading to malignant transformations.

Back 202

p53

Front 203

The types of genes involved in cancer are numerous, with two main categories being the _________, which control cell growth and replication, and tumor _______ genes, which are growth-inhibiting regulatory genes.

Back 203

protooncogenes; suppressor

Front 204

___________ is the only known retrovirus to cause cancer in humans.

Back 204

Human T-cell leukemia virus-1

Front 205

Tumor cells must double _______ times before there will be a palpable mass.

Back 205

30

Front 206

A common manifestation of solid tumors is the cancer __________ syndrome.

Back 206

anorexia-cachexia

Front 207

As cancers grow, they compress and erode blood vessels, causing ________ and _________ along with frank bleeding and sometimes hemorrhage.

Back 207

ulceration; necrosis

Front 208

_______ is a common side effect of many cancers. It is related to blood loss, hemolysis, impaired red cell production, or treatment effects.

Back 208

Anemia

Front 209

A tissue _______ involves the removal of a tissue specimen for microscopic study.

Back 209

biopsy

Front 210

__________ therapy uses high-enerfy particles or waves to destroy or damage cancer cells.

Back 210

Radiation

Front 211

________ is a systematic treatment that enables drugs to reach the site of the tumor as well as distant sites.

Back 211

Chemotherapy

Front 212

Undefined or less differentiated cellular mass

Back 212

Malignant mass

Front 213

Defines the differentiation potential of stem cells

Back 213

Cellular potency

Front 214

Stem cells undergoing numerous mitotic divisions while maintaining an undifferentiated state

Back 214

Renewal

Front 215

Process of cell division

Back 215

Proliferation

Front 216

Cancer stem cells

Back 216

Tumor-initiating cells

Front 217

Mass of cells due to overgrowth

Back 217

Tumor

Front 218

Process that removes senescent and or damaged cells

Back 218

Apoptosis

Front 219

Well-differentiated mass of cells

Back 219

Benign mass

Front 220

Process of cell specialization

Back 220

Differentiation

Front 221

Study of tumors and their treatment

Back 221

Oncology

Front 222

Normal gene that can cause cancer if mutated

Back 222

Protooncogene

Front 223

Ratio of dividing cells to resting cells

Back 223

Growth fraction

Front 224

Promote cancer when less active

Back 224

Tumor suppressor gene

Front 225

Marked by chromosomal aberrations

Back 225

Genetic instability

Front 226

Changes in gene expression without DNA mutation

Back 226

Epigenetic effects

Front 227

Loss of cell differentiation

Back 227

Anaplasia

Front 228

Epithelial cells must be anchored to either neighboring cells or the underlying extracellular matrix to live and grow.

Back 228

Anchorage dependence

Front 229

Time it takes for the total mass of cells in a tumor to double

Back 229

Doubling time

Front 230

Tumor suppressor gene

Back 230

p53

Front 231

Five factors used to describle benign and malignant neoplasm.

Back 231

1. Cell characteristics
2. Rate of growth
3. Manner of growth
4. Capacity to invade and metastasize
5. Potential for causing death

Front 232

Which of the following is not a major example of inherited suseptibility to cancer?

a. Li-Fraumeni syndrome
b. Familial polyposis coli
c. Familial retinoblastosis
d. Paraneoplastic syndrome

Back 232

d. Paraneoplastic syndrome

Front 233

Which of the following is correct regarding all malignant tumors?

a. Anaplasia
b. Spread to distant sites
c. Invasion of surrounding tissues
d. Progressive and uncoordinated growth
e. All of the above

Back 233

e. All of the above

Front 234

Variation in size, shape, and staining of anaplastic cells is the definition of:

a. Metastasis
b. Pleomorphism
c. Lack of differentiation
d. Hyperchromatism

Back 234

b. Pleomorphism

Front 235

Which test provides the most precise information about the nature of a neoplasm?

Back 235

Biopsy

Front 236

Carcinoma is synonymous with:

Back 236

Malignant epithelial neoplasm

Front 237

Characteristics of malignant neoplasms are (a) encapsulation, (b) anaplasia, (c) invasion, (d) mitosis.

Back 237

(b) anaplasia, (c) invasion,

Front 238

The process by which unspecialized stem cells become specialized:

Back 238

Differentiation

Front 239

Which part of the cell cycle has the most redundancies, is tightly regulated by proteins called cyclins, and associated ezymes called cyclin-dependent kinases (CDKs)?

Back 239

Between G1 and S

Front 240

Correct order of the cell cycle

Back 240

G1, S, G2, M

Front 241

Which of the following is correct regarding a patient with a malignant neoplasm?

a. Hypercalcaemia due to bony metastases is an example of a paraneoplastic syndrome
b. The tumor marker a-fetoprotein is usually raised in patients with hepatocellular carnioma
c. The grade of a neoplasm refers to how far it has spread
d. Tumor markers may be used as the primary tool for cancer diagnosis

Back 241

b. The tumor marker a-fetoprotein is usually raised in patients with hepatocellular carnioma

Front 242

Which is correct regarding classification and nomenclature of neoplasms?

a. The neoplastic grading is a clinical estimate of the extent of tumor spread
b. The growth in malignant tumor is uncoordinated and autonomous, which the growth in a benign tumor is usually coordinated
c. A carcinoma is an epithelial malignancy
d. Leiomyosarcoma is a malignant tumor of skeletal muscle

Back 242

c. A carcinoma is an epithelial malignancy

Front 243

At autopsy the liver contains multiple tumor masses from 2-5 cm in size that are mostly tan and firm and that grossly exibit umbilication with central necrosis.

a. There is a multicentric origin of a benign neoplasm.
b. The neoplasm has a high grade.
c. The primary neoplasm is not in the liver.
d. A carcinogen was the underlying cause for the neoplasm.
e. The neoplasm has an advanced stage.

Back 243

c. The primary neoplasm is not in the liver.

Front 244

A 35 yr old woman had a firm nodule papable on the dome of the uterus six yrs ago. The nodule has slowly increased in size and is now twice the size. She remains asymptomatic. Which neoplasm is she most likely to have?

Back 244

Leiomyoma (Tumor of smooth muscle cell)

Front 245

2 cm firm, rounded mass is palpable beneath the left forearm. No difficulty using arm, no pain, overlying skin appears normal. Mass doesn't change in size. Which neoplasm is likely?

Back 245

Lipoma

Front 246

Chronic couch over the past 2 months. Chest x-ray shows 3 cm mass in right upper lobe. Fine needle biopsy is done. Which finding is irrelevant for determining further therapy and prognosis?

a. Is the neoplam invading the margin of resection?
b. What is the size of the neoplasm?
c. What is the degree of atypia and pleomorphism of the neoplastic cells?
d. How much inflammation is present in the neoplasm?
e. Is the neoplasm primary or metastatic?

Back 246

d. How much inflammation is present in the neoplasm?

Front 247

Oncogenes have been implicated in the development of a human neoplasms. Oncogene activation is believed to be required for oncogenesis. Which of the following potential mechanisms are relevant to these processes?

a. Chromosome translocation
b. DNA point mutation
c. Amplification
d. All of the above

Back 247

d. All of the above