Pathology- Principles Of Neoplasia

Front 1

____ refers to a "new growth" of abnormal tissue (usually derived from a single cell precursor) that serves no physiologic function and, for the most part, is independent of normal restraints on orderly growth.

Back 1

neoplasia

Front 2

In neoplasia, cells normally dont replicate unless they are stimulated by ___ released in response to physiologic, pathologic, or reparative demands.

Back 2

endogenous or exogenous growth factors

Front 3

T/F Neoplastic cells have the ability to replicate in the absence of growth factors or they may replicate excessively in response to normal stimuli.

Back 3

True

Front 4

Inherited genetic influence play a direct role in the development of certain neoplasms (retinoblastoma, neurofibromatosis, multiple endocrine neoplasia syndrome), epidemiologic evidence suggest that 75-90% of human neoplasia is due, in part, to what?

Back 4

environmental factors

Front 5

Tissues most directly exposed to the environment, such as ___, ___, and ___, tend to show higher rates of neoplastic transformation.

Back 5

skin, respiratory tract, gastrointestinal tract

Front 6

Neoplastic transformation is a (quick/progressive) process involving (one/multiple) steps and in the majority of cases involves _____.

Back 6

progressive
multiple
somatic mutations of cellular DNA

Front 7

Neoplasia is a ____ disease in that the fundamental cellular changes occur at the level of ___ but these changes are induced by ___ factors.

Back 7

genetic
DNA
environmental

Front 8

What are denoted by the suffix "-oma" which usually indicates a neoplastic process but occasionally may be applied to a non-neoplastic mass (hematoma, granuloma, xanthoma, etc).

Back 8

tumors

Front 9

An unmodified suffix generally denotes a ___ neoplasm while for malignant neoplasms the suffix is modified to either ____ (referring to epithelial malignancies) or ____ (referring to mesenchymal/connective tissue malignancies.

Back 9

carcinoma
sarcoma

Front 10

malignant neoplasm of melanocytes

Back 10

melanoma

Front 11

malignant neoplasm of lymphoid tissue

Back 11

lymphoma

Front 12

malignant neoplasms of supporting tissue of the CNS

Back 12

glioma

Front 13

malignant tumors arising from early, partially differentiated embryonal tissue

Back 13

blastoma

Front 14

neoplasm which contains cells from more than one embryonic germ cell layer and may be benign or malignant

Back 14

teratoma

Front 15

a non-neoplastic "tumor" that represents abnormal overgrowth or differentiation of cells native to the tissue of origin

Back 15

hamartoma

Front 16

presence of normal tissue in an abnormal location

Back 16

choristoma (also termed ectopic or heterotopic tissue)

Front 17

What is the prefix for glandular epithelium?

Back 17

adeno

Front 18

What is the prefix for:
-squamous epi
-transitional epi
-fibrous CT

Back 18

-squamous
-transitional
-fibro

Front 19

What is the prefix for smooth muscle?

Back 19

leiomyo

Front 20

What is the prefix for skeletal muscle?

Back 20

rhabdomyo

Front 21

What is the prefix for adipose tissue?

Back 21

lipo

Front 22

What is the prefix for:
-cartilage
-bone
-blood vessel
-lymphatic vessel

Back 22

chondro
osteo
hemangio
lymphangio

Front 23

What prefix indicates hard due to excessive production of tumor stroma?

Back 23

scirrhous

Front 24

What prefix indicates soft, resembling marrow, due to scant production of tumor stroma?

Back 24

medullary

Front 25

What prefix indicates gelatinous, mucinous?

Back 25

colloid

Front 26

What prefix indicates fluid or gas filled spaces?

Back 26

cystic

Front 27

What prefix indicates the growth pattern of forming follicles?

Back 27

follicular

Front 28

What prefix indicates the growth pattern of forming small cystic spaces?

Back 28

cyst

Front 29

What prefix indicates the growth pattern of forming "nipple-like" projections?

Back 29

papillary

Front 30

What prefix indicates the growth pattern of forming shaggy, "finger-like" projections?

Back 30

villous

Front 31

What prefix indicates a growth pattern of pierced by small holes?

Back 31

cribriform

Front 32

The distinction bw benign and malignant tumors is based on what?

Back 32

their microscopic appearance and clinical behavior

Front 33

What do the differences bw benign and malignant tumors generally relate to?

Back 33

-cellular morphology
-cellular differentiation
-rate of growth
-mode of growth
-metastasis

Front 34

___ cells resemble the normal morphology of the cell of origin while ___ cells are characterized by cellular and nuclear pleomorphism (due to alterations in the cell cytoskeleton); increased nuclear/cytoplasmic ratio; increased nuclear chromatin which is frequently "clumped" along an irregular nuclear membrane; large nucleoli; bizarre mitoses; loss of cellular orientation; and to some degree, loss of normal functional capacity.

Back 34

benign neoplastic
malignant neoplastic

Front 35

Cells of benign neoplasms (are/ are not) well differentiated (all cells closely resemble the cell of origin), have a (normal/abnormal) number of chromosomes, and (retain/ do not retain) functional capabilities.

Back 35

-are
-normal
-retain

Front 36

Which cells show abnormalities in the number or structure of chromosomes and, within the same tumor, may vary from complete lack of differentiation (___) to well differentiated?

Back 36

malignant
anaplasia ()

Front 37

What tends to parallel the degree of differentiation of neoplastic cells?

Back 37

rate of growth

Front 38

What is the rate of growth for benign neoplasias?

Back 38

slow growth or may, on occasion, spontaneously regress

Front 39

What is the rate of growth for malignant neoplasias?

Back 39

grow more rapidly and rarely cease growth or regress

Front 40

(Benign/malignant) neoplasms grow by expansion and tend to compress the surrounding tissue into a "capsule" that separates the tumor from normal tissue.

Back 40

benign

Front 41

(benign/malignant) tumors grow by infiltration and invasion of the surrounding tissue and are not confined by a capsule.

Back 41

malignant

Front 42

What refers to the spread of a neoplasm to points that are not contiguous with the primary lesion?

Back 42

metastasis

Front 43

____ tumors do NOT metastasize, but all ____ neoplasms have metastatic potential ?

Back 43

benign
malignant

Front 44

What are the different ways metastases can occur?

Back 44

-lymphatic dissemination
-hematogenous dissemination
-transcoelomic seeding
-traumatic seeding

Front 45

What is the most common route of metastasis (especially for epithelial neoplasms (carcinomas))?

Back 45

lymphatic dissemination

Front 46

____ refers to the most common route of metastasis and follows the natural lymphatic drainage of the site of malignancy; regional lymph nodes may be enlarged due to metastatic tumor or to immune reaction to the presence of tumor products.

Back 46

lymphatic dissemination

Front 47

Which metastasis route is characteristic of connective tissue neoplasms (sarcomas)? Carcinomas are also spread by this route since there are vascular-lymphatic anastomoses. Invasion and metastases are more likely to occur via the ____ system due to its thin walled structure.

Back 47

hematogenous dissemination
venous

Front 48

Metastasis may occur via ___ with malignancies that involve coelomic (peritoneal, pleural) surfaces.

Back 48

transcoelomic seeding

Front 49

Metastasis may occur via ___ when excessive manipulation or cutting into malignant tumors may detach and carry small portions of the tumor to other sites.

Back 49

traumatic seeding

Front 50

(benign/malignant) neoplasms may cause significant morbidity or kill patients by virtue of their anatomic position (pituitary adenoma, craniopharyngioma, meningioma, etc). Even small tumors may cause death by interfereing w/ vital functions (brainstem, conduction of the heart).

Back 50

both

Front 51

Local affects of neoplasia:
-(benign/malignant/both) neoplasms may cause compression of surrounding structures.
-(benign/malignant/both) are more prone to infarction, necrosis, hemorrhage, ulceration, and infection
-(benign/malignant/both) stimulate excessive production of connective tissue (desmoplasia)

Back 51

-both
-malignant
-malignant

Front 52

Systemic effects of neoplasia:
-Some tumors (benign or malignant) may produce a hormone or hormone-like substances that can have systemic effects known as ____ (ex.____). Other effects may relate to hypercoagulabilty, thrombocytopenia, migratory thrombophlebitis, cachexia, sepsis, electrolyte imbalances, etc.

Back 52

paraneoplastic syndromes (hypercalcemia, Cushing's syndrome, Syndrome of Inappropriate ADH Secretion, polycythemia, etc)

Front 53

What are considered cariogenic agents?

Back 53

chemicals
radiation
viruses

Front 54

The cariogenicity of various chemcial agents appears to be ___ dependent so that multiple fractional doses over time have the same transforming potential as a comparable one-time dose.

Back 54

dose

Front 55

Although some chemical compounds act on cells directly, most chemical substances require ____ for conversion into ultimate carcinogens.

Back 55

metabolic activation

Front 56

Most of the known carcinogens are metabolized by ___ in the ___.

Back 56

cytochrome P-450- dependent mono-oxygenases in the liver

Front 57

What factors can modify the carcinogenic effect of a chemical by affecting its metabolism?

Back 57

age, sex, nutritional status, etc

Front 58

Transformation of a normal cell to a neoplastic cell with chemical carcinogens occurs in what stages?

Back 58

Initiation
Promotion
Conversion
Progression

Front 59

Which stage in the chemical transformation of a normal cell to a neoplastic cell can produce permanent changes in the genetic make-up of a cell by reacting w/ DNA to cause strand breaks, to alter methylation, or to hinder DNA repair. The DNA changes however must not be so severe as to prevent the cell from being able to replicate. They DO NOT stimulate cell division, and do not have growth autonomy nor do they have unique, readily identifiable genotype or phenotype markers.

Back 59

chemical initiators

Front 60

Which stage in the chemical transformation of a normal cell to a neoplastic cell can induce neoplastic transformation in a previously initiated cell but cannot cause neoplastic transformation in and of themselves in a non-initiated cell. Instead of altering the DNA, their action seems to induce clonal proliferation of initiated cells by altering the regulation of mitosis and the differentiation and maturation pathways.

Back 60

chemical promoters

Front 61

Ultimately in the chemical transformation of a normal cell to a neoplastic cell the cells become ___ and are no longer dependent on the promoters for proliferation.

Back 61

converted

Front 62

During the chemical transformation of a normal cell to a neoplastic cell, once the neoplastic cells become autonomous, continued genetic mutation confers new attributes to ___ of the neoplastic cells.

Back 62

subclones

Front 63

Ionizing radiation can produce ___ that mediate cellular damage by breaking or altering chemical bonds.

Back 63

free radicals

Front 64

What can inactivate enzymes, alter proteins, and cause chromosomal breakage, translocations, and point mutations. It can also inhibit cell-mediated immunity and therefore tumor surveillance.

Back 64

Ionizing radiation

Front 65

The ability of ionizing radiation to induce neoplastic transformation correlates best with its ability to what?

Back 65

induce genetic mutation within the cell

Front 66

What viruses have been found to be associated w/ human neoplasia (carcinoma of the uterine cervix, hepatocellular carcinoma, Burkitt's lymphoma)?

Back 66

both DNA and RNA viruses

Front 67

Through what processes are viruses able to directly rearrange the structure or alter the expression of the host cell genome?

Back 67

transduction and insertional mutagenesis

Front 68

T/F In order for a cell to be transformed to a neoplastic cell via a virus, the host cell must survive the viral infection and be able to reproduce.

Back 68

true

Front 69

In tissue culture, neoplastic cells appear to be freed from normal regulatory controls and have an (increased/decreased) rate of stem cell renewal and their growth (is/ is no longer) inhibited by the presence of neighboring cells.

Back 69

increased
is no longer (loss of contact inhibition)

Front 70

Do malignant cells require attachment to a hard surface to proliferate?

Back 70

No, they have anchorage independent growth and are less cohesive (loss of surface cellular adhesion molecules)

Front 71

Malignant cells require (fewer/more) exogenous growth factors and in general are ____.

Back 71

fewer (if any)
immortal (cell lines can be kept alive indefinitely

Front 72

Malignant cells can develop ___ properties (probably related to cytoskeletal changes or production of enzymes unduced by oncogene activation) and ______ potential and when injected into other animals, these cells will prodce ___ (transplantability).

Back 72

-invasive
-metastatic
-neoplasms

Front 73

What are the specific genetic sequences called that are capable of transforming normal cells into neoplastic cells and were first identified in DNA viruses and RNA tumor viruses (retroviruses) that were known to produce malignancies in animals?

Back 73

viral oncogenes (v-onc)

Front 74

What genetic sequences were found to not be of true viral origin but instead was found to be very similar to genetic sequences found in normal cellular DNA which implies that these segments at some point in the past had been incorporated into the ancestral viral genome while the virus was replicating within an infected host and had been maintained via viral replication?

Back 74

viral oncogenes

Front 75

What is it called when a normal cell has genetic information that could potentially transform that cell into a neoplastic cell under the appropriate conditions?

Back 75

proto-oncogenes

Front 76

Genetic material from a neoplastic cell can transform a normal cell into a neoplastic cell. The genetic sequences capable of inducing this transformation are termed what?

Back 76

cellular oncogenes (c-onc)

Front 77

Cellular oncogenes are similar in sequence to normal proto-oncogene sequences and may have arisen through ____ of the proto-oncogenes. Proto-oncogenes, therefore, have the potential of being converted (through mutations, retroviral transduction, increased expression, etc) to oncogenes that can promote what?

Back 77

-simple somatic mutation
-excessive or inappropriate cell proliferation

Front 78

Like all other genes, each proto-oncogene is composed of a ____ and ____ region and changes in either region could produce an active oncogene.

Back 78

regulatory and a structural region

Front 79

What kind of mutation can lead to synthesis of a protein that has aberrant structure and function?

Back 79

structural

Front 80

How do structural mutations occur?

Back 80

through point mutations, insertions/deletions, or translocations

Front 81

What causes alteration of a single base pair which may alter the protein product of a proto-oncogene?

Back 81

point mutation

Front 82

What occurs randomly throughout proto-oncogenes, but only those occurring at certain critical "hot spots" produce oncogenic activation?

Back 82

point mutations

Front 83

Point mutations are best exemplified by what oncogenes?

Back 83

ras

Front 84

If these occur in the structural region, they may result in altering the protein product of a proto-oncogene.

Back 84

Insertions/deletions

Front 85

What can affect the biochemical functions of proto-oncogenes by fusion with new genetic sequences?

Back 85

translocations

Front 86

What results from a translocation that encodes a protein different from the normal protein?

Back 86

the c-abl oncogene (Philadelphia chromosome) in chronic myelogenous leukemia; t(9;22)

Front 87

With ___ changes, mutations affect the amount of protein product rather than the structure.

Back 87

regulatory

Front 88

What do regulatory changes occur through?

Back 88

translocations or gene amplifications

Front 89

Proto-oncogenes may become activated either because they are placed next to strong promoter/enhancer sequences or because ____ removes them from the influence of normal regulatory control sequences. ex: the ___ oncogene in Burkitt's lymphoma

Back 89

translocation
c-myc

Front 90

What produces many copies of an oncogene and therefore increases the amount of protein synthesis?

Back 90

gene amplification

Front 91

In karyotype studies, gene amplification can be observed as___ if they stay associated with the chromosome or as ___ if they break loose and replicate as extrachromosomal material.

Back 91

-homogeneously staining regions (HSR)
-double minutes (DM)

Front 92

The ___ oncogenes are amplified in neuroblastomas and small cell carcinomas of the lung; ___ is amplified in breast cancers; and ___ is amplified in glioblastoma multiforme

Back 92

-myc
-HER2/neu
-erbB

Front 93

Like the protein products of normal proto-oncogenes, the protein products of oncogenes are involved in the regulatory pathways that control ___ and ___ and are capable of transforming normal cells into neoplastic ones.

Back 93

cellular division and differentiation

Front 94

What are the growth factor proteins?

Back 94

sis, int-2

Front 95

What are the growth factor receptor proteins?

Back 95

erbB, fms

Front 96

What are the GTP-Binding proteins?

Back 96

ras family

Front 97

What are the non-receptor tyrosine kinases?

Back 97

src, abl

Front 98

What are the DNA-binding proteins?

Back 98

myc family

Front 99

What are the transcription regulators?

Back 99

fos, jun

Front 100

Which oncogenes may code for large amounts of growth factors to which the cell can respond (autocrine stimulation) or they may impart growth autonomy by deregulating genes that encode growth factors?

Back 100

c-sis

Front 101

What oncogene may encode proteins that enter the nucleus and directly stimulate cellular growth?

Back 101

c-sis

Front 102

Which family of oncogenes appear to influence signal transduction?

Back 102

ras

Front 103

Which family of oncogenes modifies the cytoskeletal protein, vinculin, which anchors actin filaments to the cell membrane and also allows expression of otherwise tightly regulated growth factor genes?

Back 103

c-src

Front 104

Which family of oncogenes seems to make cells more responsive to growth factors controlling cell proliferation and appears to confer immortality to the cell line?

Back 104

myc family

Front 105

What are tumor suppressor genes called?

Back 105

anti-oncogenes

Front 106

The expression of genes that serve to protect the cell from the events leading to neoplastic transformation are referred to as what?

Back 106

tumor suppressor genes

Front 107

The protein products of ___ modulate the activity of proto-oncogenes, oncogenes, or their protein products.

Back 107

tumor suppressor genes

Front 108

What could arise in the absence of tumor suppressor genes?

Back 108

neoplasia

Front 109

What tumor suppressor gene becomes much more active after DNA damage?

Back 109

p53 tumor suppressor gene on the short arm of chromosome 17

Front 110

What does the p53 tumor suppressor gene code for?

Back 110

a protein that binds to damaged DNA and inhibits cell mitosis until damaged DNA can be repaired by the DNA repair genes. If the damage is too sever to be repaired, the cell will undergo apoptosis.

Front 111

What happens in the absence of a functional p53 tumor suppressor gene?

Back 111

the cell may continue to reproduce incorporating the DNA mutation into the genome of the cell line.

Front 112

Mutations and inactivation of the p53 gene are seen in numerous human malignancies such as what?

Back 112

astrocytoma of the brain and carcinoma of the colon

Front 113

Defects in ___ may predispose to malignant transformation and may have been associated with various cancer syndromes such as xeroderma pigmentosum.

Back 113

DNA repair genes

Front 114

___ mutations that activate an oncogene allele or inactivate a tumor suppressor gene allele may be inherited and could be a predisposing risk factor for the development of neoplasia since that individual has inherited only one, rather than two, normal copies of the gene allele.

Back 114

heterozygous

Front 115

Oncogene activation (or tumor suppressor gene inactivation) of the corresponding locus (loss of heterozygosity) by somatic mutation may result in what?

Back 115

overt neoplastic development

Front 116

Loss of heterozygosity has been identified on the short arm of chromosome 3 in what carcinomas?

Back 116

renal cell carcinomas and small cell carcinomas of the lung

Front 117

Loss of heterozygosity has been identified on the short arm of chromosome 11 in what?

Back 117

Wilms' tumor of the kidney

Front 118

Loss of heterozygosity has been identified on the long arm of chromosome 13 in what carcinomas?

Back 118

retinoblastoma and ductal carcinoma of the breast

Front 119

When is a mutated allele present in all cells giving a greater tendency to develop multiple tumors?

Back 119

when the mutated allele is inherited

Front 120

Many of the ___ neoplasia syndromes appear to be the result of inheriting at least one mutated gene allele.

Back 120

autosomal dominant (ex. multiple endocrine neoplasia syndromes, familial polyposis coli, Von Recklingshausen disease)

Front 121

If somatic mutation and activation of an oncogene allele (or inactivation of a tumor suppressor gene allele) occurs, the chances of altering both alleles in a single cell are much less than the chance of altering one allele. When this does occur, however, the subsequent neoplasia is much more likely to be ____ than multiple as seen with the _____ neoplasia syndromes.

Back 121

-solitary
-inherited

Front 122

T/F A single oncogene can transform normal cells into neoplastic cells?

Back 122

False- no single oncogene can transform normal cells into neoplastic cells. More than one oncogene may be involved, with each supplying some of the function required to convert the cell from normal to neoplastic

Front 123

What is a distinguishing feature of neoplasia that may be the result of genetic alterations (oncogene activation, tumor suppressor inactivation) that direct the cell to replicate rather than to continue to differentiate?

Back 123

the propensity of tumor cells to reproduce

Front 124

Evidence suggest that most tumors are of what origin?

Back 124

monoclonal (a single cell from normal or pre-neoplastic tissue becomes neoplastic at a specific level of differentiation and the clonal derivatives of that cell produces the neoplasm

Front 125

In most tumors there appears to be an (increase/decrease) in the proportion of stem cells undergoing replication and a corresponding (increase/decrease) in the proportion progressing to full end-stage maturation.

Back 125

increase
decrease

Front 126

What refers to the proportion of cells within a tumor population that are in the proliferating pool?

Back 126

growth fraction (GF)

Front 127

The rate of tumor growth depends upon the ___ and the degree of imbalance between cell production and cell loss.

Back 127

growth fraction

Front 128

Most tumors have a (high/low) GF and proliferation (greatly/slightly) exceeds cell loss.

Back 128

low
slightly

Front 129

The growth fraction of a tumor has a profound effect on its susceptibility to what?

Back 129

chemotherapy

Front 130

What do cancer drugs primarily act on?

Back 130

dividing cells (therefore, tumors w/ a high growth fraction are most vulnerable)

Front 131

(Slow/Fast) growing tumors which have a high proportion of cells outside the cell cycle respond less favorably to chemotherapy and harbor cells which can potentially reenter the cycle at a later time.

Back 131

slow

Front 132

Tumor growth is dependent upon ___ without which neoplastic growth will stop at approximately 1mm diameter due to the limited diffusion capacity of oxygen and solutes.

Back 132

vascularization

Front 133

What do angiogenic factors promote and control?

Back 133

the neovascularization of the expanding cell mass (neovasculature tends to be loose abnormal due to loose endothelial junctions)

Front 134

What are considered angiogenic factors?

Back 134

fibrinogen and various substances produced by the tumor cells (angiogenin, fibroblast growth factor)

Front 135

What is not uncommon in tumors and, in the case of malignant tumors, may even help assist the tumor cells to spread to other sites?

Back 135

hemorrhage

Front 136

What in the tumor environment can significantly impair the biologic effect of radiation therapy and some forms of chemotherapy which are oxygen dependent?

Back 136

hypoxia

Front 137

What can influence the growth rate of hormonally responsive tissues?

Back 137

circulating hormones

Front 138

A greater degree of angiogenesis within a tumor is correlated with a (less/more) aggressive behavior and (poorer/better) prognosis.

Back 138

more
poorer

Front 139

As tumor size increases, the time it takes for a tumor to double in volume (increases/decreases) due to diminished blood supply, competition for metabolites, and other factors that lead to a decrease in the growth fraction and an increase in cell loss.

Back 139

increases (growth rate slows down)

Front 140

As tumors enlarge, an (increasing/decreasing) proportion of tumor cells drop out of the mitotic cycle either because of necrosis or by entering into prolonged G1 periods or the G0 phase of the cell cycle.

Back 140

increasing

Front 141

T/F Even though the doubling time slows down as tumors enlarge, by the time a solid tumor is clinically detected it has already completed a major portion of its life cycle.

Back 141

True

Front 142

T/F The later a tumor is identified, the greater the chance of successful radiation and/or chemotherapy.

Back 142

False- the earlier a tumor is identified

Front 143

Although tumors probably arise monoclonally, by the time they have reached clinical detection, the cell population is ____ in respect to morphologic appearance, karyotype, degree of differentiation, invasiveness, metastatic capabilities, etc implying that tumors can undergo ____ as they develop, probably related to DNA instability and the high rate of random mutation in neoplastic cells.

Back 143

-heterogenous
-clonal evolution

Front 144

____ cell are more likely to have characteristics that enable them to spread (increased motility, decreased adhesiveness, decreased anchorage dependence, etc).

Back 144

dedifferentiated

Front 145

_____, like the progression of pre-neoplasia to neoplasia, appears to involve a sequence of oncogene activations that, over time, leads to more highly malignant cells (those that have a survival advantage due to their growth rate, invasiveness, drug resistance, etc)

Back 145

clonal evolution

Front 146

By the time most malignant neoplasms have become clinically detectable, it is likely that they have evolved several subclones with ___ potential which implies that the earlier a cancer can be identified, the less likely it is that more aggressive subclones have developed.

Back 146

metastatic

Front 147

What type of cells have the ability to invade surrounding tissue and ultimately spread to distant sites?

Back 147

malignant cells

Front 148

What cells within a tumor have a high invasive and/or metastatic potential with a high mutation rate?

Back 148

cell clones

Front 149

Evidence suggests that ___ activation is involved in conferring metastatic potential on tumor cells by enabling the cell to attach to, degrade, and penetrate basement membranes and interstitial connective tissue.

Back 149

oncogene

Front 150

Malignant epithelial cells are (less/more) adherent to one another and become (less/more) "mobile" due to (loss/gain) of normal cell adhesion molecules.

Back 150

-less
-more
-loss (or inactivation)

Front 151

What do malignant epithelial cells bind to that are embedded in basement membranes and the extracellular matrix?

Back 151

structural glycoproteins such as laminin and fibronectins

Front 152

Since ___ adheres tightly to the type IV collagen of the basement membrane, neoplastic cells may evolve mechanisms to secrete ___ or alternatively, to produce tumor membrane receptors that binds native ___.

Back 152

laminin

Front 153

Once secured to the basement membrane, what do tumor cells secrete to dissolve the basement membrane?

Back 153

proteases such as type IV collagenase

Front 154

Once the tumor cells secrete proteases to dissolve the basement membrane, they are then free to attach to ___ with additional release of proteases.

Back 154

stromal fibronectin

Front 155

The ability of tumor cells to digest ground substance (collagen, glycoproteins, proteoglycans, and elastin) by the production of proteases and metalloproteinases is correlated with ____ potential.

Back 155

invasive

Front 156

It is likely that cancer cells interact with host fibroblasts and other mesenchymal cells and stimulate them to secrete what?

Back 156

additional collagenases

Front 157

Tumor derived growth factors as well as breakdown products of the extracellular matrix have angiogenic adn tumor chemotactic activities which promote what?

Back 157

neovascularization and recruitment of additional tumor cells

Front 158

What makes it relatively easy for tumor cells to gain access to circulation?

Back 158

loose endothelial junctions of the new vessels made via neovascularization

Front 159

Due to their lack of a basement membrane, what vessels are easily invaded by tumor cells?

Back 159

lymphatic channels (walls of venules and veins are easily invaded as well)

Front 160

T/F Hemmorhage and necrosis also promote the release of tumor cells into the circulation.

Back 160

True

Front 161

Once in circulation, what are tumor cells vulnerable to?

Back 161

-hemodynamic factors that cause cell trauma
-to immunologic recognition and attack (particulary by NK cells)
-to other adverse conditions

Front 162

How many tumor cells released into the bloodstream will ultimately metastasize?

Back 162

fewer than 1 in 1000

Front 163

In circulation, what do tumor cells tend to do?

Back 163

aggregate into clumps

Front 164

T/F Clumps of five to ten tumor cells appear less effective in producing metastases than either single cells or larger clumps.

Back 164

F- more effective

Front 165

Some clumps of tumor cells adhere to platelets or produce procoagulants which form "shields" of precipitated ___ to ward off immunologic recognition. These procoagulants may partly explain some of the hypercoagulable states seen in patients w/ desseminated cancer.

Back 165

fibrin

Front 166

What is the regional spread of tumors primarily influenced by?

Back 166

the anatomy of regional lymphatics

Front 167

Does metastases from malignant tumors display preferences for some tissue sites over others?

Back 167

yes, a variety of malignant tumors do

Front 168

T/F Metatastic deposits, like primary tumors, are clonal in origin and the survival and growth of the metatastic lesion generally depends on the same factors that enable growth of the primary lesion.

Back 168

True

Front 169

What type of antigen refers to antigens that are found on neoplastic cells and not on normal cells?

Back 169

tumor specific antigens

Front 170

In animals, each individual tumor induced by a given chemical carcinogen frequently (carries its own unique tumor antigen/share a common antigen) while all tumors produced by a given virus (carries its own unique tumor antigen/share a common antigen).

Back 170

-carries its own unique tumor antigen
-share a common antigen

Front 171

___ antigens can activate host immunologic destruction of cancer cells in animals but whether this occurs in humans to any significant extent is not known.

Back 171

tumor-specific antigens

Front 172

What type of antigens are found in normal cells but which are present in higher concentration in tumor cells?

Back 172

tumor associated antigens

Front 173

What type of tumor associated antigens are expressed at certain stages of a cell's maturation?

Back 173

differentiation antigens (beta HCG)

Front 174

What type of tumor associated antigens are expressed during embryonic development but normally repressed during adult life?

Back 174

oncofetal antigens (CEA, AFP)

Front 175

What refers to the microscopic pathologic determination of tumor aggressiveness based on the degree of differentiation of the neoplastic cells and the number of mitoses as an estimate of the rate of growth?

Back 175

Grading

Front 176

Most tumors are graded from I (low/high grade; undifferentiated/well differentiated) through IV (low/high grade; undifferentiated/well differentiated)?

Back 176

-low grade; well differentiated
-high grade; undifferentiated

Front 177

Many malignant neoplasms progress to a (lower/higher)grade over time as (less differentiated/undifferentiated) clones of cells become dominant.

Back 177

-higher
-less differentiated

Front 178

Is a lower or higher grade a better prognosis?

Back 178

lower

Front 179

What refers to the clinical and pathologic determination of tumor aggressiveness based on the size of the neoplasm, the presence or absence of regional lymph node involvement, and the presence or absence of distant metastases?

Back 179

Staging

Front 180

Staging is the basis of what?

Back 180

the TNM (tumor size, node involvement, metastasis) staging system

Front 181

How are tumors staged?

Back 181

numerically from 0 (localized tumor) through IV (distant metastases), and some are staged alphabetically from A (localized tumor) to D (metastatic tumor)

Front 182

The (smaller/larger) the tumor and the more localized it is, the (better/worse) the prognosis.

Back 182

-smaller
-better