Neoplasia - Cellular Adaptation

Front 1

what happens if a cell doesn't adapt to injury

Back 1

they undergo necrosis

Front 2

neoplasia means

Back 2

'new form'

Front 3

what is the downside to cellular adaptation to injury

Back 3

can lead to growth disturbances which predispose to neoplastic disease

Front 4

point of loss of reversibility = ?

Back 4

the point where tissues no longer respond to normal signals

Front 5

non-neoplastic growth disturbances are responsive to _______________. (what about neoplastic?)

Back 5

normal controls for growth; in neoplastic growth disturbances, response to normal controls for growth is lost. They ignore the body's signals

Front 6

non-neoplastic growth disturbances occur _________________________. (what about neoplastic?)

Back 6

separately or in combination; neoplastic are usually multiple

Front 7

how do you reverse a non-neoplastic growth disturbance? neoplastic?

Back 7

remove the stimulus. neoplastic are irreversible

Front 8

how do you determine the point of loss of reversibility?

Back 8

you can't, you can only observe the consequences

Front 9

what type of growth disturbance is most significant in neoplasms

Back 9

dysplasia (or combinations with dysplasia)

Front 10

rank growth disturbances in terms of significance in causing neoplasms

Back 10

hypertrophy < atrophy < hyperplasia < prosoplasia < metaplasia < dysplasia < combos with dysplasia

Front 11

atrophy

Back 11

shrinkage of a tissue due to a reduction in number of cells

Front 12

hyperplasia

Back 12

increase in the size of tissue due to increase in number of cells

Front 13

hypertrophy

Back 13

increase in size of tissue due to increase in size of cells

Front 14

prosoplasia

Back 14

substitution of a more highly specialized tissue for a less specialized tissue

Front 15

metaplasia

Back 15

substitution of a less specialized tissue for a more highly specialized tissue

Front 16

dysplasia

Back 16

abnormal pattern of maturation

Front 17

examples of atrophy

Back 17

cancers of the prostate & stomach

Front 18

example of hyperplasia

Back 18

reaction to irritation or hormones

Front 19

examples of hypertrophy

Back 19

physical stresses or exercise of muscle

Front 20

examples of prosoplasia

Back 20

GERD, barrett's esophagus

Front 21

examples of metaplasia

Back 21

smoker's bronchi

Front 22

examples of dysplasia

Back 22

CIN, oral precancer

Front 23

one way in which neoplastic cells differ from normal cells

Back 23

they don't respond to normal controls for growth

Front 24

which neoplastic diseases are caused by hypertrophy

Back 24

hypertrophy is not known to lead to neoplastic disease

Front 25

various injuries to cells may damage ________

Back 25

DNA

Front 26

what types of injuries create the conditions favorable to the production of free radicals that attack DNA

Back 26

ischemia and ischemia-re-profusion injuries

Front 27

nutritional deficiencies can lead to ______________________________

Back 27

a lack of adequate levels of essential components for cell growth, maturation

Front 28

downregulation of PTEN stimulates _____________________________

Back 28

cell cycle progression

Front 29

in hyperplasia there is an increased chance for _______________________________

Back 29

spontaneous DNA errors or action of deleterious agents on replication DNA

Front 30

promotors

Back 30

increase the number of tumors that form

Front 31

initiators

Back 31

cause mutations

Front 32

example of epithelial hyperplasia of the oral cavity

Back 32

acanthosis with hyperkeratosis (leukoplakia)

Front 33

what must you do if you find leukoplakia

Back 33

- remove stimulus
- biopsy! 5% of leukoplakias are already malignant

Front 34

what does it mean if a leukoplakia does not reverse after the stimulus is removed

Back 34

it is headed towards carcinoma

Front 35

what % of high-grade dysplastic barrett's esophagus become malignant

Back 35

10%

Front 36

what must happen in order for adenocarcinoma of the esophagus to occur

Back 36

a preceding change from stratified squamous epithelium to gastric-like mucosa (often followed by dysplasia)

Front 37

example of prosoplasia in the oral cavity

Back 37

erythroplakia

Front 38

what % of low-grade dysplastic barrett's esophagus become malignant

Back 38

1%

Front 39

cells present in premalignant barrett's esophagus

Back 39

normal cells and prosoplastic cells

Front 40

what happens ti TP53 in oral cancer

Back 40

mutated

Front 41

during immortilization, invasion and metastasis, there is upregulation of ________

Back 41

VEGFA

Front 42

metaplasia represents ________________________________

Back 42

adaptive substitution - cells sensitive to stress are substituted by cells better able to withstand it

Front 43

most common epithelial metaplasia

Back 43

ciliated columnar epithelium to simple squamous epithelium in the trachea and bronchi in response to chronic irritation

Front 44

vitamin A deficiency induces

Back 44

squamous metaplasia in the respiratory epithelium

Front 45

vitamin A excess suppresses

Back 45

keratinization

Front 46

what important function is lost in respiratory squamous metaplasia

Back 46

mucous secretion

Front 47

the most common form of cancer in the respirtatory tract is composed of _______________________

Back 47

squamous cells

Front 48

most cancer appear to arise from tissues that exhibit

Back 48

prior dysplasia

Front 49

microscopic characteristics of dysplatic cells are similar to (or very often indistinguishable from) _______________________________

Back 49

cytologic features of malignancy

Front 50

microscopic features of displasia

Back 50

- hyperkeratosis*
- acanthosis*
- increased numbers and/or abnormal mitosis
- keratin pearls
- individual cell keratinization
- loss of polarity and cellular orientation
- large, prominent nucleoli
- dyskarynosis
- basilar hyperplasia
- increased nuclear:cytoplasmic ratio
- poikilocarynosis
- hyperchromatism

HA! I KILL'D BIPH! (i know it's lame)

Front 51

what protein plays a pivotal roll in maintaining cell proliferation

Back 51

Ki-67

Front 52

Ki-67 is present in which phases of the cell cycle

Back 52

all non-G0 phases (G1 --> S --> G2 --> M)

Front 53

in which phase of the cell cycle does Ki-67 peak

Back 53

M

Front 54

what happen to Ki-67 after M phase

Back 54

it is rapidly catabolized

Front 55

Ki-67 labeling index = ?
Represents?

Back 55

the percentage of cells in a tissue staining for Ki-67; represents the growth fraction

Front 56

for dysplasia in barrett's esophagus Ki-67 LI is associated with

Back 56

progression

Front 57

in benign tumors, high LI is associated with

Back 57

high recurrence rate

Front 58

LI greater than 20% is seen in ___________

Back 58

high grade non-hodgkins lymphoma

Front 59

in low grade lymphomas, LI>______ have a worse prognosis than those with LI<______

Back 59

5%

Front 60

p27 protein encodes _______________________

Back 60

encodes a cell cycle inhibitor protein that binds to cyclin D and CDK4 and causes arrest in G1 phase

Front 61

p27 is activated by

Back 61

transforming growth factor beta

Front 62

mutation to p27 may lead to

Back 62

loss of control of cell cycle ---> uncontrolled cellular proliferation

Front 63

minichromosome maintenance proteins are essential for ____________________________

Back 63

initiation of DNA replication

Front 64

what proteins are relevant markers for prognosis in various types of tumors

Back 64

MCM proteins

Front 65

how can MCM2 be used?

Back 65

- assess tumor proliferation
- prognostic tool to predict the outcome in a variety of cancers

Front 66

which is useful as a prognosticator in mucoepidermoid carcinoma of intraoral minor salivary glands, Ki-67 or p27?

Back 66

p27

Front 67

hallmark of many tumors:

Back 67

p53 gene is mutated and expressed at greatly elevated levels

Front 68

a normal p53 gene encodes

Back 68

a DNA binding transcription factor that is responsible for cell cycle checkpoints that are activated after exposure to DNA-damaging agents

Front 69

in a normal cell p53 is inactivated by

Back 69

mdm2

Front 70

what does p53 do once activated

Back 70

it causes cell cycle arrest to allow for cell repair or causes apoptosis of damaged cell to occur

Front 71

p53 gene is a ____________ gene. its function?

Back 71

tumor suppressor; stops the formation of tumors

Front 72

p53 has been mapped to what chromosome

Back 72

chromosome 17

Front 73

li-fraumeni syndrome

Back 73

inheritance of only one functional copy of p53 --> prediposes to cancer --> individuals develop several tumors in different tissues in early adulthood

Front 74

mutations to __________ are found in most tumor types

Back 74

p53

Front 75

in the normal cell p53 protein binds ________ which in turn stimulates another gene to form ____________

Back 75

DNA; protein p21

Front 76

what happens when p21 interacts with cdk2

Back 76

the cell cannot pass through to the next stage of cell division

Front 77

why is mutated p53 ineffective

Back 77

it cannot bind DNA in an effective way

Front 78

which gene is known as the 'guardian of the genome'

Back 78

p53