Neoplasia Cellular Adaptation

Front 1

What are the conditions for a NON-neoplastic growth disturbance? (reversible)

Back 1

1. Responsive to normal controls for growth
2. Reversible when stimulus is removed
3. May occur separately or in combination
4. Precise point of loss of reversibility (transformation) cannot be accurately determined; only the consequences can be observed

Front 2

What pre-neoplastic growth disturbances contribute to neoplasia?

Back 2

1. Atrophy**
2. Hyperplasia**
3. Prosoplasia**
4. Metaplasia***
5. Dysplasia****
6. Combination w/Dysplasia*******

Front 3

What is of shrinkage in the size of a tissue due to a reduction in number of cells (cancers of prostate and stomach)

Back 3

Atrophy

Front 4

What is a increase in the size of a tissue due to an increase in the number of cells (reaction to irritation or hormones)

Back 4

Hyperplasia

Front 5

What is an increase in the size of a tissue due to an increase in the size of cells (physical stresses or exercise of muscle)

Back 5

Hypertrophy

Front 6

What is a substitution of a more highly specialized tissue for a less specialized tissue (GERD-Barrett's esophagus)

Back 6

Prosoplasia

Front 7

What is a substitution of a less specialized tissue for a more highly specialized tissue (smokers bronchi)?

Back 7

Metaplasia

Front 8

What is an abnormal pattern of maturation (CIN; oral precancer)?

Back 8

Dysplasia

Front 9

What does the word neoplasia mean?

Back 9

The emergence of a new form of tissue (altered cells that form a mass or tumor)

Front 10

What is a main way that neoplastic cells vary from normal cells?

Back 10

Neoplastic cells are not responsive to the normal controls for growth.

Front 11

T/F
Hypertrophy causes neoplastic disease

Back 11

False
Hypertrophy is not know to predispose to neoplastic disease

Front 12

What type of pre-neoplastic condition occurs from ischemia and ischemia reprofusion injury in particular creates the conditions favorable to the production of free radicals that attack DNA and in nutritional deficiencies, there can be a lack of adequate levels of essential components for normal growth and/or maturation of cells?

Back 12

Atrophy

Front 13

What are the causes of atrophy?

Back 13

1. Damaged DNA due to cell injury
2. Ischemia and reprofusion produce free radicles that attack DNA
3. Nutritional deficiencies
4. Cell Aging

Front 14

What type of preneoplastic condition is evident in Prostate Carcinogenesis and what are the stages?

Back 14

Atrophy
Columnar cells shrink causing proliferative inflammatory atrophy. Then the cells undergo prostatic intraepithelial Neoplasia and become prostate cancer

Front 15

What are the steps for atrophy as a pre-neoplastic condition?

Back 15

Proliferative inflammatory atrophy (PIA)
Low-grade PIN
High-grade PIN
Invasive carcinoma

Front 16

In the carcinogenesis model of hyperplasia, ______ increase the number of tumors that form, _______ cause the mutations.

Back 16

Promoters
Initiators

Front 17

What are the properties of hyperplasia as a premalignant condition?

Back 17

1. Intrinsic/extrinsic stimulated cell replication
2. Enlarged pool of cells duplicating DNA
3. Increased chance for spontaneous DNA errors or action of deleterious agents on replication DNA (mutation)
4. In the carcinogenesis model, promoters increase the number of tumors that form, whicle initiators cause the mutations
e. Association with many types of cancers (including oral SCC)

Front 18

What is the best example of Prosoplasia as a pre-neoplastic condition?

Back 18

Barrett esophagus in longstanding GERD (often referred to as intestinal metaplasia)

Front 19

What is the progression of barrett's esophagus to adenocarcinoma?

Back 19

Prosoplasia occurs changing the epithelium to gastric-like mucosa.
That is followed by dysplasia then adenocarcinoma

Front 20

What pre-neoplastic condition is a reversible change in which one adult cell type is replaced by another adult cell type?

Back 20

Metaplasia

Front 21

What type of pre-neoplastic condition represents an adaptive substitution of cells sensitive to stress by cell types better able to withstand the adverse environment?

Back 21

Metaplasia

Front 22

What is the most common epithelial metaplasia?

Back 22

Pseudostratified Columnar to squamous cells in the respiratory tract in response to chronic irritation as in the habitual cigarette smoker.

Front 23

What are some factors that can induce metaplasia in the respiratory tract?

Back 23

Vitamin A deficiency
Chronic smoking irritation

Front 24

Which pre-neoplastic condition has microscopic characteristics of the cells are very similar to the cytologic features of malignancy?

Back 24

Dysplasia

Front 25

What is this abnormal maturation of the covering epithelium?

Back 25

Epithelial Dysplasia

Front 26

What are two microscopic features of epithelial dysplasia that do not indicate dysplasia by themselves but may be present in conjunction with other features such as hyperchromatism?

Back 26

Hyperkeratosis (hyperorthokeratosis; hyperparakeratosis) and Acanthosis

Front 27

What protein plays a pivotal role in maintaining cell proliferation?

Back 27

Ki-67
is used as a labelling index (the % of cells in a tissue staining for Ki-67 indicates the growth fraction)

Front 28

What is used for grading and lebelling index?

Back 28

Ki-67 Protein

Front 29

A labelling index greater than 20% is seen in high grade ____________

Back 29

Non-hodgkin's lymphomas

Front 30

Low grade lymphomas with a labelling index in excess of 5% have a ____ prognosis than those with an index of less than 5%.

Back 30

Worse

Front 31

In soft tissue sarcomas, Ki-67 index is positively correlated with _________, ________, and the histological ________.

Back 31

mitotic count
cellularity
histological grade

Front 32

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

Back 32

p27 protein

Front 33

How is p27 activated?

Back 33

TGF-β (transforming growth factor β)

Front 34

What might a mutation in p53 lead to?

Back 34

Loss of control over the cell cycle leading to uncontrolled cellular proliferation.

Front 35

What are essential for the initiation of DNA replication and have been found to be releveant markers for prognosis in a variety of tumors?

Back 35

Minichromosome Maintenance (MCM) proteins

Front 36

What can Mcm2 expression be used to assess?

Back 36

Tumor proliferation and may be useful as an additional prognostic marker to refine the prediction of outcome in a variety of cancers.

Front 37

T/F
p27 and Ki-67 may be useful in estimating prognosis of the patients who have mucoepidermoid carcinoma of intraoral minor salivary glands.

Back 37

False
p27 is useful (NOT Ki-67)

Front 38

What color stain indicates protein Ki-67 presence?

Back 38

Brown

Front 39

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

Back 39

p53 gene

Front 40

What is true about the p53 gene's expression in tumors?

Back 40

it is mutated and expressed at much higher levels

Front 41

In a normal cell, what inactivates the p53 protein?

Back 41

p53 is inactivated by its negative regulator mdm2 (murine double minute 2 protein)

Front 42

Upon DNA damage or other stress, various pathways lead to the dissociation of the p53 and mdm2 complex. Once activated, p53 will either_________?

Back 42

Induce a cell cycle arrest to allow repair and survival of the cell OR apoptosis to discard the damaged cell.

Front 43

What does the p53's activity do to formation of tumors?

Back 43

p53 Stops the formation of tumors
(it is a tumor supressor gene)

Front 44

If only one functional copy of the p53 gene is inherited what happens to the patient?

Back 44

They are predisposed to cancer and develop several independent tumors in a variety of tissues in early adulthood. This condition is rare and is known as LyFraumeni syndrome.

Front 45

How does p53 protein prevent tumors?

Back 45

1. p53 binds DNA
2. protein p21 is made
3. p21 binds to cdk2 (cell division-stimulating protein)
4. Once the p21 complexes with cdk2 the cell cannot pass through to the next stage of cell division

Front 46

When p53 is mutated, what happens?

Back 46

it can't bind to DNA effectively and does not perform the stop signal for cell division.

Front 47

What proteins are the key element down regulated in prostate cancer?

Back 47

Pten proteins - repair DNA damage

Front 48

What is the literal translation of pleomorphsim?

Back 48

"Pleomorphism" literally mean "many shapes" (pleo- = many; -morph = shapes). It is a characteristic of anaplasia