Neoplasia IV Flashcards

(50 cards)

1
Q

_________ is disordered, non-neoplastic abnormal cell growth with loss of cellular orientation, shape and size in comparison to normal tissue maturation.

A

Dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Dysplasia used only with _________

A

Epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Mild dysplasia is usually _________; severe dysplasia usually progresses to _________

A

Reversible

carcinoma in situ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does CIN and SIL mean?

A

CIN = cervical intra-epithelial neoplasia

SIL = squamous intra-epithelial lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the CIN and SIL for mild dysplasia?

A

CIN 1 - confined to basal 1/3 of epithelium

Low grade SIL (LSIL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the CIN and SIL for moderate dysplasia?

A

CIN2 - confined to basal 2/3 of epithelium

High grade SIL (HSIL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the CIN and SIL for severe dysplasia?

A

CIN 3 (>2/3, but <3/3)

HSIL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the CIN and SIL for carcinoma in situ (CIS)?

A

CIN 3 = 3/3 full thickness dysplasia

HSIL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

The grade of cervical intra-epithelial neoplasia (CIN) is defined by ___________

A

the proportion of epithelium occupied by immature cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Invasive carcinoma occurs when _________

A

abnormal cells invade through the basement membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

__________ refers to full thickness dysplasia extending from BM to surface of epithelium. Only applicable to epithelial neoplasms

A

Carcinoma in situ (CIS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

_________ refers to growth into surrounding tissue by direct expansion

A

Invasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the progression of carcinoma in the oral cavity?

A

Oral leukoplakia

Dysplasia

Squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the progression of adenocarcinoma of esophagus?

A

Barret esophagus (metaplasia)

Dysplasia

Adenomacarcinoma of esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the progression of adenocarcinoma of colon?

A

Chronic ulcerative colitis

Dysplasia

Adenocarcinoma of colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the progression of hepatocellular carcinoma?

A

Hep B or C

Macronodular cirrhosis

Hepatocellular carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Tumor is a ________ of a mutated cell

A

monoclonal expansion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

New subclones arise from descendants of the ___________ by multiple mutations. With progression, the tumor mass becomes enriched for variants that are more adept at ________ and are likely to be more ________

A

original transformed cell

Evading host defenses

aggressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are essential alterations for malignant transformation? x7

A
  1. Defects in DNA repair
  2. Self-sufficiency in growth signals
  3. Insensitivity to growth inhibitory signals
  4. Limitless replicative potential
  5. Evasion of apoptosis
  6. Sustained angiogenesis
  7. Ability to invade and metastasize
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the 4 classes of normal regulatory genes?

A
  1. Growth promoting proto-oncogenes
  2. Growth inhibiting tumor suppressor genes
  3. Genes regulating apoptosis
  4. Genes regulating DNA repair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

After activation of protooncogenes, two categories of chain exist and they are______

A
  1. Normal protein is overproduced
  2. Mutant protein is produced and has an aberrant function
22
Q

What mechanisms lead to activation of a proto-oncogene?

A

Chemical carcinogens
Radiation
Infectious agents

Those 3 lead to DNA damage and transformation

23
Q

What translocation occurs with chronic myelogenous leukemia (CML)? Then what occurs?

A

c-abl proto-oncogene on chromosome 9 is translocated to bcr, an oncogene on chromosome 22

bcr-abl hybrid/fusion gene on chromosome 22 encoding for a protein with increased tyrosine kinase activity

24
Q

With chronic myelogenous leukemia, increased tyrosine kinase activity stimulates ________

A

Proliferation of granulocytic precursors giving rise to a CML

25
What is used to treat CML?
Imatinib mesylate (Gleevec) Inhibits tyrosine kinase
26
What chromosome is involved with CML?
Philadelphia chromosome
27
What translocation occurs with Burkitt lymphoma?
Translocation of c-myc protooncogene from chromosome 8 to a site adjacent to Ig heavy chain (IgH) locus on chromosome 14
28
With Burkitt lymphoma, overexpression due to translocation or amplification of c-myc leads to __________.
Excess transcription signals
29
Translocation of c-myc can also be seen in other________
B and T cell tumors
30
Amplification of c-myc can also be found in ________
breast, colon, lung, and other cancers
31
Amplication of n-myc are seen in 30-40% of _________ and is associated with poor prognosis
Neuroblastomas
32
How can neuroblastomas be identified? Where do they usually arise?
Homogenous staining region (HSR) or double minutes seen on a karyotype Occur in children and usually arise in the adrenals or sympathetic nerve ganglia.
33
Proto-oncogene is responsible for _________
Regulation of growth and differentiation
34
How are proto-oncogenes activated? x3
1. Point mutation 2. Chromosomal translocation 3. Amplification
35
Once activated, proto-oncogene becomes ________ causing overproduced __________ with an aberrant function.
oncogene normal protein or mutant protein
36
An ___________ is the cancer causing gene.
oncogene
37
Neoplastic clonal expansion is not only because activation of proto-oncogenes, but also_______
1. inactivation of tumor suppressor genes 2. Decreased apoptosis due to imbalance between pro and anti-apoptotic genes
38
What gene is involved with B cell follicular lymphoma? What gene products are produced?
BCL-2 genes Produce gene products that prevent mitochondrial leakage of cytochrome c (signal for apoptosis)
39
Overexpression of BCL-2 protein product -->
prevents apoptosis of B lymphocytes then leads to follicular lymphoma
40
What translocation occurs with B cell follicular lymphoma?
Translocation t(14; 18)
41
What are the key gene translocations that occur with activation of pro-oncogene?
CML = t(9; 22) Burkitt's lymphoma t(8; 14)
42
What are the key gene translocations that occur with activation of anti-apoptotic gene?
Follicular lymphoma: t(14; 18)
43
What is the gene product and neoplasm for the oncogene BCR-ABL?
Tyrosine kinase CML, ALL
44
What is the gene product and neoplasm for the oncogene BCL-2?
Antiapoptotic molecule (inhibits apoptosis) Follicular and diffuse large B cell lymphomas
45
What is the gene product and neoplasm for the oncogene BRAF?
Serine/threonine kinase Melanoma, non-Hodgkin lymphoma, papillary
46
What is the gene product and neoplasm for the oncogene c-myc?
Transcription factor Burkitt lymphoma
47
What is the gene product and neoplasm for the oncogene HER2/neu (c-erbB2)?
Receptor tyrosine kinase Breast and gastric carcinomas
48
What is the gene product and neoplasm for the oncogene MYCL1?
Transcription factor Lung tumor
49
What is the gene product and neoplasm for the oncogene MYCN?
Transcription factor neuroblastoma
50
What is the gene product and neoplasm for the oncogene RET?
Receptor tyrosine kinase MEN2A and 2B, medullary thyroid cancer