Neoplasia IV Flashcards

1
Q

definition: dysplasia

A

disordered growth, pleomorphism, mitoses, loss of polarization

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

leukoplakia can develop into what type of cancer?

A

squamous cell carcinoma (via dysplasia)

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

Barrett esophagus can transform into what type of cancer?

A

adenocarcinoma (via dysplasia / metaplasia)

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

chronic atrophic gastritis of pernicious anemia can transform into what type of cancer?

A

gastric adenocarcinoma (via dysplasia)

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

chronic UC can transform into what type of cancer?

A

adenocarcinoma of colon (via dysplasia)

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

hep B or C can transform into what type of cancer?

A

hepatocellular carcinoma (via macronodular cirrhosis)

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

what are the roles of proto-oncogenes?

A

regulation of growth and differentiation

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

what are the activation mechanisms for proto-oncogenes?

A

mutation, chromosomal translocation, amplification

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

what are the two main categories of cellular / molecular change following activation of an oncogene?

A
  1. normal protein is overproduced 2. mutant protein is produced and has an aberrant function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ERBB2 / Her-2 / Neu is associated with what type of cancer? how?

A

breast / ovarian - amplification

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

RET is associated with what type of cancer? how?

A

MEN 2a / 2b, familial medullary thyroid carcinomas - point mutation

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

KRAS is associated with what type of cancer? how?

A

pancreas, colon, lung - point mutation

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

ABL is associated with what type of cancer? how?

A

chronic myeloid leukemia, acute lymphoblastic leukemia - translocation

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

B-catenin is associated with what type of cancer? how?

A

hepatoblastomas (point mutation), hepatocellular carcinoma (overexpression)

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

C-myc is associated with what type of cancer? how?

A

Burkitt lymphoma - translocation

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

N-myc is associated with what type of cancer? how?

A

neuroblastoma, small cell CA of lung - amplification

17
Q

cyclin D is associated with what type of cancer? how?

A

mantle cell lymphoma (translocation), breast and esophageal (amplification)

18
Q

what are the important clinical features of multiple endocrine neoplasia 2a / 2b?

A
  1. mutation of RET 2. many endocrine organs can be involved 3. most are tumors, but can be hyperplasia
19
Q

what is the pathogenesis of chronic myelogenous leukemia (CML)?

A
  1. c-abl oncogene on chromosome 9 translocated to bcr on chromosome 22 2. increase in tyrosine kinase activity 3. proliferation of granulocytic precursors
20
Q

what drug inhibits tyrosine kinase in CML?

A

Imatinib mesylate (Gleevec)

21
Q

what is the pathogenesis of burkitt lymphoma?

A
  1. translocation of c-myc proto-oncogene from chromosome 8 to Ig heavy chain on chromosome 14 2. overexpression of c-myc leads to excess transcription signals
22
Q

what is the pathogenesis of B cell follicular lymphoma?

A
  1. translocation 14-18 2. over expression of BCL-2 protein product 3. prevents apoptosis of B cells
23
Q

what is the most common lymphoma?

A

follicular lymphoma (evasion of apoptosis)

24
Q

what is the pathogenesis of neuroblastoma?

A

amplification of N-myc

25
Q

how is neuroblastoma diagnosed? how do they manifest?

A
  1. homogenously stained regions (HSRs) or double minutes on a karyotype 2. arise in adrenal glands or kidney, present as abdominal masses