Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

General Pathology > Exam #2: Neoplasia IV > Flashcards

Exam #2: Neoplasia IV Flashcards

1
Q

What is dysplasia? What are the characteristics of dysplasia?

A

Dysplasia refers to disordered growth in epithelial cells that includes:

1) Loss of uniformity of individual cells
2) Loss of architectural orientation

*****This is a precursor to cancer, but does NOT invariably progress to cancer

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

Describe the spectrum of neoplasia in the cervix.

A 
CIN1 
CIN2 
CIN3 
CIS 
Invasive carcinoma

CIN is defined by the epithelium occupied by immature cells i.e. undifferentiated

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

What is CIN1?

A
  • 1/3 of the full-thickness of the cervical epithelium from the basement membrane contains immature cells
  • This is also called mild dysplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the definition of CIN2?

A
  • 1/3 - 2/3 of the full-thickness of the cervical epithelium from the basement membrane contains immature cells
  • This is also called moderate dysplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the definition of CIN3?

A
  • > 2/3 of the full-thickness of the cervical epithelium from the basement membrane contains immature cells
  • This is also called severe dysplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the definition of CIS?

A

Carcinoma in situ refers to full thickness of the cervical epithelium containing immature cells

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

What is the difference between carcinoma in situ and invasive carcinoma?

A

CIS= full-thickness WITHOUT breach of the basement membrane

Invasive carcinoma= invasion of the basement membrane

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

What can oral hairy leukoplakia transform into?

A

Squamous cell carcinoma

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

What can Barett’s esophagus transform into?

A

Adenocarcinoma of the esophagus

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

Describe the different stages of GERD, Barrett’s Esophagus, and Adenocarcinoma?

A

1) Esophagitis i.e. inflammation of the esophagus
2) Barrett’s Esophagus (metaplasia–columnar epithelium)
3) Dysplasia
4) Carcinoma

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

What can chronic atrophic gastritis lead to? What about chronic ulcerative colitis?

A
  • Gastric adenocarcinoma
  • Adenocarcinoma of the colon

*Note that only ulcerative colitis transforms to cancer, Chron’s Disease DOES NOT

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

What cancerous progression can occur following Hepatitis B or C infection?

A

1) Hepatitis B or C
2) Macronodular cirrhosis
3) Hepatocellular carcinoma

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

What can be the result of simple/complex hyperplasia of the endometrium?

A

Endometrial adenocarcinoma

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

What can solar keratosis of skin lead to?

A

Skin cancer (usually squamous cell carcinoma)

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

What is the definition of a tumor?

A

Monoclonal expansion of a mutated cell

*****Teratomar still follows this rules; originally from one cell that immediately goes to three different lineages.

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

What is carcinogenesis? What does carcinogenesis lead to?

A

Carcinogenesis is non-lethal genetic damage that leads to:

1) Inherited germline mutations
2) Acquired mutations

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

What are the three outcomes of genetic mutations that are carcinogenic?

A

1) Activation of growth promoting genes i.e. “proto-oncogenes”
2) Inactivation of tumor suppressor genes i.e. “anti-oncogenes”
3) Alteration in genes that regulate apoptosis

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

What is heterogeneity?

A

Heterogeneity is the process by which new subclones arise from the descendants of the original transformed cell by multiple mutations

  • Remember, a tumor cell comes from one cell i.e. “monoclonal”
  • This cell divides and leads to diverging cellular lineages with different adaptations and characteristics

Thus, in a tumor, there are a number of different cells with different characteristics i.e. the tumor is “heterogenous”

19
Q

What are the seven essential alterations for malignant transformation?

A

1) Self-sufficiency in growth signals
2) Insensitivity to growth-inhibitory signals
3) Evasion of apoptosis
4) Limitless replicative potential
5) Sustained angiogenesis
6) Ability to invade and metastasize
7) Defects in DNA repair

**Note that not ALL of these are needed for malignant transformation

20
Q

What are the four 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

**MircoRNA is a new class of regulatory molecules

21
Q

What is the difference between a proto-oncogene & an oncogene?

A

Proto-oncogenes are NORMAL

Oncogenes are proto-oncogenes that have undergone mutations to promote “autonomous” cell growth that is devoid of regulatory elements

22
Q

How many alleles are there of tumor suppressor genes? What is the clinical implication of heterzygous vs. homozygous mutations?

A

2x

  • Heterozygous mutations do NOT result in cancer (increased risk)
  • Homozygous mutations result in cancer
23
Q

What are the different classes of oncogenes?

A

1) Growth factors synthesis
2) Growth factor receptor synthesis
3) Signal transduction
4) Nuclear transcription
5) Cell cycle regulators

24
Q

What are the mechanisms that can activation of an oncogene?

A

1) Point mutation
2) Translocation
3) Amplification

25
Q

What are the two potential results of the activation of oncogenes?

A
  • Normal protein is overproduced

- Mutant protein is produced and has an aberrant function

26
Q

What are ERBB2 (HER-2/NEU) mutations associated with?

A
  • ERBB2 is the receptor for EGF
  • Mutation results in amplification
  • Implicated in breast & ovarian cancer
27
Q

What are RET mutations associated with?

A
  • RET= Receptor for Neurotrophic Factors
  • Point mutation
  • Multiple endocrine neoplasia types 2a & 2b (MEN 2A & MEN 2B
28
Q

What are KRAS mutations associated with?

A
  • KRAS= GTP-binding protein
  • Point mutation
  • Pancreatic, colon, and lung cancer
29
Q

What are ABL mutations associated with?

A
  • ABL= Non-receptor tyrosine kinase
  • Translocation
  • CML & ALL i.e. Chronic myeloid leukemia & Acute lymphoblastic leukemia
30
Q

What are BRAF mutations associated with?

A
  • Ras signal transduction pathway
  • Point mutation
  • Melanoma
31
Q

What are B-Catenin mutations associated with?

A
  • WNT signal transduciton

Liver cancer:
- Hepatoblastomas & -hepatocellular carcinoma

32
Q

What are C-myc mutations associated with?

A
  • Transcriptional activator
  • Translocation
  • Burkitt’s Lymphoma
33
Q

What are N-myc mutations associated with?

A
  • Transcriptional activator
  • Amplification
  • Neuroblastoma & small cell cancer of the lung
34
Q

What are Cyclin D mutations associated with?

A
  • Cell cycle regulator
  • Translocation= Mantle cell lymphoma
  • Amplification= Breast & esophageal cancer
35
Q

What is MEN-2a or MEN-2b?

A
  • Multiple endocrine neoplasia types 2a & 2b
  • Caused by RET mutations
  • Symptoms include the familial occurrence of a combination of:
    1) Medullary thyroid carcinoma
    2) Bilateral pheochromocytoma
    3) Hyperparathyroidism due to hyperplasia or tumor
36
Q

Outline the chromosomal translocation that occurs in CML.

A
  • “Philadephila chromosome”
  • c-abl proto-oncogene on chromosome 9 is translocated to bcr, and oncogene on chromosome 22 i.e. 9x22
  • Resulting fusion gene encodes for a protein with increased tyrosine kinase activity
37
Q

What is the treatment for CML? What is the mechanism of action of the drug?

A

Imatinib mesylate (Gleevec) inhibits tyrosine kinase

38
Q

Outline the translocation that occurs in Burkitt Lymphoma

A
  • Translocation of c-myc proto-oncogene from chromosome 8 to a site adjacent to the Ig heavy chain locus on chromosome 14 i.e. 8x14
39
Q

What is the difference between endemc, sporadic, and HIV-associated Burkitt’s Lymphoma?

A

Endemic/ African= patients present with a jaw mass
Sporadic= patients present with an abdominal mass
HIV-associated

40
Q

What is the mechanism of B-cell follicular lymphoma?

A

Translocation of 14x18 leads to overexpression of BCL-2

  • BCL-2 produces a gene product that prevents the leakage of cytochrome c
  • This prevents the apoptosis of B-lymphocytes
41
Q

What cancer is caused exclusively by the evasion of apoptosis?

A

B-cell follicular lymphoma

42
Q

What is neuroblastoma?

A

Aggressive childhood tumor with marked N-MYC amplicfication

43
Q

Outline the pathogenesis of neuroblastoma.

A

Amplification of N-myc, which is a transcriptional activator

44
Q

How does neuroblastoma commonly present in children?

A

Abdominal masses

General Pathology (33 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions