Exam #2: Neoplasia IV Flashcards
What is dysplasia? What are the characteristics of dysplasia?
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
Describe the spectrum of neoplasia in the cervix.
CIN1 CIN2 CIN3 CIS Invasive carcinoma
CIN is defined by the epithelium occupied by immature cells i.e. undifferentiated
What is CIN1?
- 1/3 of the full-thickness of the cervical epithelium from the basement membrane contains immature cells
- This is also called mild dysplasia
What is the definition of CIN2?
- 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
What is the definition of CIN3?
- > 2/3 of the full-thickness of the cervical epithelium from the basement membrane contains immature cells
- This is also called severe dysplasia
What is the definition of CIS?
Carcinoma in situ refers to full thickness of the cervical epithelium containing immature cells
What is the difference between carcinoma in situ and invasive carcinoma?
CIS= full-thickness WITHOUT breach of the basement membrane
Invasive carcinoma= invasion of the basement membrane
What can oral hairy leukoplakia transform into?
Squamous cell carcinoma
What can Barett’s esophagus transform into?
Adenocarcinoma of the esophagus
Describe the different stages of GERD, Barrett’s Esophagus, and Adenocarcinoma?
1) Esophagitis i.e. inflammation of the esophagus
2) Barrett’s Esophagus (metaplasia–columnar epithelium)
3) Dysplasia
4) Carcinoma
What can chronic atrophic gastritis lead to? What about chronic ulcerative colitis?
- Gastric adenocarcinoma
- Adenocarcinoma of the colon
*Note that only ulcerative colitis transforms to cancer, Chron’s Disease DOES NOT
What cancerous progression can occur following Hepatitis B or C infection?
1) Hepatitis B or C
2) Macronodular cirrhosis
3) Hepatocellular carcinoma
What can be the result of simple/complex hyperplasia of the endometrium?
Endometrial adenocarcinoma
What can solar keratosis of skin lead to?
Skin cancer (usually squamous cell carcinoma)
What is the definition of a tumor?
Monoclonal expansion of a mutated cell
*****Teratomar still follows this rules; originally from one cell that immediately goes to three different lineages.
What is carcinogenesis? What does carcinogenesis lead to?
Carcinogenesis is non-lethal genetic damage that leads to:
1) Inherited germline mutations
2) Acquired mutations
What are the three outcomes of genetic mutations that are carcinogenic?
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
What is heterogeneity?
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”
What are the seven essential alterations for malignant transformation?
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
What are the four classes of normal regulatory genes?
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
What is the difference between a proto-oncogene & an oncogene?
Proto-oncogenes are NORMAL
Oncogenes are proto-oncogenes that have undergone mutations to promote “autonomous” cell growth that is devoid of regulatory elements
How many alleles are there of tumor suppressor genes? What is the clinical implication of heterzygous vs. homozygous mutations?
2x
- Heterozygous mutations do NOT result in cancer (increased risk)
- Homozygous mutations result in cancer
What are the different classes of oncogenes?
1) Growth factors synthesis
2) Growth factor receptor synthesis
3) Signal transduction
4) Nuclear transcription
5) Cell cycle regulators
What are the mechanisms that can activation of an oncogene?
1) Point mutation
2) Translocation
3) Amplification
