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Patho Unit6 Neoplasia Cheat Sheet (DRAFT) by

Personal exam revision use hehe

This is a draft cheat sheet. It is a work in progress and is not finished yet.


Mesenc­hymal tumors
Epithelial tumors

Epidem­iology (Acquired predis­posing condit­ions)

1. Chronic inflam­mation
2. Immuno­def­iciency states
3. Precursor lesion

Clinical aspects

1. Local effects of tumor encroa­chment of tissues/ organs
2a. Functional activity e.g. Hormone synthesis
2b. Parane­opl­astic syndromes -> Ectopic hormone secretion
3. Bleeding & infections when tumor ulcerates thru adjacent surface
4. Rupture/ infarction
5. Cachexia (Weakness, e.g. weight loss)

Molecular basis of cancer

Nonlethal genetic damage
Hallmark: Genetic alteration
Cancer genes (Target of genetic damage)
1. Oncogene (Mutated gene)
- Mutation from proto-­onc­ogenes
2. Tumor suppressor genes
- Prevent uncont­rolled growth
3. Apopto­sis­-re­gul­ating gene
- Overex­pressed in cancer cell-> Protect against apoptosis
4. Regulate intera­ctions between tumor and host cells
- Change recogn­ition of tumor by host immune system

2. Insens­itivity to Tumor suppressor signals

Retino­bla­stoma Gene
- Active hypoph­osp­hor­ylated state: Halts cell cycle
- Inactive hyperp­hos­pho­rylated state
-Hetero­zyg­osity: X Affect cell function
- Both to be inacti­vated to affect function
1. Cell cycle arrest
2. DNA repair
3. Apoptosis

4. Evasion of cell death

- Overex­pre­ssion of BCL-2 protein -> Long life

8. Evasion of immune survei­llance

Host defence against tumor -- Tumor immune
Tumor antigens
Antitumor effectors
- Overex­pressed cellular proteins, Oncogenic viral products, Differ­ent­iation antigens
- CD8+
- Oncogenic viral products
- NK lympho­cytes
- Differ­ent­iation antigens
- Macrop­hages
- Humoral immunity
Immune evasion
- Immuno­sup­pre­ssion
- Selective outgrowth
- Antigen masking
- X MHC expression
- Apoptosis of CD8+
- X Costim­ulation

10. Tumor-­pro­moting inflam­mation

- Intera­ction between inflam­matory cell& tumor
1. Prolif­era­tio­n-p­rom­oting factor release
2. Growth suppressor removal
3. Cell death resistance
4. Angiog­enesis
5. Invasion & Metastasis
6. Immune evasion

Benign Malignant differ­ent­iation

Differ­ent­iation & anaplasia
1. Well differ­ent­iated
1. Well to undiff­ere­ntiated (Anapl­asia: Functi­ona­l& structural differ­ent­iation loss)
- Dysplasia (Disor­dered growth)
- Carcinoma in situ (Non-i­nvasive malignant tumor)
Rate of growth
- Correlates w./ level of differ­ent­iation
2. Progre­ssive & slow
2. Erratic (Unpre­dic­table)
Local invasion
3. No, expansion w./ clear boundaries
4. Yes, infiltrate & destroy
(1)Seeding of body cavities (2) Lymphatic spread (3) Hemato­genous spread
4. Absent
4. Frequently present

1. Self-s­uff­iciency in growth signals

-Normal genes, promote prolif­eration
-Mutant version, function anonym­ously w./o growth­-pr­omoting signals
-Proteins encoded
Self-s­uff­icient in:
1. Growth factors & receptors
3. Transc­ription factors
2. Signal transd­uction proteins
4. Cyclins & CDKs

3. Altered cellular metabolism

Warbug effect
- Aerobic situation: Distinct form of cellular metabolism
- High levels of glucose uptake
- Increased conversion of glucose to lactose via glycoyitic pathway

5. Limitless replic­ative potential: Telomerase

- Telomerase shorten with each cell division
- Cancer cell have enzyme that regenerate telomerase

6. Sustained angiog­enesis

- Controlled by balance between angiog­enesis promoter (VEGF) and inhibitors (bFGF)

7. Invasion & Metastasis

- Invasion of extrac­ellular matrix
a. Loosening of intrac­ellular junctions
b. Degrad­ation
c. Attatc­hment
d. Migration
- Embolus: Evade WBC killing

9. Genetic instab­ility

- Both copies of DNA repair proteins are lost
1. Hereditary Nonpol­yposis Cancer Syndrome
2. BRCA-1 & BRCA-2 (80% familial breast cancer, not sporad­ic-­ass­oci­ated)

Carcin­ogenic Agents

1. Chemical Carcin­oge­nesis
- Carcinogen exposure -> permanent DNA
- Promoter induce tumor in initiated cell (Nontu­mor­igenic)
- Promoting agent enhance prolif­eration & results in cancer
2. Radiation Carcin­oge­nesis
- UV rays (UVB, 280-320nm)
- Ionizing radiation (X-ray, gamma ray, particles)
3. Oncogenic DNA viruses
1. Papill­oma­viruses (HPV)
2. Epstei­n-Barr virus (EBV)
3. Hep B virus (HBV)
4. Kaposi sacroma herpes virus (KSHV)