1.
2 types of classification schemes for cancer types: 1. Tissue & cell type of origin
2. Invasiveness --benign or malignant
2.
2 types of genes involved in endogenous causes of cancer: Proto-oncogens & tumor suppression genes
3.
Alpha-fetoprotein: marker for hepatocellular carcinoma & certain germ cell tumors that contain yolk sac components. Tumor in ovary or testes. Need further testing
4.
amplificaiton: overproduced normal proteins
5.
Anchorage dependence in normal cells:: Usually anchored to extracellular matrix by anchoring proteins; if not properly anchored, cells destroyed by apoptosis (suicide).
6.
At which steps of oncogenesis must mutagens be present. WHY?: Must be present at both initiation phase and promotion phase. Otherwise, tumour suppression cells will destroy mutated cells if present at initiation phase.
7.
Benign vs malignancy: Architecture: B(resembles normal tissue of origin), M(Does not resemble normal tissue of origin)
8.
Benign vs malignancy: Capsule: B(yes), M(no)
9.
Benign vs malignancy: Cells: B(well differentiated), M(poorly differentiated)
10.
Benign vs malignancy: External surface: B(smooth), M(irregular)
11.
Benign vs malignancy: Growth: B(slow & expansive), M(fast, invasive)
12.
Benign vs malignancy: Hemorrhage: B(no), M(yes)
13.
Benign vs malignancy: Metastatis: B(no), M(yes)
14.
Benign vs malignancy: Mitosis: B(few), M(many, irregular)
15.
Benign vs malignancy: Necrosis: B(no), M(yes)
16.
Bladder cancer: Risk: excretory carcinogens (industrial chemicals)
17.
Cancer cachexia syndrome (generalized effects of cancer): weight loss, muscle wasting, weakness, anorexia (liver dysfunction decreases appetite), Anemia (loss of blood due to bleeding, blood clots--deep vein thrombosis
18.
Carcinoembryonic antigen (CEA): marker for adenocarcinoma of the colon
19.
Cervical cancer: Risk: HPV (human papillovirus)
20.
Change in cell surface in cancer: 1. Surface glycoproteins & glycolipids are lost or modified = decreased communication between cells
2. Change in anchoring & gap junctions proteins = exhibit anchorage independence & enzymes altered on cell surface and in cytoplasm so cells might digest through basement membrane and leak into blood vessels
21.
Characteristics of tumour cells. Name 5: 1. Local hyperplasia
2. Loss of normal cell arrangement
3. Pleimorphism: variation of cells in size and shape
4. Increase in nuclear size and total DNA
5. Increase in mitotic activity
22.
chromosome rearrangement: overproduced or oncogenic protein
23.
Concept map of metastasis: primary malignant neoplasm, release of angiogenesis factor & vascularization, secretion of proteases and collagenase, lysis of basement membrane, invasion into lymphatics & blood vessels (venules & capillaries), transport/interaction with other blood elements --> escape from vessel (extravasation), adherence of tumour cells, establishment of microenvironment & growth into metastasis, release of angiogenesis factor and vascularization
24.
Crushing's syndrome: Paraneoplastic disorder: cortisol from small-cell carcinoma of the lung
25.
Cyclins: Proteins that monitor cell cycle by ensuring enough proteins are produced to separate the chromosomes and checking DNA being correctly replicated and measuring whether cell is big enough to divide
26.
Describe the 3 steps of metastasis: 1. transformed cells loosen adhesion to original neighbours & escape from original tissue
2. Burrow through other tissues basement membrane to reach a blood vessel or lymphatic vessel
3. Exit from circulation elsewhere and surviv, proliferate in a new environment
27.
Difference between stem cells and fully differentiated cells: Stem cells are not differentiated and divide very rapidly. Differentiated cells divide slowly, or not at all; also have specialized functions.
28.
Factors that determine clinical features of tumors: Expansive or invasive / Location /Histologic grade/clinical stage / immune status of the host / sensitivity of the tumor to therapy
29.
GI cancer: Risk: dietary carcinogen (smoked foods)
30.
Growth factors: Interfere @ G1 of cell cycle & guide stable cells to enter the cell cycle & divide
31.
How does tissue tropism affect metastasis?: tumour cells metastasize to preferred size due to presence of hormones/growth factors in the target tissue, tissue-selective homing receptors, or cells are physically trapped in the nearest narrow capillary beds.
32.
Hypercalcemia: Paraneoplastic disorder: parathyroid hormone squamous cell carcinoma of the lung
33.
Immune response to tumors: Natural killer cells, macrophages, cytotoxic T cells, B lymphocytes, neutrophils
34.
Initiation phase: Normal cell experiences DNA damage and cell mutation under carcinogenic agent (chemical, radiation, viruses)
35.
Labile cells: (Normal cells) cells in the mitotic phase of the cell cycle divide and form stable cells (dividable formed in G1) and permanent cells (non-dividable, e.g., muscle/neurons)
36.
LIST 3 routes of metastasis: 1. circulation
2. lymphatics
3. seeding through body cavities
37.
LIST 4 mechanisms to produce abnormal proteins: Point mutation; Amplification, Chromosome rearrangement, Viral insertion
38.
List 5 local effects of tumour growth: 1. Bleeding (broken blood vessels)
2. Compression of blood vessels
3. Compression of lymph vessels
4. Compression of hollow organs
5. Compression of nerves
39.
LIST the 3 steps of oncogenesis: Initiation, promotion, progression
40.
Liver cancer: Risk: Liver carcinogen (mildewed grain)
41.
Lung cancer: Risk: inhalation carcinogens (cigarette smoke)
42.
Lymphoma (cancer of the thymus, lymph nodes): Risk: viruses
43.
nomenclature:
1-benign
2-malignant
3. lymphoid tissue
4. blood cells
5. glial cells
6. embryonic cells
7. adrenal medulla or neural cells)
8. liver
9. kidney
10. epithelial cells
11. connective tissue/muscle cells: 1. -oma
2. -carcinoma, -sarcoma
3. lymphoma
4. leukemia
5. glioma
6. blastoma
7. neuroblastoma
8. hepatoblastoma
9. nephroblastoma
10. carcinoma
11. sarcoma
44.
Oncogenes: Mutated proto-oncogenes that direct formation of proteins for cell division that produce abnormal proteins OR too many proteins.
45.
Paraneoplastic disorders: consequences of the presence of tumour , but due to hormones & cytokines secreted by tumour cells or immune cells. Occurs when tumour cells secret hormones typically produced elsewhere
46.
Point mutation: forms oncogenic proteins
47.
Polycythemia: Paraneoplastic disorder: erythropoietin from renal cell carcinoma
48.
Progression: Tumor cells compete with one another and develop more mutations which make them more aggressive. Malignant tumor forms
49.
Promotion stage: Mutated cells are stimulated by oncogenes (activated by promoter agent) to divide
50.
Properties of tumour cells. Name 5: 1. Proliferate without body signals
2. Ignore signals to stop dividing
3. Do not mature to perform normal tissue function
4. Do not undergo apoptosis
5. Exhibit anchorage independence-->metastasis follows
51.
Prostat-specific antigen (PSA): marker for prostate cancer. Normally present in blood in small amounts
52.
Proto-oncogens contribution to cancer development: Usually this protein directs formation of normal proteins used in cell division. Includes growth factors, growth factor receptors, & other proteins in cell growth. Mutations to this gene results in overactivity of genes that control growth.
53.
Ratio of cells produced to cell death in Normal cells: 1:1
Cell death = cell proliferation
54.
Skin cancer: Risk: sunlight (UV), contact carcinogens
55.
Thyroid cancer: Risk: radiation
56.
Tumor Grading: Grade 1: well-differentiated
Grade 2: moderately differentiated
Grade 3: poorly differentiated
57.
Tumor markers: antigens that indicate the presence of tumors
58.
Tumor Staging: based on tumor size, invasiveness and spread
59.
Tumour suppression genes contribution to cancer development: Usually this protein stops divisions of mutated cells and keeps most mutations from developing into cancer. Inactivation of these genes result in no suppression of possible tumour cells
60.
viral insertion: produce oncogenic protein
61.
What abilities would a transformed cell need to metastasize?: Aggressiveness/competitive; abnormal digestive enzyme production; ability to survive in a new environment
62.
What abilities would a transformed cell need to survive in a tumor?: Production of angiogenic factor (FGF) to bring in more nutrients; Ignore social controls; Ability to divide quickly; camouflage (so it can evade immune system)
63.
What is Carcinogenesis: development of cancer
64.
What is de-differentiation?: process of differentiated cells becoming less mature or specialized. Cancer cells' daughter cells retain an ability to carry on dividing indefinitely.
65.
What is the central property of cancer cells: Defiance of social controls on cell division
66.
What is tumour angiogenesis: Tumour cells release tumour angiogenic factors (FGF) that induce the growth of endothelial cells to form blood vessels and bring O2 and nutrients
