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66 terms

Unit 8 Neoplasia

STUDY
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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)
Ratio of cells produced to cell death in Normal cells
1:1
Cell death = cell proliferation
Growth factors
Interfere @ G1 of cell cycle & guide stable cells to enter the cell cycle & divide
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
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.
Anchorage dependence in normal cells:
Usually anchored to extracellular matrix by anchoring proteins; if not properly anchored, cells destroyed by apoptosis (suicide).
What is the central property of cancer cells
Defiance of social controls on cell division
Skin cancer
Risk: sunlight (UV), contact carcinogens
Lung cancer
Risk: inhalation carcinogens (cigarette smoke)
Thyroid cancer
Risk: radiation
Lymphoma (cancer of the thymus, lymph nodes)
Risk: viruses
Liver cancer
Risk: Liver carcinogen (mildewed grain)
GI cancer
Risk: dietary carcinogen (smoked foods)
Bladder cancer
Risk: excretory carcinogens (industrial chemicals)
Cervical cancer
Risk: HPV (human papillovirus)
2 types of genes involved in endogenous causes of cancer
Proto-oncogens & tumor suppression genes
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.
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
Oncogenes
Mutated proto-oncogenes that direct formation of proteins for cell division that produce abnormal proteins OR too many proteins.
LIST 4 mechanisms to produce abnormal proteins
Point mutation; Amplification, Chromosome rearrangement, Viral insertion
Point mutation
forms oncogenic proteins
amplificaiton
overproduced normal proteins
chromosome rearrangement
overproduced or oncogenic protein
viral insertion
produce oncogenic protein
What is Carcinogenesis
development of cancer
LIST the 3 steps of oncogenesis
Initiation, promotion, progression
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.
Initiation phase
Normal cell experiences DNA damage and cell mutation under carcinogenic agent (chemical, radiation, viruses)
Promotion stage
Mutated cells are stimulated by oncogenes (activated by promoter agent) to divide
Progression
Tumor cells compete with one another and develop more mutations which make them more aggressive. Malignant tumor forms
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.
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
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
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
2 types of classification schemes for cancer types
1. Tissue & cell type of origin
2. Invasiveness --benign or malignant
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
Benign vs malignancy: Growth
B(slow & expansive), M(fast, invasive)
Benign vs malignancy: Metastatis
B(no), M(yes)
Benign vs malignancy: External surface
B(smooth), M(irregular)
Benign vs malignancy: Capsule
B(yes), M(no)
Benign vs malignancy: Necrosis
B(no), M(yes)
Benign vs malignancy: Hemorrhage
B(no), M(yes)
Benign vs malignancy: Architecture
B(resembles normal tissue of origin), M(Does not resemble normal tissue of origin)
Benign vs malignancy: Cells
B(well differentiated), M(poorly differentiated)
Benign vs malignancy: Mitosis
B(few), M(many, irregular)
LIST 3 routes of metastasis
1. circulation
2. lymphatics
3. seeding through body cavities
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
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
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.
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
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
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
Crushing's syndrome
Paraneoplastic disorder: cortisol from small-cell carcinoma of the lung
Hypercalcemia
Paraneoplastic disorder: parathyroid hormone squamous cell carcinoma of the lung
Polycythemia
Paraneoplastic disorder: erythropoietin from renal cell carcinoma
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
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
Tumor Grading
Grade 1: well-differentiated
Grade 2: moderately differentiated
Grade 3: poorly differentiated
Tumor Staging
based on tumor size, invasiveness and spread
Tumor markers
antigens that indicate the presence of tumors
Carcinoembryonic antigen (CEA)
marker for adenocarcinoma of the colon
Alpha-fetoprotein
marker for hepatocellular carcinoma & certain germ cell tumors that contain yolk sac components. Tumor in ovary or testes. Need further testing
Prostat-specific antigen (PSA)
marker for prostate cancer. Normally present in blood in small amounts
Immune response to tumors
Natural killer cells, macrophages, cytotoxic T cells, B lymphocytes, neutrophils
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)
What abilities would a transformed cell need to metastasize?
Aggressiveness/competitive; abnormal digestive enzyme production; ability to survive in a new environment