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247 Cards in this Set
- Front
- Back
Five phases of the cell cycle
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G0, G1, G2, M, S
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The first gap of the cell cycle.
Where RNA and protein synthesis occurs. The end of this phase marks a critical event that occurs that commits the cell to continue through all phases of the gap cycle. |
G1
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The resting stage. Cells can leave G1 and enter this stage.
Time spent in this stage varies and not all cells enter this stage. |
G0
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DNA synthesis occurs here.
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S
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Premitotic phase.
Cell engages in RNA and protein synthesis again. |
G2
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Mitosis where cell divides
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M
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Cell that cannot enter cell cycle. Permanently differentiated.
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Permanent cells (Amitotic Cells)
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Examples of permanent cells
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Neurons, striated muscle cells (skeletal and cardiac muscle)
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Cells usually in G0 (resting) phase.
Cells can still divide, but can only give rise to daughter cells of the same cell type. Cellular injury stimulates to enter G1 phase. |
Stable Cells
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Examples of Stable Cells
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Hormones (estrogen), Growth factors (epidermal derived growth factor), Progenitor blood cells, skin cells, liver cells, smooth muscle, and most other cells.
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Cells constantly making new cells.
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Labile Cells
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Examples of labile cells
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Stem cells, cancer or tumor cells
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The act or process in development in which unspecialized cells or tissues acquire more specialized characteristics.
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Cell differentiation
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The reproduction or multiplication of similar forms, especially cells.
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Proliferation
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Tissue name + -oma
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Benign tumor
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Any cancer that arises from epithelial cells (90%)
Based on appearance Based on putative cell of origin |
Carcinoma
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A cancer that arises from mesenchymal tissue, the connective or supportive tissue (bone, cartilage, fat, muscle, blood vessels)
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Sarcoma
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Adenoma
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Benign epithelial neoplasm of glandular tissue
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Osteoma
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Benign bone tumor
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Chondoma
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Benign cartilage tumor
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Lipoma
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Benign adipose tumor
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Melanoma
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Skin cancer
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Adenocarcinoma
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Malignancies that originate from glandlike structures
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Fibrosarcoma
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Cancer of fibrous tissue
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Chondrosarcoma
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Malignant tumor composed of chondrocytes
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Myeloma
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Cancer of plasma cells
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Lymphoma
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Cancer of the lymphocytes
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Hepatoma
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Liver cancer
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Osteosarcoma
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Malignant Bone Tumor
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Liposarcoma
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Malignant Adipose Tumor
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Angiosarcoma
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Cancer of the vessel walls
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Leiomyosarcoma
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Smooth muscle cancer
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A variety of cancer that originates in lymphocytes, originate in lymph nodes
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Lymphoma
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A cancer of the blood or bone marrow characterized by an abnormal proliferation of blood cells, usually WBCs
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Leukemia
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Well-differentiated cells that resemble cells in the tissue of origin
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Benign Tumor Cells
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Undifferentiated cells, do not resemble cells in the tissue of origin
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Malignant Tumor Cells
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Slow growth
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Benign Tumor Cells
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Expansion and not invasion, usually encapsulated
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Benign Tumor Cells
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Grows at periphery and invades
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Malignant Tumor Cells
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Involves metastasis
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Malignant Tumor Cells (via blood and lymph)
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Small size
Slow growing Encapsulated or well demacrated borders Well differentiated Non-invasive Never metastasize |
Benign Tumor Cell
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Larger in size
Rapid growth Necrosis and hemorrhage common Poorly demacated borders Anaplastic Vary in size and shape (Pleomorphism) Increased nuclear/cytoplasmic ratios Nuclear hyperchromasia (dark) and prominent nucleoli High mitotic activity Invasive growth Metastasizes |
Malignant Tumor Cells
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A multistep process
Requires the accumulation of multiple genetic changes (inherited or aquired) |
Cancer
|
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Cancer mutations (genes)
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Growth promoting
Growth inhibiting Apoptosis regulating |
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Normal cellular genes involved with growth and cellular differentiation
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Protooncogenes (growth promoting oncogenes)
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Mechanisms of oncogene activation
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Point mutations
Chromosomal translocations Gene amplification Insertional mutagenesis |
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__________ oncogenes lack regulatory control and are _____________, resulting in ______________ ____________ ___________.
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Activated;
overexpressed; unregulated cellular proliferation. |
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A multistep process
Requires the accumulation of multiple genetic changes (inherited or aquired) |
Cancer
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Encode proteins that regulate and supress cell proliferation by inhibiting progression of the cell through the cell cycle
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Tumor suppressor genes
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Cancer mutations (genes)
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Growth promoting
Growth inhibiting Apoptosis regulating |
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Mechanisms of tumor suppressor genes
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p53 prevents a cell with damaged DNA from entering S-phase
Rb prevents the cell from entering S-phase until the appropriate growth signals are present |
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Normal cellular genes involved with growth and cellular differentiation
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Protooncogenes (growth promoting oncogenes)
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Prevents a cell with damaged DNA from entering S-phase
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p53
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Mechanisms of oncogene activation
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Point mutations
Chromosomal translocations Gene amplification Insertional mutagenesis |
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Prevents the cell from entering S-phase until the appropriate growth signals are present
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Rb
|
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__________ oncogenes lack regulatory control and are _____________, resulting in ______________ ____________ ___________.
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Activated;
overexpressed; unregulated cellular proliferation. |
|
Both genes must be inactivated for oncogenesis
|
Two hit hypothesis
|
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Encode proteins that regulate and supress cell proliferation by inhibiting progression of the cell through the cell cycle
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Tumor suppressor genes
|
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Mechanisms of tumor suppressor genes
|
p53 prevents a cell with damaged DNA from entering S-phase
Rb prevents the cell from entering S-phase until the appropriate growth signals are present |
|
Prevents a cell with damaged DNA from entering S-phase
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p53
|
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Prevents the cell from entering S-phase until the appropriate growth signals are present
|
Rb
|
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Both genes must be inactivated for oncogenesis
|
Two hit hypothesis
|
|
A multistep process
Requires the accumulation of multiple genetic changes (inherited or aquired) |
Cancer
|
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Cancer mutations (genes)
|
Growth promoting
Growth inhibiting Apoptosis regulating |
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Normal cellular genes involved with growth and cellular differentiation
|
Protooncogenes (growth promoting oncogenes)
|
|
Mechanisms of oncogene activation
|
Point mutations
Chromosomal translocations Gene amplification Insertional mutagenesis |
|
__________ oncogenes lack regulatory control and are _____________, resulting in ______________ ____________ ___________.
|
Activated;
overexpressed; unregulated cellular proliferation. |
|
Encode proteins that regulate and supress cell proliferation by inhibiting progression of the cell through the cell cycle
|
Tumor suppressor genes
|
|
Mechanisms of tumor suppressor genes
|
p53 prevents a cell with damaged DNA from entering S-phase
Rb prevents the cell from entering S-phase until the appropriate growth signals are present |
|
Prevents a cell with damaged DNA from entering S-phase
|
p53
|
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Prevents the cell from entering S-phase until the appropriate growth signals are present
|
Rb
|
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Both genes must be inactivated for oncogenesis
|
Two hit hypothesis
|
|
A multistep process
Requires the accumulation of multiple genetic changes (inherited or aquired) |
Cancer
|
|
Cancer mutations (genes)
|
Growth promoting
Growth inhibiting Apoptosis regulating |
|
Normal cellular genes involved with growth and cellular differentiation
|
Protooncogenes (growth promoting oncogenes)
|
|
Mechanisms of oncogene activation
|
Point mutations
Chromosomal translocations Gene amplification Insertional mutagenesis |
|
__________ oncogenes lack regulatory control and are _____________, resulting in ______________ ____________ ___________.
|
Activated;
overexpressed; unregulated cellular proliferation. |
|
Encode proteins that regulate and supress cell proliferation by inhibiting progression of the cell through the cell cycle
|
Tumor suppressor genes
|
|
Mechanisms of tumor suppressor genes
|
p53 prevents a cell with damaged DNA from entering S-phase
Rb prevents the cell from entering S-phase until the appropriate growth signals are present |
|
Prevents a cell with damaged DNA from entering S-phase
|
p53
|
|
Prevents the cell from entering S-phase until the appropriate growth signals are present
|
Rb
|
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Both genes must be inactivated for oncogenesis
|
Two hit hypothesis
|
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Inherited germ-line mutation
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First hit (two hit hypothesis)
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Acquired somatic mutation
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Second hit (two hit hypothesis)
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Germ-line mutation of Rb on chromosome 13
High rate of retinoblastoma and osteosarcoma |
Familial retinoblastoma
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Germ-line mutation of p53 on chromosome 17
High rate of many types of tumors |
La-Fraumeni syndrome
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Top 3 incidences of cancer (male)
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Prostate
Lung Colon & rectum |
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Top 3 incidences of cancer (female)
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Breast
Lung Colon & rectum |
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Top 3 mortalities of cancer (male)
|
Lung
Prostate Colon & rectum |
|
Top 3 mortalities of cancer (female)
|
Lung
Breast Colon & rectum |
|
Top 3 causes of death in U.S.
|
Heart disease
Cancer Cerebrovascular disease |
|
Stomach cancer
Japan or US? |
Japan
|
|
Breast cancer
US or Japan |
US
|
|
Liver hepatoma
Asia or US |
Asia (Hep B)
|
|
Prostate Cancer
African American or Caucasian |
African American
(higher androgen) |
|
Predispositions to cancer
|
Age
Heredity Acquired preneoplastic disorders |
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Rb gene mutation
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Familial retinoblastoma
|
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MEN gene mutation
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Multiple endocrine neoplasia => thyroid cancer
|
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Familial adenomatous polyps (FAP)
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Colon cancer
|
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Cervical dysplasia =>
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Cervical cancer
|
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Endometrial hyperplasia =>
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Endometrial carcinoma
|
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Cirrhosis =>
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Liver cancer
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Ulcerative colitis =>
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Colon cancer
|
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Chronic atrophic gastritis =>
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Gastric cancer
|
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Most common carcinogen
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Chemical carcinogens
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Multi-step process involving a sequence of mutation (initiation) followed by proliferation (promotion)
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Carcinogenesis
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Mutations that cause cancer directly or indirectly by modifying DNA
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Indicators
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Cause cellular proliferation of mutated (initiated) cells
Proliferation of a mutated cell may lead to accumulation of additional mutations |
Promoters
|
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Most common carcinogenic agent
|
Cigarette smoke
|
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Asbestos
Radiation Oncogenic bacteria and viruses |
Carcinogenic agents
|
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Ultraviolet radiation _____________ and ionizing radiation ____________ damage DNA.
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UVB sunlight; x-rays
|
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Helicobacter Pylori => Peptic Ulcer =>
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Gastric carcinoma
|
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Human T-cell leukemia virus (HTLV-1) =>
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Adult T-cell leukemia/lymphoma
|
|
DNA oncogenic viruses
|
Hep B
Epstein-Barr virus Human papilloma virus (HPV) Kaposi-sarcoma-associated herpesvirus (HHV8) |
|
Epstein-Barr virus =>
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Burkitt lymphoma (African)
B-cell lymphoma (Immunosuppressed patients) Nasopharyngeal carcinoma (S. China) |
|
Hep B virus =>
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Hepatocellular carcinoma
|
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Human papilloma virus (HPV) =>
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Cervical cancer
|
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Kaposi-sarcoma-associated herpesvirus (HH8V) =>
|
Kaposi sarcoma (skin cancer)
|
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bcl-2
|
Prevents apoptosis;
Overexpressed in follicular B-cell lymphomas |
|
Human T-cell leukemia virus (HTLV-1) =>
|
Adult T-cell leukemia/lymphoma
|
|
Genes promoting apoptosis
|
bax; bad; bcl-xS; bid; p53
|
|
DNA oncogenic viruses
|
Hep B
Epstein-Barr virus Human papilloma virus (HPV) Kaposi-sarcoma-associated herpesvirus (HHV8) |
|
p53
|
Promotes apoptosis in mutated cells by stimulating bax synthesis
|
|
Epstein-Barr virus =>
|
Burkitt lymphoma (African)
B-cell lymphoma (Immunosuppressed patients) Nasopharyngeal carcinoma (S. China) |
|
c-myc
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Causes Burkitt lymphoma;
Promotes cellular proliferation; With p53 leads to apoptosis; With bcl-2 inhibits apoptosis |
|
Hep B virus =>
|
Hepatocellular carcinoma
|
|
Human papilloma virus (HPV) =>
|
Cervical cancer
|
|
Kaposi-sarcoma-associated herpesvirus (HH8V) =>
|
Kaposi sarcoma (skin cancer)
|
|
bcl-2
|
Prevents apoptosis;
Overexpressed in follicular B-cell lymphomas |
|
Genes promoting apoptosis
|
bax; bad; bcl-xS; bid; p53
|
|
p53
|
Promotes apoptosis in mutated cells by stimulating bax synthesis
|
|
c-myc
|
Causes Burkitt lymphoma;
Promotes cellular proliferation; With p53 leads to apoptosis; With bcl-2 inhibits apoptosis |
|
Human T-cell leukemia virus (HTLV-1) =>
|
Adult T-cell leukemia/lymphoma
|
|
DNA oncogenic viruses
|
Hep B
Epstein-Barr virus Human papilloma virus (HPV) Kaposi-sarcoma-associated herpesvirus (HHV8) |
|
Epstein-Barr virus =>
|
Burkitt lymphoma (African)
B-cell lymphoma (Immunosuppressed patients) Nasopharyngeal carcinoma (S. China) |
|
Hep B virus =>
|
Hepatocellular carcinoma
|
|
Human papilloma virus (HPV) =>
|
Cervical cancer
|
|
Kaposi-sarcoma-associated herpesvirus (HH8V) =>
|
Kaposi sarcoma (skin cancer)
|
|
bcl-2
|
Prevents apoptosis;
Overexpressed in follicular B-cell lymphomas |
|
Genes promoting apoptosis
|
bax; bad; bcl-xS; bid; p53
|
|
p53
|
Promotes apoptosis in mutated cells by stimulating bax synthesis
|
|
c-myc
|
Causes Burkitt lymphoma;
Promotes cellular proliferation; With p53 leads to apoptosis; With bcl-2 inhibits apoptosis |
|
c-myc + p53 =
|
apoptosis
|
|
c-myc + bcl-2 =
|
inhibited apoptosis
|
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New growth, non-adaptive, uncoordinated, autonomous, proliferation and differentiation out of control, competitive and parasitic
|
Neoplasm
|
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Hallmark of malignant transformation
|
Anaplasia
|
|
Histologic estimate of the malignancy of a tumor (I-IV)
|
Grade of tumor
|
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Criteria of tumor grade
|
Degree of differentiation
Number of mitosis |
|
Clinical estimate of the extent of tumor spread
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Stage of tumor
|
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TNM staging system
|
T= Tumor size (0-4)
N= Node of involvement (0-3) M= Metastasis (0/1) |
|
Better predictor of tumor prognosis?
|
Staging
|
|
Key distinction between benign and malignant tumors
|
Capacity of malignant tumors to invade and metastasize (except basal cells of carcinoma do not metastasize)
|
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In situ
|
Original site
|
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Tx
|
Tumor removed
|
|
Use of tumor markers
|
Screening
Monitoring Detecting recurrance |
|
Common tumor marker
|
Prostate specific antigen (PSA)
|
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True or False;
Tumor markers, usually proteins can not tell if cells are cancerous or not and should not be used as the primary diagnostic tool. |
True
|
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The spread of cancer from its primary site to other places in the body
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Metastasis
|
|
Cancer cells use these enzymes to invade the basement membrane
|
Type IV collagenases. hydrolases, and protease
|
|
Transforming growth factors (TGF) that promote angiogenesis
|
a (alpha) and B (beta)
|
|
When cancer cells spread to form a new tumor, it is called a ___________, or __________ tumor.
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Secondary; Metastatic
|
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Types of Metastasis
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Lymphatic
Hematogenous Seeding |
|
Cancer cells break away from a primary tumor and penetrate into lymphatic vessels
|
Lymphatic Metastasis
|
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Cancer cells break away from a primary tumor and penetrate into blood vessels.
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Hematogenous Metastasis
|
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Malignant cells exfoliate and implant/invade tissue
|
Seeding Metastasis
|
|
Most common route of spread for epithelial carcinomas
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Lymphatic Metastasis
|
|
Most common sites for hematogenous metastatsis
|
Lung and brain
|
|
Certain tumors seed in particular organs:
Prostate cancer => Colon cancer => Stomach cancer => |
Bones
Liver Ovary in women (Krukenberg tumor) |
|
Local symptoms of cancer
|
Lumps or swelling
Hemorrhage Necrosis Pain Ulceration Jaundice (compression of surrounding tissues) |
|
Systems of metastasis
|
Enlarged lymph nodes
Cough Hemoptysis Hepatomegaly (enlarged liver) Bone pain Fracture of affected bones Neurological symptoms |
|
Systematic symptoms of cancer
|
Weightloss and cachexia
Paraneoplastic syndromes Fatigue Anorexia Low-grade fever Excessive sweating Anemia |
|
Factors (cytokines) released directly effect satiety centers in hypothalamus or indirectly by injuring tissues
|
Cachexia
|
|
Occur when a neoplasm elaborates a substance that results in an effect that is not directly related to growth, invasion, or metastasis
Most result from elaboration or hormone-like substances |
Paraneoplastic syndromes
|
|
PTH control Ca 2+ concentration =>
|
Too much Ca 2+ => Stone formation
|
|
ADH => decrease urination => H20 => dilute plasma =>
|
Decrease sodium
|
|
Insulin =>
|
Lowers blood sugar
|
|
Erthroprotein-like substance =>
|
Polycythemia
|
|
Cytotoxic drugs used to treat cancer
|
Chemotherapy
|
|
Chemotherapy drugs:
a. Alkylating agents b. Anti-metabolites c. Anti-tumor antibiotics .d. Plant alkaloids e. Topoisomerase inhibitors f. Monoclonal antibodies g. Anti-tumor agents |
a. Cyclophosphamide
b. Methotrexate, 5-fluorouracil c. Dactinomycin d. vinca alkaloids, Taxanes e. flouroquinolones f. Rituximab g. a-interferon, IL-2 |
|
Drugs that affect cell division or DNA synthesis and function in some way
|
Chemotherapy
|
|
Tamoxifen
|
Selective estrogen receptor modulator, reduces the risk of breast cancer
|
|
Finasteride
|
5-a reductase inhibitor, lowers risk of prostate cancer
|
|
Aspirin
|
Reduces the incidence of stomach, esophogeal, colorectal cancers
|
|
Types of cells mostly affected by anti-cancer drug
|
Bone marrow
Mucosal cells of GI tract Gonadal cells |
|
Cancer is a disorder of altered cell ___________ and ___________.
|
Differentiation; growth
|
|
The process of cell division results in cellular _________.
|
Proliferation
|
|
__________ is the process of specialization whereby new cells acquire the structure and function of the cells they replace.
|
Differentiation
|
|
Proteins called _________ control entry and progression of cells through the cell cycle.
|
Kinases
|
|
Kinases are enzymes that __________ proteins.
|
phosphorylate
|
|
Continually renewing cell populations rely on __________ cells of the same lineage that have not yet differentiated to the extent that they have lost their ability to divide.
|
progenitor
|
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__________ cells remain incompletely undifferentiated throughout life.
|
Stem
|
|
____________ stem cells are pluripotent cells derived from the inner cell mass of the blastocyst stage of the embryo.
|
Embryonic
|
|
The term _________ refers to an abnormal mass of tissue in which the regrowth exceeds and is uncoordinated with that of the normal tissues.
|
neoplasm
|
|
__________ do not usually cause death unless the location interferes with a vital organ's function.
|
Benign tumors
|
|
Malignant neoplasms are less well __________ and have the ability to break loose, enter the circulatory or lymphatic systems, and form secondary malignant tumors at other sites.
|
differentiated
|
|
Tumors usually are named by adding the suffix -____ to the parenchymal tissue type from which the growth originated.
|
-oma
|
|
A ________ is a growth that protects from a mucosal surface.
|
polyp
|
|
The term __________ is used to designate malignant tumor of epithelial tissue organ.
|
carcinoma
|
|
There are two categories of malignant neoplasms, _________ and _______ cancers.
|
solid tumors; hematological
|
|
The term ________ is used to describe the loss of cell differentiation in cancerous tissue.
|
anaplasia
|
|
A characteristic of of cancer cells is the ability to proliferate even in the absence of _________.
|
growth factors
|
|
With homologous loss of _________ gene activity, DNA damage goes unrepaired and mutations occur in dividing cells, leading to malignant transformations.
|
p53
|
|
The types of genes involved in cancer are numerous, with two main categories being the _________, which control cell growth and replication, and tumor _______ genes, which are growth-inhibiting regulatory genes.
|
protooncogenes; suppressor
|
|
___________ is the only known retrovirus to cause cancer in humans.
|
Human T-cell leukemia virus-1
|
|
Tumor cells must double _______ times before there will be a palpable mass.
|
30
|
|
A common manifestation of solid tumors is the cancer __________ syndrome.
|
anorexia-cachexia
|
|
As cancers grow, they compress and erode blood vessels, causing ________ and _________ along with frank bleeding and sometimes hemorrhage.
|
ulceration; necrosis
|
|
_______ is a common side effect of many cancers. It is related to blood loss, hemolysis, impaired red cell production, or treatment effects.
|
Anemia
|
|
A tissue _______ involves the removal of a tissue specimen for microscopic study.
|
biopsy
|
|
__________ therapy uses high-enerfy particles or waves to destroy or damage cancer cells.
|
Radiation
|
|
________ is a systematic treatment that enables drugs to reach the site of the tumor as well as distant sites.
|
Chemotherapy
|
|
Undefined or less differentiated cellular mass
|
Malignant mass
|
|
Defines the differentiation potential of stem cells
|
Cellular potency
|
|
Stem cells undergoing numerous mitotic divisions while maintaining an undifferentiated state
|
Renewal
|
|
Process of cell division
|
Proliferation
|
|
Cancer stem cells
|
Tumor-initiating cells
|
|
Mass of cells due to overgrowth
|
Tumor
|
|
Process that removes senescent and or damaged cells
|
Apoptosis
|
|
Well-differentiated mass of cells
|
Benign mass
|
|
Process of cell specialization
|
Differentiation
|
|
Study of tumors and their treatment
|
Oncology
|
|
Normal gene that can cause cancer if mutated
|
Protooncogene
|
|
Ratio of dividing cells to resting cells
|
Growth fraction
|
|
Promote cancer when less active
|
Tumor suppressor gene
|
|
Marked by chromosomal aberrations
|
Genetic instability
|
|
Changes in gene expression without DNA mutation
|
Epigenetic effects
|
|
Loss of cell differentiation
|
Anaplasia
|
|
Epithelial cells must be anchored to either neighboring cells or the underlying extracellular matrix to live and grow.
|
Anchorage dependence
|
|
Time it takes for the total mass of cells in a tumor to double
|
Doubling time
|
|
Tumor suppressor gene
|
p53
|
|
Five factors used to describle benign and malignant neoplasm.
|
1. Cell characteristics
2. Rate of growth 3. Manner of growth 4. Capacity to invade and metastasize 5. Potential for causing death |
|
Which of the following is not a major example of inherited suseptibility to cancer?
a. Li-Fraumeni syndrome b. Familial polyposis coli c. Familial retinoblastosis d. Paraneoplastic syndrome |
d. Paraneoplastic syndrome
|
|
Which of the following is correct regarding all malignant tumors?
a. Anaplasia b. Spread to distant sites c. Invasion of surrounding tissues d. Progressive and uncoordinated growth e. All of the above |
e. All of the above
|
|
Variation in size, shape, and staining of anaplastic cells is the definition of:
a. Metastasis b. Pleomorphism c. Lack of differentiation d. Hyperchromatism |
b. Pleomorphism
|
|
Which test provides the most precise information about the nature of a neoplasm?
|
Biopsy
|
|
Carcinoma is synonymous with:
|
Malignant epithelial neoplasm
|
|
Characteristics of malignant neoplasms are (a) encapsulation, (b) anaplasia, (c) invasion, (d) mitosis.
|
(b) anaplasia, (c) invasion,
|
|
The process by which unspecialized stem cells become specialized:
|
Differentiation
|
|
Which part of the cell cycle has the most redundancies, is tightly regulated by proteins called cyclins, and associated ezymes called cyclin-dependent kinases (CDKs)?
|
Between G1 and S
|
|
Correct order of the cell cycle
|
G1, S, G2, M
|
|
Which of the following is correct regarding a patient with a malignant neoplasm?
a. Hypercalcaemia due to bony metastases is an example of a paraneoplastic syndrome b. The tumor marker a-fetoprotein is usually raised in patients with hepatocellular carnioma c. The grade of a neoplasm refers to how far it has spread d. Tumor markers may be used as the primary tool for cancer diagnosis |
b. The tumor marker a-fetoprotein is usually raised in patients with hepatocellular carnioma
|
|
Which is correct regarding classification and nomenclature of neoplasms?
a. The neoplastic grading is a clinical estimate of the extent of tumor spread b. The growth in malignant tumor is uncoordinated and autonomous, which the growth in a benign tumor is usually coordinated c. A carcinoma is an epithelial malignancy d. Leiomyosarcoma is a malignant tumor of skeletal muscle |
c. A carcinoma is an epithelial malignancy
|
|
At autopsy the liver contains multiple tumor masses from 2-5 cm in size that are mostly tan and firm and that grossly exibit umbilication with central necrosis.
a. There is a multicentric origin of a benign neoplasm. b. The neoplasm has a high grade. c. The primary neoplasm is not in the liver. d. A carcinogen was the underlying cause for the neoplasm. e. The neoplasm has an advanced stage. |
c. The primary neoplasm is not in the liver.
|
|
A 35 yr old woman had a firm nodule papable on the dome of the uterus six yrs ago. The nodule has slowly increased in size and is now twice the size. She remains asymptomatic. Which neoplasm is she most likely to have?
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Leiomyoma (Tumor of smooth muscle cell)
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2 cm firm, rounded mass is palpable beneath the left forearm. No difficulty using arm, no pain, overlying skin appears normal. Mass doesn't change in size. Which neoplasm is likely?
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Lipoma
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Chronic couch over the past 2 months. Chest x-ray shows 3 cm mass in right upper lobe. Fine needle biopsy is done. Which finding is irrelevant for determining further therapy and prognosis?
a. Is the neoplam invading the margin of resection? b. What is the size of the neoplasm? c. What is the degree of atypia and pleomorphism of the neoplastic cells? d. How much inflammation is present in the neoplasm? e. Is the neoplasm primary or metastatic? |
d. How much inflammation is present in the neoplasm?
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Oncogenes have been implicated in the development of a human neoplasms. Oncogene activation is believed to be required for oncogenesis. Which of the following potential mechanisms are relevant to these processes?
a. Chromosome translocation b. DNA point mutation c. Amplification d. All of the above |
d. All of the above
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