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43 Cards in this Set
- Front
- Back
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What was the oldest description of cancer? |
3000 BC - Edwin Smith Papyrus |
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What does the term "cancer" mean? |
Crab (because of finger-like projections of cancer) |
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Who first used the term "carcinos" and "carcinoma?" |
Hippocrates: Carcinos: non-ulcer forming tumors Carcinoma: ulcer-forming tumors |
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Who first used the term "cancer?" |
Celcus (Roman, 28-50 BC) |
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Who first used the term "oncos?" |
Galen (130-200 AD) |
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What two Renaissance scientists developed & used autopsies? |
Harvey (1862) Morgagni (1761) |
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Who was the father of cellular pathology? (BIG HINT: Rudolf, the Red-Nosed Reindeer) |
Rudolf Virchow |
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What does neoplasia mean? |
-"New formation" or Tumor -State of poorly regulated cell growth |
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What are types of neoplasia? |
-Benign neoplasma -Malignant neoplasm -Carcinoma in situ (in its place) |
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Histological Difference #1 - Differentiation Benign vs. Malignant |
Benign: Well-differentiated
Malignant: Poorly-differentiated |
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Histological Difference #2 - Size and Shape Benign vs. Malignant |
Benign: Uniform cell size and shape
Malignant: Variable size and shape |
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Histological Difference #3 - Demarcation (Boundaries/Edges) Benign vs. Malignant |
Benign: Well-demarcated
Malignant: Poorly demarcated |
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Histological Difference #4 - Nucleus Benign vs. Malignant |
Benign: One nucleus
Malignant: Occasional multiple nuclei |
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Histological Difference #5 - Tumor Growth Benign vs. Malignant |
Benign: Tumor is not within blood vessels, does not metastasize, grows slowly
Malignant: Invades lymphs and veins; areas of necrosis and hemorrhage; invades past the the "basement membrane" (the area separating the epithelium from the underlying connective tissue) |
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What are the phases of the cell cycle regulation? |
-G0 -Interphase ....G1 ....S phase ....G2 phase -M phase |
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What is the G0 phase? |
This is the quiescent (dormant) phase. |
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What is the Interphase? |
The preparation period for the cell to take in nutrients.
Three stages: G1; S, and G2 |
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What is the G1 phase and its substages? |
This is the Gap between the end of M phase and beginning of S phase. G1 has 5 substages: a. Early G1 stage b. G0 stage c. R stage d. Late G1 stage e.G1/S checkpoint
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Early G1 stage? |
Mitogens (signals) tell the cell to proceed! Mitogens trigger mitosis. |
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G0 stage? |
Cells exit due to absence of mitogens (generally small cells) |
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R phase? |
Retinoblastoma protein (Rb) normally prevents cell growth by inhibiting cell cycle progression. But in this phase, it undergoes "hyperphosphorylation" by cyclin D. (This means phosphate is added to the compound) When Rb is hyperphosphorylated by cyclin D, it becomes inactive and cell cycle progression resumes. |
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Late G1 phase? |
Signals from mitogens are no longer needed for the cell to proceed. |
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G1/S checkpoint? |
Checks for existence of all conditions (nutients, enzymes), DNA damage |
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What does S stand for (S phase)? |
Synthesis |
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What occurs during the S phase? |
DNA replication (Amount of DNA doubles) -At the end of this phase, each chromosome will have 2 chromatids |
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What is the G2 phase? |
The second gap phase. The DNA which was replicated during the S phase is checked before mitosis at the GS/M checkpoint. |
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What is the M phase? |
The mitosis phase. It includes a spindle assembly checkpoint to make sure chromosomes are attached to the spindle. Mitosis occurs here: prophase, metaphase, anaphase, telophase, and cytokinesis. |
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What are the three ways that tumors metastasize (travel)? |
1. Lymphatic spread
2. Hematogenous spread
3. Direct seeding |
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What is the difference between carcinomas and sarcomas? |
Carcinomas start in the epithelial tissue, such as the lining of the breast, colon, lung, prostrate.
Sarcomas start in the mesodermal tissue, such as the bone, muscle, nervous system, or blood. They are sometimes called mesenchymal tumors. |
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What is the most common pathway for carcinoma to spread? |
Through lymphatic spread
Follows the route of lymphatic drainage
Example: Lymphadenopathy (increase in size of lymph nodes)
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What is the typical metastatic route for sarcomas? |
Through hematogenous spread (blood system)
Veins more readily invaded than arteries
Examples: Portal vein: Liver metastasis Inferior vena cava: Lung metastasis Thyroid: Lung metastasis |
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What is direct seeding? |
Cancer cells break away from the original tumor and begin seeding in body cavities
Examples: Pleural cavity, peritoneal cavity |
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What is a proto-oncogene? |
It's a normal part of the genome that promotes cell growth and differentiation in normal cells. |
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What is an oncogene? |
Oncogenes are mutated proto-oncognes that give a proliferative advantage (replicative advantage) to the tumor.
They can cause apoptotic cells (those supposed to die) to survive and proliferate (normally also requires environmental factors, viruses, etc.) |
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How do proto-oncogenes become oncogenes? |
1. Mutation 2. Increased concentration of certain proteins 3. Chromosomal translocation |
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How does mutation activate oncogenes? |
Mutations within the regulatory area of the proto-oncogene causes disturbances in regulation of the cell's growth and replication. |
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How does increased protein concentration activate oncogenes? |
Misregulation of protein snthesis leads to abnormal increase of protein expression and duplication of genes. |
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How does chromosomal translocation activate oncogenes? |
-Relocation of proto-oncogene to a new chromosomal site (increased expression) and fusion with another gene (increased cancerous activity) |
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What do tumor suppressor genes do? |
They restrict cell proliferation by: -Controlling cell division I-Inducing apoptosis |
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What kind of tumor suppressor genes stop cell cycle progression when DNA damage is detected? |
Gatekeeper genes |
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What are two gatekeeper genes? |
1. p53 It's activated when the cell has DNA damage. It activates p21 which stops the cyclin complex which stops the cell cycle. 2. pRB (retinoblastoma) Its prevents the cell cycle from progressing by inhibiting the S phase (where DNA is replicated) |
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What are caretaker genes? |
They repair DNA. |
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What are two caretaker genes? |
1. BRCA It repairs DNA. It loss causes aneuploidy(chromosome number not a multipleof 23)
2. Mismatch repair genes (MMR) -Fix mismatched nucleotides during DNA replication. -Without it, unstable microsatellite regions of repeating nucleotides develop. |
