Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
62 Cards in this Set
- Front
- Back
|
Totipotent Cells |
Fertilized ova capable of differentiating into any type of cell in the human body |
|
|
Multipotent Cells |
Differentiated cells that have eliminated many types of cells by permanently turning off associated genes (endoderm/mesoderm/ectoderm) |
|
|
Pluripotent Cells |
Cells are narrowed down to a few related cells (bone marrow, tissues) |
|
|
Unipotent Cells |
Can only become one type of cell but still retain the properties of a stem cell (RBC) |
|
|
Mature Differentiated Cell |
Functional tissue cell that is unresponsive to growth factors |
|
|
Regulation of Cell Division |
Growth factors Cell-cell communication --> gap junctions Terminal differentiation |
|
|
Grading of Cancer as a Stem Cell Disease |
Grade I: Both cells are not differentiated Grade II: Both cells proliferate extensively Grade III: Both cells self-generate (are "immortal") Grade IV: Both cells are sensitive to radiation therapy (cell can go through reverse differentiation) Grade V: Both cells can be induced in-vitro to differentiate with proper differentiation factors |
|
|
Tumor |
Abnormal growth due to uncontrolled cell proliferation that serves no function |
|
|
Neoplasm |
New growth |
|
|
Benign Tumor |
Not referred to as cancers, growths that are encapsulated and well differentiated, cell retains normal tissue functions |
|
|
Cancer |
Reserved for malignant neoplasms, characterized by rapid growth, loss of differentiation, and lack of normal tissue organization |
|
|
Cancer Nomenclature |
Tissue name Grade Stage |
|
|
Carcinoma |
Cancer of epithelial tissue |
|
|
Adenocarcinoma |
Cancer of glandular epithelial tissue |
|
|
Sarcoma |
Cancer of connective tissue (very hard to treat) |
|
|
Leukemia |
Cancer of blood forming organs |
|
|
Glioma |
Cancer of glial cells of CNS (Brain --> typically are inoperable) |
|
|
Lymphoma |
Cancer of lymphatic tissue |
|
|
Cancer Grading vs Staging |
Grading estimates the degree of differentiation (or lack thereof) and staging rates the degree of invasiveness |
|
|
Tumor Grading |
Grade I: Closely resembles tissue of origin, retains some specialized functions, hasn't invaded capsule (benign neoplasm) Grade II: Less resemblance, more variation in size/shape, increased mitosis, has begun invading capsule (malignant neoplasm) Grade III: Does not closely resemble tissue of origin, much variation in size/shape, greatly increased mitosis (poorly differentiated malignant neoplasm) Grade IV: No resemblance to tissue of origin, great variation of size/shape (anaplastic metastatic neoplasm) |
|
|
Cancer Staging |
Stage I: Confined to organ of origin (carcinoma in situ) Stage II: Locally invasive and has broken through capsule Stage III: Spread to regional structures (lymph nodes --> most common route of metastasis) Stage IV: Spread to distant organs (lymph nodes to circulation --> first capillary beds hit are usually the liver and the lungs) |
|
|
Tumor Suppressor Gene |
Genes which inhibit cell growth and division and promotes terminal maturation ***Requires two mutations for control of cell growth/differentiation to be lost |
|
|
Proto-oncogene |
Growth related gene that codes for proteins that control growth and differentiation, act as a dominant trait, only need one mutation to cause cancer |
|
|
Oncogene |
Over-expressed growth stimulating one of two homologous genes, causes abnormal growth, overstimulation of these genes causes cancer, only requires one mutation |
|
|
Caretaker Genes |
Genes that repair damaged DNA/DNA replication mistakes, when these are dysfunctional that number of mutations increases dramatically |
|
|
Tumor Virus |
Virus that inserts its DNA into the host cells and causes uncontrolled cell growth and division |
|
|
Mutations Necessary for Normal Cells to Become Cancer Cells (Does Not Include Blood Cancers) |
1. One mutation in an oncogene (growth stimulated in absence of growth factor) 2. Two mutations in Tumor Suppressor Gene (decreased sensitivity to antigrowth signals) 3. Mutations in genes regulating glycosphingolipids (increased responsiveness to GF) 4. Mutations disabling apoptosis (usually TP53) 5. Mutations in genes expressing telomerase (immortal growth) 6. Mutations in genes involved with expression of fibronectin (cell adhesion) 7. Mutations of genes regulating gap junctions 8. Abnormal secretion of angiogenic growth factors |
|
|
Mutations Necessary for Blood Cancers to Occur |
1. One mutation in an oncogene (growth stimulated in absence of growth factor)
2. Two mutations in Tumor Suppressor Gene (decreased sensitivity to antigrowth signals) 3. Mutations in genes regulating glycosphingolipids (increased responsiveness to GF) 4. Mutations in genes expressing telomerase (immortal growth) 5. Abnormal secretion of angiogenic growth factors |
|
|
Leukemia vs Other Cancers |
Normally it takes seven mutations for a tumor to become cancerous and usually this takes years, leukemia only requires three mutations |
|
|
Glycosphingolipids |
Normally decrease cell responsiveness to growth factors, in cancer glycosphingolipids are decreased and this increases the cell's responsiveness to growth factors
|
|
|
Changes in Glycoproteins and Glycolipids |
This causes decreased communication between cells, may increase immune response to the cancer cells |
|
|
Fibronectin |
A cell-surface protein that mediates cellular adhesive interactions (cadherins and integrins form the adhesion junctions), loss of fibronectin occurs in cancer |
|
|
Protease Secretion |
Proteases are enzymes that break down proteins and peptides, as these are secreted during cancer the extracellular matrix is disrupted and adhesiveness is decreased, this allows cancer cells to escape the capsule |
|
|
Anchorage Proteins (Decreased) |
Ex. Desmosomes, adherens, junctions Normal cells need to be anchored to undergo mitosis, but in the event of cancer cells undergo anchorage independent mitosis and are allowed to metastasize, this is linked to changes in fibronectin |
|
|
Gap Junctions |
Many tumors alter/block/down-regulate gap junction function and block cell-cell communication, implies reduced/absent communication and decreased contact inhibition |
|
|
Tumor Cell Marker Definition |
Substances secreted by cancer onto tumor cell membranes or released into ECF compartments, assists in identifying people with high risk for cancer, diagnosing cancer, and effectiveness of treatment |
|
|
Tumor Cell Markers: Hormones |
Ectopic hormones (produced by tumor cells of non-endocrine origin) --> ACTH/catecholamines Immature/fetal forms of a hormone --> hCG, AFP |
|
|
Tumor Cell Markers: Enzymes |
Immature/fetal types of enzymes or enzymes in abnormal proportions |
|
|
Tumor Cell Markers: Genes |
Oncogenes or mutated forms - Phophokinases (turn pathways on and off) - DNA binding proteins - Cellular growth factors |
|
|
Tumor Cell Markers: Antigens |
Production of neoantigens (newly formed antigen that is not recognized by immune system) --> may help immune system response Normal antigens: prostate specific antigen --> causes prostate growth stimulated by testosterone --> increased growth --> mutations (increased levels of cells increases the likelihood of cancer) |
|
|
Tumor Cell Markers: Antibodies
|
Ineffectual immunnoglobins (IgM antibodies in multiple myeloma) |
|
|
Tumor Cell Markers: Proteins |
Secretions in response to certain cancers AFP (alpha fetal protein) secreted by liver cancer cells and germ line cancers |
|
|
How Are Tumor Cell Markers Used in a Clinical Setting |
Present in blood, spinal fluid, or urine Tumor markers can cause symptoms Helps identify/confirm type of cancer |
|
|
Epigenetic Suppression |
Silencing of normal gene through deacetylation or methylation, this mutation can be passed on genetically |
|
|
Inherited Mutation vs Spontaneous Mutation |
Most mutations that lead to cancer occur during life time of individual within the somatic tissues, mutations that occur in the germ-line can be passed on through generations Inherited: genetic Spontaneous: "natural" mutation |
|
|
Complications of Cancer and Cancer Treatments |
Cushings Syndrome, inappropriate ADH secretion, Hypercalcemia, hypoglycemia, Carcinoid Syndorme, polycythemia Pain, fatigue, cachexia, anemia, leukopenia, thrombocytopenia, infection, GI distress, alopecia, skin breakdown |
|
|
Mechanisms of Local Invasion |
A. Cellular multiplication (high mitosis rate and low death rate)
B. Release of lytic enzymes (digests ECM and enters organ --> diapedesis) C. Mechanical pressure (projections compress local cells/blood vessels and cause damage and hypoxia) D. Decreased cell-cell adhesion (loss of fibronectin) E. Increased motility |
|
|
Steps of Metastasis |
1. Local invasion 2. Penetration into blood vessels/lymph system 3. Released into lymphatic system or blood 4. Transport to a secondary site by blood or lymph 5. Arrest/adherence/proliferation at secondary site 6. Neovascularization (secretion of VEGF and PDGF to stimulate new vessel growth and nutrient delivery to sustain tumor) |
|
|
Metastasis to Different Organs |
1. Loss of cell adhesion --> movement into circulation/lymph 2. First capillary bed encountered (typically lungs or liver) 3. Organ trophism (tumors themselves are heterogenous but individual cells are attracted to certain organs/tissues) |
|
|
Invasion of Distant Organs |
1. Laminin receptors attach to basement membrane and actively invade capillary wall 2. Proteolytic enzymes are released to degrade basement membrane/ECM (removes barriers) 3. Pseudopodia extended into tissue as an anchor 4. Angiogenesis 5. TAMS (block Tc and NK cell functions, prevent immune response) |
|
|
Angiogenesis |
Formation of new blood vessel into tumor (secondary tumor requires vascular network to continue growth), requires angiogenic growth factors --> VEGF (vascular endothelial growth factor), PDGF (platelet derived growth factor), and TGF-a (transforming growth factor alpha) *Normal cells prevent new blood vessel development by secreting thrombospondin |
|
|
Immunological Defenses the Body has Against Tumors |
NK cells and Tc cells Tumor markers |
|
|
Ways Cancer Cells are Able to Avoid Immunological Detection |
Anchorage independent, resistant to apoptosis (telomerase), clonal proliferation, inactivate tumor suppressor genes, silence genes, alter progrowth and antigrowth signals |
|
|
General Cancer Treatment Modalities |
1. Chemotherapy 2. Radiation 3. Surgery 4. Immunotherapy |
|
|
Chemotherapy |
Kills cells that are capable of mitosis, hope is to eradicate enough cells that body can kill the rest, combinations have been the most successful (drugs attack different weaknesses/pathways), some cells may be resistant (as body releases GF to replace cells, cancer cells increase and the prognosis for second chemo treatments is poor) |
|
|
Radiation |
Focuses only tumor and hopefully doesn't damage tissue around it too severely, damages large macromolecules (ex. DNA) |
|
|
Surgery |
Typically "debulking" followed by chemo Objective is to remove tumor before it metastasizes, preventative surgery (mastectomy), and remove pressure to alleviate pain, debulk, or determine staging/nodal involvement |
|
|
Immunotherapy |
How our immune system can kill cancer, selectively kills tumor cells while sparing normal cells, memory cells are created for prevention of primary tumor Ex. BCG, DNCB, LAK, and Monoclonal Antibodies |
|
|
BCG |
Bacterial wall extracts are injected into tumor, activated macrophages and NK cells because immune system no longer recognizes cell as self, success with urogenital and lung cancers |
|
|
DNCB (Dinitrochlorobenzene) |
Body first sensitized (applied to normal skin) than DNCB is painted on skin tumor and causes a hypersensitivity response (Type IV) similar to poison ivy |
|
|
LAK (Lymphokine Activated Killer) |
Tc cells are removed from patient, cultured, and sensitized to tumor specific antigens, cells reinserted into patient and cause lysis of tumor cells, used successfully against melanoma and renal cell carcinoma |
|
|
Monoclonal Antibodies |
Used to diagnose and monitor treatment results, goal is to mediate tumor rejections, has been successful against hematologic and lymphatic cancers, conjugated antibodies attach radioactive isotopes and when the antibodies bind to the tumor cells they kill the target with radioactive iodine (thyroid cancer) *Fluorescent antibody attaches to tyrosine kinase and injects cancer specific toxin |
