20998799
Beschreibung
Karteikarten von Pooja Acharya, aktualisiert more than 1 year ago
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Erstellt von Pooja Acharya
vor mehr als 4 Jahre
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| Frage | Antworten |
| Neoplasia | New growth; the formation of clonal tumors by the uncontrolled proliferation of cells triggered by a series of genomic alterations and independent of physiological growth signals |
| Metaplasia | Differentiated cell type is replaced by a different mature cell type Found in association with tissue damage/ repair/ regeneration (ex: smokers bronchi - ciliated columnar epithelium replaced by squamous metaplasia) |
| Pleomorphism | variable size and shape of cells/nuclei histologic feature of malignant cells |
| Dysplasia | Precursor to cancer confined to epithelium by basement membrane |
| Carcinoma in situ | dysplastic cells involving full thickness of epithelium but still confined by basement membrane; patient can still be cured by complete surgical excision |
| Teratoma | rare benign tumor containing cells/tissues from more than one germ layer |
| Hamartoma | benign proliferation of cells indigenous to involved site (ie odontoma - toothlets) Hamartoma of lung |
| Choristoma | benign proliferation of cells in non-native site (ie small nodule of pancreatic tissue in submucosa of stomach) |
| What four classes of normal regulatory genes are the principal targets of cancer-causing mutations? | 1. Proto-oncogenes (growth promoting) 2. Tumor suppressor genes (growth-inhibiting) 3. Genes that regulate programmed cell death/apoptosis 4. Genes involved in DNA repair |
| Oncoproteins | Mutant proteins that have gained function to promote cell growth independently of normal extracellular growth-promoting signals (traffic light is always green) |
| Most commonly mutated proto-oncogene | RAS |
| Most common mitogen activated protein kinase (MAPK) pathway alteration present in 78-88% of ameloblastomas | BRAF (BRAFV600E mutation - valine is substituted for glutamine at codon 600) |
| MYC mutation | Oncogene that activates expression of many genes involved in cell growth Can reprogram banal somatic cells into pluripotent stem cells Upregulates telomerase in some contexts (Contributes to stem-cell like immortalization of tumor cells) |
| Abnormalities in tumor suppressor genes are characterized by __________-of-function mutations | Loss Encode proteins that have lost function to regulate signal transduction pathways and other critical cellular functions |
| Restinoblastoma gene (RB) | Governor of the cell. Regulates expression of genes necessary for dividing cells to pass through G1/S cell cycle checkpoint |
| Knudson "two-hit" hypothesis | With tumor suppressor genes, both alleles must be mutated for all loss of function to occur (one allele can pick up the slack for its mutated counterpart) explains why retinoblastoma has a hereditary pattern |
| Most frequently mutated gene in human cancers | TP53 (guardian of the genome) Central monitor of DNA damage and cell stress Regulates cell cycle progression, DNA repair, cellular senescence, apoptosis |
| APC | Gatekeeper of colonic neoplasia (APC mutations present in 70-80% of colorectal carcinoma) Tumor suppressor that downregulates Wnt/β-catenin signaling pathway |
| Familial adenomatous polyposis (FAP) | Cancer predisposition syndrome characterized by polyps caused by germline APC mutations Risk of colorectal cancer approaches 100% |
| Enzyme whose activation causes apoptosis | caspase activated either by mitochondrial or death receptor pathways |
| Follicular lymphoma | a neoplasm that evades cell death Characterized by overexpression of Bcl-2 via a specific chromosomal translocation |
| Result of translocation of the philadelphia chromosome t(9;22): | Chronic myelogenous leukemia |
| Xeroderma pigmentosum | Cancer predisposition syndrome characterized by impaired ability to repair UV-induced DNA damage Abnormal cross-linking of pyrimidine bases prevents error-free DNA replication |
| Lynch Syndrome (HNPCC) | Hereditary nonpolyposis colon cancer syndrome characterized by loss of DNA proof-reading microsatellite instability-high (MSh2/mlh1) |
| Aflatoxin B1 | Fungal food contaminant that results in increased risk of hepatocellular carcinoma in Africa and the Far East |
| Warburg effect | Cancer cells use aerobic glycolysis generating just 2 ATP = inefficient pathway for energy production, but generates metabolic intermediates necessary for frequent cell division / synthesis |
| Neoangiogenesis | development of new blood vessels from previously existing capillaries; allow malignancies to enlarge (create its own blood supply) accomplished by VEGF - Vascular endothelial growth factor |
| 8 hallmarks of cancer | Self-sufficiency in growth signals (Oncogenes - gain of function - green light) Insensitivity to growth-inhibition (tumor suppressor loss of function) Evasion of apoptosis (follicular lymphoma) Ability to evade the host immune response (immune surveillance; immunoediting; downregulate T-cells) Limitless replicative potential (immortality; upregulate telomerase ) Altered cellular metabolism (Warburg effect) Sustained angiogenesis (blood vessel formation) Ability to invade and metastasize (spread) |
| Cancer cachexia | progressive loss of body fat and lean body mass, accompanied by profound weakness, anorexia and anemia (TNF-A) |
| Eaton-Lambert syndrome | SCLC, myasthenia-gravis-like symptoms but gets better with exercise and doesn't respond to Ach-esterase inhibitors, antibodies against presynaptic Ca channels |
| Nephrotic syndrome | Lung, breast, stomach cancer. Diffuse membranous glomerulopathy |
| Cushing syndrome | SCLC, secretes ACTH, moon face, weight gain |
| Hypercalcemia | SCC lung, ectopic production of parathrelated peptide |
| Polycythemia | Renal and liver cancer, erythropoietin |
| Loss of function of E-cadherin | Binds to B-Catenin / growth inhibition of epithelial cells Familial Gastric Cancer (AD) -- (CDH1) |
| mechanism for tumor invasion | invade ECM detach from E-cadherin and N-CAM attach to matrix degrade ECM (metalloproteinases and cathepsin D) migrate vascular dissemination attach to another organ |
| tumor viruses | acute transforming retrovirus = contains active oncogene slow transforming retrovirus = inserts itself, does not have own oncogene |
| human T-cell leukemia virus (HTLV) | has TAX protein, which increases survival and growth of infected cells, increases genomic instability adult T-cell leukemia (ATL) |
| high risk HPV types | 16, 18 can cause invasive cancers proteins E6 and E7 promote growth and proliferation of cancer |
| HPV E6 | blocks p53 stimulates temolerase expression increased tumor proliferation |
| HPV E7 | blocks p21 blocks RB-E2F increased tumor proliferation |
| EBV associated cancers | Burkitt's & Hodgkin's lymphoma nasopharyngeal cancers CNS-Lymphoma in HIV |
| LMP-1 | EBV oncogenes Activates signaling pathways for B-cell via CD40 Activates BCL-2 |
| Helobacter pylori and cancer | lymphoma (MALT) due to chronic gastritis = polyclonal/monoclonal b cell proliferation monoclonal cured by eradicating HP carcinoma due to chronic gastritis = intestinal metaplasia, dysplasia, takes decades, not seen w ulcers |
| CA-125 | Surface epithelial ovarian cancers |
| PSA | Prostatic cancer |
| AFP | HCC, GERM CELL TUMORS OF TESTIS |
| CEA | Colon cancer |
| CA19-9 | Pancreatic cancer |
| NMYC oncogene amplication | Neuroblastoma |
| t(8:14) | Burkitt lymphoma |
| t(11:22) | Ewing sarcoma |
| IHC: Cytokeratin | Epithelial cancers |
| Vimentin | sarcomas: Mesenchymal cancers |
| Desmin | Rhabdomyosarcoma: striated muscle |
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