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Neoplasia Flashcards

Deleted user User has deleted their subject information English 55 cards

Cards in this deck (55)

  1. 1NeoplasiaNew 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
  2. 2MetaplasiaDifferentiated 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)
  3. 3Pleomorphismvariable size and shape of cells/nuclei
    histologic feature of malignant cells
  4. 4DysplasiaPrecursor to cancer confined to epithelium by basement membrane
  5. 5Carcinoma in situdysplastic cells involving full thickness of epithelium but still confined by basement membrane; patient can still be cured by complete surgical excision
  6. 6Teratomarare benign tumor containing cells/tissues from more than one germ layer
  7. 7Hamartomabenign proliferation of cells indigenous to involved site (ie odontoma - toothlets)
    Hamartoma of lung
  8. 8Choristomabenign proliferation of cells in non-native site (ie small nodule of pancreatic tissue in submucosa of stomach)
  9. 9What 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
  10. 10OncoproteinsMutant proteins that have gained function to promote cell growth independently of normal extracellular growth-promoting signals
    (traffic light is always green)
  11. 11Most commonly mutated proto-oncogeneRAS
  12. 12Most common mitogen activated protein kinase (MAPK) pathway alteration present in 78-88% of ameloblastomasBRAF (BRAFV600E mutation - valine is substituted for glutamine at codon 600)
  13. 13MYC mutationOncogene 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)
  14. 14Abnormalities in tumor suppressor genes are characterized by __________-of-function mutationsLoss
    Encode proteins that have lost function to regulate signal transduction pathways and other critical cellular functions
  15. 15Restinoblastoma gene (RB)Governor of the cell. Regulates expression of genes necessary for dividing cells to pass through G1/S cell cycle checkpoint
  16. 16Knudson "two-hit" hypothesisWith 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
  17. 17Most frequently mutated gene in human cancersTP53 (guardian of the genome)
    Central monitor of DNA damage and cell stress
    Regulates cell cycle progression, DNA repair, cellular senescence, apoptosis
  18. 18APCGatekeeper of colonic neoplasia (APC mutations present in 70-80% of colorectal carcinoma)
    Tumor suppressor that downregulates Wnt/β-catenin signaling pathway
  19. 19Familial adenomatous polyposis (FAP)Cancer predisposition syndrome characterized by polyps caused by germline APC mutations
    Risk of colorectal cancer approaches 100%
  20. 20Enzyme whose activation causes apoptosiscaspase
    activated either by mitochondrial or death receptor pathways
  21. 21Follicular lymphomaa neoplasm that evades cell death
    Characterized by overexpression of Bcl-2 via a specific chromosomal translocation
  22. 22Result of translocation of the philadelphia chromosome t(9;22):Chronic myelogenous leukemia
  23. 23Xeroderma pigmentosumCancer predisposition syndrome characterized by impaired ability to repair UV-induced DNA damage
    Abnormal cross-linking of pyrimidine bases prevents error-free DNA replication
  24. 24Lynch Syndrome (HNPCC)Hereditary nonpolyposis colon cancer syndrome characterized by loss of DNA proof-reading
    microsatellite instability-high (MSh2/mlh1)
  25. 25Aflatoxin B1Fungal food contaminant that results in increased risk of hepatocellular carcinoma in Africa and the Far East
  26. 26Warburg effectCancer cells use aerobic glycolysis generating just 2 ATP = inefficient pathway for energy production, but generates metabolic intermediates necessary for frequent cell division / synthesis
  27. 27Neoangiogenesisdevelopment of new blood vessels from previously existing capillaries; allow malignancies to enlarge (create its own blood supply)
    accomplished by VEGF - Vascular endothelial growth factor
  28. 288 hallmarks of cancerSelf-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)
  29. 29Cancer cachexiaprogressive loss of body fat and lean body mass, accompanied by profound weakness, anorexia and anemia
    (TNF-A)
  30. 30Eaton-Lambert syndromeSCLC, myasthenia-gravis-like symptoms but gets better with exercise and doesn't respond to Ach-esterase inhibitors, antibodies against presynaptic Ca channels
  31. 31Nephrotic syndromeLung, breast, stomach cancer. Diffuse membranous glomerulopathy
  32. 32Cushing syndromeSCLC, secretes ACTH, moon face, weight gain
  33. 33HypercalcemiaSCC lung, ectopic production of parathrelated peptide
  34. 34PolycythemiaRenal and liver cancer,
    erythropoietin
  35. 35Loss of function of E-cadherinBinds to B-Catenin / growth inhibition of epithelial cells
    Familial Gastric Cancer (AD) -- (CDH1)
  36. 36mechanism for tumor invasioninvade ECM
    detach from E-cadherin and N-CAM
    attach to matrix
    degrade ECM (metalloproteinases and cathepsin D)
    migrate
    vascular dissemination
    attach to another organ
  37. 37tumor virusesacute transforming retrovirus = contains active oncogene
    slow transforming retrovirus = inserts itself, does not have own oncogene
  38. 38human T-cell leukemia virus (HTLV)has TAX protein, which increases survival and growth of infected cells, increases genomic instability
    adult T-cell leukemia (ATL)
  39. 39high risk HPV types16, 18 can cause invasive cancers
    proteins E6 and E7 promote growth and proliferation of cancer
  40. 40HPV E6blocks p53
    stimulates temolerase expression
    increased tumor proliferation
  41. 41HPV E7blocks p21
    blocks RB-E2F
    increased tumor proliferation
  42. 42EBV associated cancersBurkitt's & Hodgkin's lymphoma
    nasopharyngeal cancers
    CNS-Lymphoma in HIV
  43. 43LMP-1EBV oncogenes
    Activates signaling pathways for B-cell via CD40
    Activates BCL-2
  44. 44Helobacter pylori and cancerlymphoma (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
  45. 45CA-125Surface epithelial ovarian cancers
  46. 46PSAProstatic cancer
  47. 47AFPHCC, GERM CELL TUMORS OF TESTIS
  48. 48CEAColon cancer
  49. 49CA19-9Pancreatic cancer
  50. 50NMYC oncogene amplicationNeuroblastoma
  51. 51t(8:14)Burkitt lymphoma
  52. 52t(11:22)Ewing sarcoma
  53. 53IHC: CytokeratinEpithelial cancers
  54. 54Vimentinsarcomas: Mesenchymal cancers
  55. 55DesminRhabdomyosarcoma: striated muscle

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Description
User has deleted their subject information Flashcards on Neoplasia Flashcards, created by Deleted user on 25/02/2020.
Created by
Deleted user · Feb 2020
Updated
Feb 25, 2020
Views
76
History
  • Created by Pooja Acharya · Feb 24, 2020
  • Copied by Pooja Acharya · Feb 25, 2020
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