Patho Unit 1

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Author:
rstoth
ID:
102378
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Patho Unit 1
Updated:
2011-09-18 21:46:42
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neoplasia
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chapter 7
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  1. benign neoplasms
    well-differentiated cells that resemble normal counterpart in structure & function but lost ability to control proliferation
  2. malignant neoplasms
    • less differentiated
    • lost ability to control cell proliferation & differention
  3. parenchymal tissue
    • transformed or neoplastic cells
    • determines behavior of cells
  4. supporting tissue
    connective tissue, ECM & blood vessels around neoplasm
  5. benign tumor suffix
    -oma
  6. mesenchymal tumor suffix
    -sarcoma
  7. differences of benign & malignant tumor
    • characteristic of cells- benign resemble origin cells; malignant less differentiated
    • rate of growth- benign slow
    • local invasion- benign fibrous capsule
  8. cancer in situ
    localized preinvasive lesion
  9. anaplastic malignant neoplasm
    poorly differentiated cells
  10. pleomorphism
    undifferentiated cells that vary in size and shape
  11. aneuploidy
    malignant cells w/ abnormal # chromosomes
  12. growth properties of malignant cells
    • growth factor independence- make own growth factor
    • lack of cell density-dependent inhibition- cells should stop dividing when close together
    • impaired cohesiveness & adhesion
    • loss of anchorage dependence- grow w/out attach to ECM
    • faulty cell-to-cell communication-
    • indefinite cell life span
  13. antigen expression in neoplasm
    • immunologically distinct from original tissue
    • produce fetal antigens
  14. paraneoplastic syndromes
    abnormal production of substances that affect body function
  15. growth fraction
    ratio of dividing cells to resting
  16. Gompertzian model
    initial growth rate of tumor exponential then tends to decrease with time due to limitations in blood supply & nutrients
  17. sentinel node
    initial lymph node to which primary tumor drains
  18. chemokines
    chemoattractant cytokines regulate leukocytes play role in invasion & metastisis
  19. epigenetic factors
    • silence genes
    • may be factor in pathogenesis of cancer
  20. proto-oncogenes
    normal genes that become cancer causing if mutated
  21. tumor-suppressor genes
    when less active create environment where cancer promoted
  22. genetic events leading to oncogene formation/activation
    • point mutation- single nucleotide base change
    • RAS oncogene: signal-relaying proteins transmit growth signals to cell nucleus
    • chromosomal translocations- gene sites change from one chromosome to another displacing other genes (philadelphia +)
    • multiple copies of certain genes overexpress higher # proteins (HER human epidermal growth factor in breast cancer)
  23. genetic events leading to loss ot tumor-suppressor gene function
    • recessive- cells behave normally until both genes are effected
    • suppressor gene p53- prevents propogation of defective cells stopping G1 for repair; loss of activity promotes angiogenesis & removes antiangiogenesis switch
    • retinoblastoma gene (suppressor gene)- both alleles inactivated
  24. two hit hypothesis of carcinogenesis
    • one genetic change is inheredited (1st hit)
    • second mutation occurs to express the cancer (2nd hit)
  25. molecular & cellular pathway of neoplasm
    • defect in DNA repair mechanism- chemical, free radical
    • disorders in growth factor signaling pathways- couple growth factor receptors to nuclear target
    • evasion of apoptosis
    • development of sustained angiogenesis
    • evasion of metastasis
  26. epigenic mechanisms
    • changes in gene expression w/out change in DNA
    • may silence genes like tumor suppressor
    • may be hit in 2 hit hypothesis
  27. kinases
    proteins involved in signalingpathways; factors that control growth factors
  28. micro RNA genes
    • can be tumor suppressor if critical target is oncogene
    • can be oncogene if target is tumor suppressor gene
  29. reasons for failure of cells to undergo apoptosis
    • altered cell survival signaling
    • down-regulation of death receptors
    • stabilization of mitochrondia
    • inactivation of apoptotic proteins
  30. MET proto-oncogene
    • key regulator of invasive growth
    • expressed in both stem & cancer cells
  31. initiation in tumor cell transformation
    • exposure of cells to appropriate doses og carcinogenic agent that makes them susceptable to malignancy
    • chemical, physical, biologic
    • cells most vulnerable are actively synthesizing DNA
  32. promotion of tumor cell transformation
    • induction of unregulated accelerated growth in already initiated cells by various chemicals and growth factors
    • reversible of promotor substance removed
  33. complete carcinogens
    can initiate & promote neoplasm
  34. progression in tumor cell transformation
    process where tumor cells get malignant phenotype changes that promote invasiveness, metastatic competence, autonomous growth tendicies, increased karyotypic instability
  35. autosomal dominant inheritance pattern in neoplasm
    • point mutation in single allele to tumor-suppressor gene
    • one normal & one mutant gene
    • for cancer to develop, mutation must occur in normal gene
  36. hormones in cancer
    • action unknown
    • may drive cell division in malignant phenotype
  37. obsesity in neoplasm
    • increased sex hormones (androgens & estrogens)
    • insulin resistance & increased production of pancreatic insulin
    • insulin-like growth factor stimulates cell proliferation & inhibit apoptosis
    • inflammation w/ production of cytokines
  38. tumor antigens
    molecular configurations that can be recognized by immune T cells or antibodies
  39. T-cell response in cancer
    • important host responses for controlling growth of antigenic cells & activation of immune system
    • T-cell immunity of cancer cells reflects action of CD4 helper T cells & CD8 cytotoxic T cells
  40. 2 groups of chemical carcinogens
    • direct-reacting; do not need activation to become carcinogenic
    • indirect-reacting (procarcinogens or initiators); active only after metabolic conversion
  41. promotors
    • enhance carcinogenicity of other agents
    • change expression of genetic material
    • increase DNA synthesis
    • alter intercellular communication
  42. effects of ionizing radiation
    causes chromosomal breakage, translocations, point mutations
  43. effects of ultraviolet radiation
    • low energy rays; sallow penetration
    • effects additive
    • long delay from exposure & cancer
  44. oncogenic viruses
    • HPV-cervical
    • EBV-burkitts, NP cancer, lymphoma
    • hepBV- liver
    • HHV-8 (herpes)
    • HTLV-1 (human T-cell leukemia virus)
  45. anorexia & cachexia
    • persistent inflammatory response in conjunction w/ production of cytokines & catabolic factors from tumor
    • people w/ cachexia poorer outcomes
    • TNF & IL 1&2 produce wasting syndrome
  46. cancer related fatigue
    • peripheral- inability of neuromuscular apparatus to do task in response to central stimulation;lack of ATP
    • build up of metabolic products (lactic acid)
    • central- difficulty initiating voluntary activities; poor regulation of 5-HT (serotonin)
  47. paraneoplastic syndromes
    manifestations in sites not affected in cancer
  48. paraneoplastic hormones
    • peptic hormones (ADH)- SIADH
    • adrenocorticotropic (ACTH)- Cushings
    • parathyroid hormone (PTH)- hypercalcemia
  49. paraneoplastic hematolic complications
    • procoagulation factors that cause thromboembolism
    • mucin-producing adenocarcinoma release thromboplastin
  50. Lambert Eaton Syndrome
    • small lung cell cancer
    • muscle weakness in limbs
    • immune mediated
  51. tumor markers
    • expressed from tumor cells
    • screening, establishing prognosis, monitoring tx, detect recurrent disease
  52. oncofetal antigens
    • AFP-liver
    • CEA (carcinoembryonic antigen)-colorectal, pancreas, lung
  53. hormone tumor marker
    • hCG- gestational trophoblastic, germ cell
    • calcitonin- thyroid
    • catecholamines- pheochromocytoma
  54. specific proteins tumor markers
    • monoclonal immunoglobin- multiple myeloma
    • PSA- prostate
  55. mucin/glycoproteins tumor markers
    • CA-125: ovarian
    • CA-19-9: pancreas, colon
  56. papanicolaou test
    • cancer cells lack cohesive intercellular junctions
    • cnacer cells exfoliate & mix w/ secretions
  57. immunohistochemisrty
    • use monoclonal antibodies to ID cell products or surface markers
    • ID site of origin
  58. microarray technology
    gene chips that can simultaneously perform miniature assays to detect and quantify expression of large numbers of genes at the same time
  59. grading of tumors
    • microscopic exam of tissue to determine level of differentiation & # of mitoses
    • the close the cells resemble the normal cells the lower the grade
  60. clinical staging of tumors
    • size of primary tumor
    • extent of local growth
    • lymph node involvement
    • presence of distant metastisis
  61. TNM staging system
    • T 1-4 increasing size of primary tumor
    • N 0-3 advancing node involvement
    • M0-1 ansence or presence of distant mets
  62. radiation therapy
    • indirect ionization- cellular damage when x-rays absorbed into tissue & give up fast moving electrons which are absorbed & produce free radicals
    • immediately kill cells, delay cell cycle progression, nuclear damage
    • rapidly dividing & poorly differentated
  63. exponential killing
    number of survivingcells proportionate to drug dose & # cells at risk porporitonate to destructive action of drug
  64. cell-cycle specific drugs
    exert action during specific phase on cell cycle
  65. hormone/antihormone therapy
    deprive cancer cell of hormonal signals that stimulate them to survive
  66. GnRH gonadotropin-releasing hormone
    pharmocologic suppression of hormones at level of hypothalmus
  67. biologic response modifiers- interferons
    • inhibit tumor protein synthesis
    • prolong cell cycle
    • increase % cells in G0
    • stimulate NK & T-cells
    • types alpha, beta, gamma
  68. biologic response modifiers- interleukins
    cytokines that bind to reseptor sites on surface membrane of target cells

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