Chapter 11: Oncology Flashcards

1
Q

MC cancer related death in women

A

Lung cancer

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2
Q

MC Cancer in men

A

Prostate cancer

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3
Q

Need MHC complex to attack tumor

A

Cytotoxic T cells

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4
Q

Can independently attack tumor cells

A

Natural killer cells

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5
Q

Tumor marker: colon ca

A

CEA

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6
Q

Tumor marker: liver CA

A

AFP

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7
Q

Tumor marker: pancreatic CA

A

CA 19-9

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8
Q

Tumor marker: Ovarian ca

A

CA 125

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9
Q

Tumor marker: testicular Ca, choriocarcinoma

A

Beta-HCG

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10
Q

Tumor marker: prostate CA

A

PSA

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11
Q

Prostate CA: thought to be tumor marker with the highest sensitivity, although specificity is low

A

PSA

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12
Q

Tumor marker: small cell lung CA, neuroblastoma

A

NSE

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13
Q

Tumor marker: breast CA

A

BRCA I and II

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14
Q

Tumor marker: carcinoid tumor

A

Chromogranin A

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15
Q

Tumor marker: thyroid medullary CA

A

Ret oncogene

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16
Q

Half life: CEA

A

18 days

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17
Q

Half life: PSA

A

18 days

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18
Q

Half life: AFP

A

5 days

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19
Q

Oncogenesis: time between exposure and formation of clinically detectable tumor

A

Latency period

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20
Q

Three phases of latency period

A
  1. Initiation (carcinogen acts with DNA)
  2. Promotion (then occurs)
  3. Progression (cancers cells to clinically detectable tumor)
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21
Q

What do retroviruses contain?

A

Oncogenes

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22
Q

Associated with Burkitt’s lymphoma (8:14 translocation) and nasopharyngeal CA (c-myc)

A

Ebstein-Barr Virus

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23
Q

Infectious agent: nasopharyngeal carcinoma

A

EBV

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24
Q

Infectious agent: Burkitt’s lymphoma

A

EBV

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25
Q

Infectious agent: various lymphomas

A

HIV

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26
Q

Most vulnerable stage of cell cycle for XRT

A

M phase

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27
Q

Radiation therapy: what causes most of the damage?

A

Most damage to DNA done by formation of oxygen radicals -> maximal effect with high oxygen levels

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28
Q

How does high-energy radiation have a skin–preserving effect?

A

Maximal ionizing potential not reached until deeper structures

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29
Q

What do fractionate XRT doses allow?

A
  • Repair of normal cells
  • Re-oxygenation of tumor
  • Redistribution of tumor cells in the cell cycle
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30
Q

Very radiosensitive tumors

A

Seminomas, lymphomas

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31
Q

Very radioresistant tumors

A

Epithelial, sarcomas

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32
Q

Brachytherapy

A

Source of radiation in or next to tumor (Au-198, I-128); delivers high, concentrated doses of radiation

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33
Q

Chemo Agent: exhibit plateau in cell-killing ability

A

Cell cycle-specific agents (5FU, methotrexate)

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34
Q

Chemo Agent: Linear response to cell killing

A

Cell cycle-nonspecific agents

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35
Q

Chemo Agent: Decreases short-term (5 year) risk of breast CA 45%

A

Tamoxifen (blocks estrogen receptor)

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36
Q

Complications: tamoxifen therapy

A

1% risk of blood clots

0.1 % risk of endometrial cancer

37
Q

Chemo Agent: promotes microtubule formation and stabilization that cannot be broken down; cells are ruptures

A

Taxol

38
Q

Chemo Agent: can cause pulmonary fibrosis

A

Bleomycin

Busulfan

39
Q

Chemo Agent: nephrotoxic, neurotoxic, ototoxic

A

Cisplatin (platinum alkylating agent)

40
Q

Chemo Agent: bone (myelo) suppression

A

Carboplatin (platinum alkylating agent) and

Vinblastine (microtubule inhibitor)

41
Q

Chemo Agent: peripheral neuropathy, neurotoxic

A

Vincristine (microtubule inhibitor)

42
Q

Cyclophosphamide

A

Alkylating agent: transfer alkyl groups; forms covalent bonds to DNA

  • Acrolein is the active metabolite.
  • Side effects: gonadal dysfunction, SIADH, hemorrhagic cystitis
43
Q

Tx: hemorrhagic cystitis s/t cyclophosphamide

A

Mesna

44
Q

Chemo Agent: antihelminthic drug thought to stimulate immune system against cancer

A

Levamisole

45
Q

Methotrexate

A

Chemo Agent: inhibits dihydrofolate reductase (DHFR), which inhibits purine and DNA synthesis
- Side effects: renal toxicity, radiation recall

46
Q

Reverses effects of methotrexate by re-supplying folate

A

Leucovorin rescue (folinic acid)

47
Q

5-fluorouracil (5FU)

A

Chemo Agent: inhibits thymidylate synthetase, which inhibits purine and DNA syntehsis

48
Q

Increases toxicity of 5-fluorouracil

A

Leucovorin (folinic acid)

49
Q

Doxorubicin

A

Chemo Agent: DNA intercalator, oxygen radical formation

50
Q

Side effects: doxorubicin

A

Heart toxicity secondary to oxygen radicals at total doses > 500 mg/m^2.

51
Q

Etoposide (VP-16)

A

Chemo Agent: inhibits topoisomerase (which normally unwinds DNA)

52
Q

Chemo Agents: least myelosuppression

A

Bleomycin, vincristine, busulfan, cisplatin

53
Q

GCSF (granulocyte colony-stimulating factor

A

Used for neutrophil recovery after chemo

Side effect - Sweet’s syndrome (acute febrile neutropenic dermatitis)

54
Q

When to consider resection of a normal organ to prevent cancer -> breast

A

BRCA I or II with strong family history

55
Q

When to consider resection of a normal organ to prevent cancer -> thyroid

A

RET proto-oncogene with family history thyroid cancer

56
Q

Tumor suppressor gene: chromosome 13; involved in cell cycle regulation

A

Retinoblastoma

57
Q

p53

A

Tumor suppressor gene: chromosome 17; involved in cell cycle
Normal gene induces cell cycle arrest and apoptosis; abnormal gene allows unrestrained cell growth

58
Q

APC

A

Tumor suppressor gene: chromosome 5, involved with cell cycle regulation and movement

59
Q

DCC

A

Tumor suppressor gene: chromosome 18; involved in cell adhesion

60
Q

bcl

A

Tumor suppressor gene: involved in apoptosis (programmed cell death)

61
Q

Chromosome: p53

A

17

62
Q

Chromosome: APC

A

5

63
Q

Chromosome: DCC

A

18

64
Q

ras

A

Proto-oncogene: G protein defect

65
Q

src

A

Proto-oncogene: tyrosine kinase defect

66
Q

sis

A

Proto-oncogene: platelet-derived growth factor receptor defect

67
Q

erb B

A

Proto-oncogene: epidermal growth factor receptor defect

68
Q

myc (c-myc, n-myc, l-myc)

A

Proto-oncogenes: transcription factors

69
Q

Li-Fraumeni syndrome

A

Defect in p53 gene -> patients get childhood sarcomas, breast CA, brain tumors, leukemia, adrenal CA

70
Q

Colon cancer

A
  • Gene involved in development include APC, p53, DCC, and K-ras
  • APC though to be initial step in evolution
  • Does not usually go to bone
71
Q

Carcinogens: coal tar

A

Larynx, skin, bronchial CA

72
Q

Carcinogens: beta-naphthylamine

A

Urinary tract CA (bladder CA)

73
Q

Carcinogens: benzene

A

Leukemia

74
Q

DDX: suspicious supraclavicular node

A

Neck, breast, lung, stomach (Virchow’s node), pancreas

75
Q

DDX: suspicious axillary node

A

Lymphoma (#1), breast, melanoma

76
Q

DDX: suspicious periumbilical node

A

Pancreas (Sister Mary Joseph’s node)

77
Q

DDx: ovarian metastases

A

Breast (#1), prostate

78
Q

DDx: skin metastases

A

Breast, melanoma

79
Q

DDx: small bowel metastases

A

Melanoma (#1)

80
Q

Clinical trials:

  • Phase 1
  • Phase 2
  • Phase 3
  • Phase 4
A
  • Phase 1: Is it safe and at what dose?
  • Phase 2: Is it effective?
  • Phase 3: Is it better than existing therapy?
  • Phase 4: implementation and marketing
81
Q

What is induction therapy?

A

Sole treatment; use for advanced disease or when no other treatment exists

82
Q

En bloc multiorgan resection

A

Can be attempted for some tumors (colon into uterus, adrenal into liver, gastric into spleen); aggressive local invasiveness is different from metastatic disease

83
Q

Colon metastases to the liver: prognosis

A

35% 5-year survival rate if successfully resected

84
Q

Prognostic indictors for survival after resection of hepatic colorectal metastases

A

Disease-free interval > 12 months, tumor number

85
Q

One of the few tumors for which surgical debunking improves chemotherapy (not seen in other tumors)

A

Ovarian CA

86
Q

Curable solid tumors with chemotherapy only

A

Hodgkin’s and non-Hodgkin’s lymphoma

87
Q

T cell lymphomas

A
HTLV-1 (skin lesions)
Mycosis fungoides (Sezary cells)
88
Q

HIV related malignancies

A

Kaposi’s sarcoma, non-Hodgkin’s lymphoma

89
Q

Causes angiogenesis; involved in tumor metastasis

A

V-EGF (Vascular epidermal growth factor)