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ABSITE > 11 Oncology > Flashcards

11 Oncology Flashcards

1
Q

what cancer (with mets) are most successfully cured with surgery?

A

colon ca in liver and sarcoma to lung but survival will STILL be low overall

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2
Q

which protein causes angiogenesis and is involved with tumor mets?

A

V-EGF (vascular epidermal growth factor)

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3
Q

what cancer (with mets) are most successfully cured with surgery?

A

colon ca in liver and sarcoma to lung but survival will STILL be low overall

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4
Q

which malignancies are HIV-related?

A

kaposi’s sarcoma and non-hodgkin’s lymphoma

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5
Q

what are the cutaneous T-cell lymphomas?

A

HTLV-1 (skin lesions) and mycosis fungoides (sezary cells)

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6
Q

which solid tumors are curable with chemotherapy only?

A

hodgkin’s and nonhodgkin’s lymphoma

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7
Q

what are prognostic indicators for survival after resection of hepatic colorectal mets?

A

disease-free interval > 12 months tumor number < 3 CEA < 200 size < 5 cm negative nodes

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8
Q

can en bloc multi-organ resection attempted?

A

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

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9
Q

what is 5 year survival for colon mets to liver if successfully resected?

A

35%

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10
Q

when is palliative surgery considered?

A

for tumors of hollow viscus causing obstruction or bleeding (colon ca), or breast ca with skin or chest wall involvement

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11
Q

how are lymph nodes good signs of probable mets?

A

they have poor barrier function

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12
Q

when is salvage therapy given?

A

for tumors that fail to respond to initial chemotherapy

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13
Q

what is adjuvant therapy?

A

combined with another modality; given after other therapy is used

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14
Q

what is primary therapy, when is it used? what is another name?

A

neoadjuvant. chemo given 1st (usually), followed by another (secondary) therapy

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15
Q

what is induction therapy, when is it used?

A

sole treatment; used for advanced disease or when no other tx exists

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16
Q

what are the types of therapy?

A

induction, primary, adjuvant, salvage

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17
Q

what question does a phase IV clinical trial answer?

A

implementation and marketing

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18
Q

what question does a phase III clinical trial answer?

A

is it better than existing therapy?

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19
Q

what question does a phase II clinical trial answer?

A

is it effective?

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20
Q

what question does a phase I clinical trial answer?

A

is it safe and at what dose?

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21
Q

which cancers cause small bowel mets?

A

melanoma (#1)

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22
Q

which cancers cause skin mets?

A

breast, melanoma

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23
Q

which cancers cause bone mets?

A

breast (31), prostate

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24
Q

which cancers can cause ovarian mets?

A

stomach (krukenberg tumor), colon

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25
Q

which cancers are associated with a suspicious periumbilical node? what is that node called?

A

pancreas. Sister Mary Joseph’s node

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26
Q

which cancers are associated with suspicious axillary node?

A

lymphoma (#1), breast, melanoma

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27
Q

what cancers can give you suspicious supraclavicular nodes?

A

neck, breast, lung, stomach (virchow’s node), pancreas

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28
Q

what cancer does asbestos give you?

A

mesothelioma

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29
Q

what cancer does benzene give you?

A

leukemia

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30
Q

what cancer does beta-naphthylamine give you?

A

urinary tract ca (bladder ca)

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31
Q

what cancer does coal tar give you?

A

larynx, skin, bronchial ca

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32
Q

what are common carcinogens?

A

coal tar, beta-naphthylamine, benzene, asbestos

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33
Q

does colon ca met to bone?

A

not usually

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34
Q

which gene is the initial step in teh evolution of colorectal ca?

A

APC

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35
Q

which genes are involved in colon cancer?

A

APC, p53, DCC, K-ras

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36
Q

what is li-fraumeni syndrome?

A

defect in p53 gene. childhood sarcomas, breast ca, brain tumors, leukemia, adrenal ca

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37
Q

when mutated, which proto-oncogene is responsible for unregulated production of ranscription factors?

A

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

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38
Q

when mutated, which proto-oncogene is responsible for an epidermal growth factor receptor defect?

A

erb B

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39
Q

when mutated, which proto-oncogene is responsible for a G protein defect?

A

ras

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40
Q

when mutated, which proto-oncogene is responsible for a platelet derived growth factor receptor defect?

A

sis

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41
Q

when mutated, which proto-oncogene is responsible for a tyrosine kinase defect?

A

src

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42
Q

what are the proto-oncogenes?

A

ras, src, sis, erb B, myc

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43
Q

what are the tumor suppressor genes?

A

Rb1, p53, APC, DCC, bcl, BRCA

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44
Q

which tumor suppressor gene is located on chromosome 18?

A

DCC.

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45
Q

what does APC gene do?

A

tumor suppressor gene involved with cell cycle regulation and movement

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46
Q

which tumor suppressor gene is located on chromosome 5?

A

APC

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47
Q

what does normal p53 gene do, and what happens when it is abnormal?

A

p53 normally induces cell arrest and apoptosis. abnormal p53 allows unrestrained cell growth

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48
Q

which tumor suppressor gene is located on chromosome 17?

A

p53

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49
Q

which tumor suppressor gene is located on chromosome 13?

A

Rb1

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50
Q

which tumor suppressor genes are involved in apoptosis?

A

bcl

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51
Q

which tumor suppressor genes are involved in cell adhesion?

A

DCC

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52
Q

which tumor suppresor genes are involved with cell cycle regulation?

A

retinoblastoma (Rb1), P53, APC

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53
Q

which organs can you resect to PREVENT cancer (resecting normal organs)?

A

Breast: BRCA I or II w strong family history

Thyroid when pt has RET proto-oncogene with FH of thyroid ca

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54
Q

what is GCSF side effect?

A

sweet’s syndrome (acute febrile neutropenic dermatitis)

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55
Q

what is GCSF used for?

A

neutrophil recovery after chemo

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56
Q

what is GCSF?

A

granulocyte colony-stimulating factor

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57
Q

which cancer drugs have the least myelosuppression?

A

bleomycin, vincristine, busulfan, cisplatin

58
Q

what does topoisomerase do?

A

unwinds DNA

59
Q

what is another name for etoposide?

60
Q

what does etoposide do?

A

inhibits topoisomerase.

61
Q

what are teh toxicities of doxorubicin and at what doses?

A

heart toxicity 2/2 O2 radicals at doses >500mg/m^2

62
Q

what does doxorubicin do?

A

DNA intercalator. creates O2 radicals

63
Q

what cancer-related drug should you avoid with 5FU?

A

leucovorin (folinic acid). it increases toxicity of 5FU

64
Q

what does thymidylate synthetase do?

A

inhibits purine and DNA synthesis

65
Q

what does 5-fluorouracil do?

A

5FU inhibits thymidylate synthetase

66
Q

how do you reverse effects of methotrexate?

A

leucovorin rescue (folinic acid): resupplyies folate

67
Q

what are side effects of methotrexate?

A

renal toxicity, radiation recall

68
Q

how does methotrexate work?

A

inhibits dihydrofolate reductase (DHFR), which inhibits purine and DNA synthesis.

69
Q

what is levamisole?~ what does it do?

A

anthelminthic drug. thought to stimulate immune system against cancer

70
Q

what drug can help with hemorrhagic cystitis that is given with cyclophosphamide?

71
Q

what are the side effects of cyclophosphamide?

A

gonadal dysfunction, SIADH, hemorrhagic cystitis

72
Q

what is the active metabolite in cyclophosphamide?

73
Q

how do alkylating agents work?

A

transfer alkyl groups; form covalent bonds to DNA.

74
Q

what are the toxicities of vinblastine?

A

bone (myelo) suppression. vinBlastine

75
Q

how does vinblastine work?

A

microtubule inhibitor

76
Q

what are the toxicities of vincristine?

A

peripheral neuropathy, neurotoxic

77
Q

how does vincristine work?

A

microtubule inhibitor

78
Q

what are the toxicities of carboplatin?

A

bone (myelo) suppression. carBoplatin

79
Q

what is carboplatin?

A

platinum alkylating agent.

80
Q

what are the toxicities of cisplatin?

A

nephrotoxic, neurotoxic, ototoxic

81
Q

how does cisplatin work?

A

platinum alkylating agent

82
Q

what are the risks of bleomycin and busulfan?

A

cause pulmonary fibrosis

83
Q

how does taxol work?

A

promotes microtubule formation and stabilization that can’t be broken down; cells are ruptured

84
Q

what happens to the risk of blood clots and endometrial cancer when taking tamoxifen?

A

blood clot risk inc by 1%, endometrial ca risk by 0.1%

85
Q

how much does tamoxifen decrease short term (5 year) risk of breast ca?

86
Q

how does tamoxifen work?

A

blocks estrogen receptor

87
Q

what is the difference in response between cell cycle specific and nonspecific agents?

A

specific agents have a plateau in cell-killing ability. nonspecific agents have a linear response to cell killing

88
Q

what are the cell-cycle specific agents?

A

5FU, methotrexate.

89
Q

hwat is brachytherapy, what are the elements used?

A

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

90
Q

why are large tumors less responsive to XRT?

A

they lack oxygen in the tumor

91
Q

which tumors are very radioresistant?

A

epithelial, sarcomas

92
Q

which tumors are very radiosensitive?

A

seminomas, lymphomas

93
Q

what is fractionate XRT?

A

an xr dose that is distrubted over multiple courses

94
Q

what are the benefits of fractionate XRT doses?

A

allows repair of normal cells (tumor cells can’t repair as fast), allows re-oxygenation of tumor, allows redistribution of tumor cells in cell cycle

95
Q

why is lower energy radiation worse than higher energy radiation?

A

high energy radiation has skin preserving effect (max ionizing potential isn’t reached until deeper structures)

96
Q

what is the main target for oxygen radicals and XRT?

97
Q

what causes the most carcinogenic damage to cells/DNA and in what situation is can you get the max effect?

A

formation of oxygen radicals. maximal effect with high oxygen levels

98
Q

when is the most vulnerable stage of the cell cycle for cancer when undergoing XRT?

99
Q

what is the infectious agent for various lymphomas?

100
Q

what is the infectious agent for burkitt’s lymphoma?

101
Q

what is the infectious agent for nasopharyngeal carcinoma?

102
Q

what is the infectious agent for hepatocellular carcinoma?

A

hep B and hep C viruses

103
Q

what is the infectious agent for gastric cancer?

104
Q

what is the infectious agent for cervical cancer?

A

human papillomavirus (HPV)

105
Q

what are proto-oncogenes?

A

human genes w malignant potential

106
Q

what is an example of a retrovirus that contains oncogenes?

A

EBV, associated with burkitt’s lymphoma (8:14) translocation) and nasopharyngeal CA (c-myc)

107
Q

how do retroviruses give cancer?

A

they contain oncogene

108
Q

how do neoplasms arise?

A

carcinogenesis (eg smoking), viruses (eg EBV), or immunodeficiency (eg HIV)

109
Q

what are the steps of cancer within the latency period?

A

initiation: carcinogen acts with DNA
promotion of cancer cells then occurs
progression of cancer cells to clinically detectable tumor.

110
Q

what is the definition of latency period?

A

time between exposure and formation of clinically detectable tumor

111
Q

what is the definition of cancer transformation?

A

heritable alteration in genome AND loss of growth regulation

112
Q

what is the half life of AFP?

113
Q

what is the half life of PSA?

114
Q

what is the half life of CEA?

115
Q

what is the tumor marker for thyroid medullary ca?

A

Ret oncogene

116
Q

what is the tumor marker for carcinoid tumor?

A

chromogranin A

117
Q

what is the tumor marker for breast ca?

A

BRCA I and II

118
Q

what is the tumor marker for neuroblastoma?

119
Q

what is the tumor marker for small cell lung cancer?

120
Q

what is sensitivity and specificity of PSA?

A

high sensitivity, low specificity

121
Q

what is the tumor marker for prostate ca?

122
Q

what is the tumor marker for choriocarcinoma?

123
Q

what is the tumor marker for testicular cancer?

124
Q

what is the tumor marker for ovarian ca?

125
Q

what is the tumor marker for pancreatic ca?

126
Q

what is the tumor marker for liver cancer?

127
Q

what is the tumor marker for colon ca?

128
Q

what is dysplasia?

A

altered size, shape, organization (eg Barrett’s dysplasia)

129
Q

what is an example of metaplasia?

A

GERD squamous epithelium in esophagus changed to columnar gastric tissue (eg Barrett’s esophagus)

130
Q

what is metaplasia?

A

replacement of one tissue with another

131
Q

what is hyperplasia?

A

increased number of cells

132
Q

how do you know if a cell is a tumor based on antigen?

A

you don’t know. tumor antigens are random unless it’s a viral-induced tumor

133
Q

what do natural killer cells need to attack tumor cells?

A

they dont need anything. they can independently attack tumor cells

134
Q

what do cytotoxic T cells need to attack a tumor?

A

the MHC complex

135
Q

what type of molecules does PET detect?

A

fluorodeoxyglucose molecules

136
Q

what is PET used for?

A

identify mets

137
Q

what is the MC cancer in men?

138
Q

what is the MC cause of cancer related death in women?

A

lung cancer

139
Q

what is the MC Ca in women?

140
Q

what is the #2 cause of death in the US?

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