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444-Oncology and Neurology > Introduction to Oncology > Flashcards

Introduction to Oncology Flashcards

1
Q

cancer occurs when there is a genetic mutation that leads to

A

proliferation of a colony of malignant cells

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2
Q

define uncontrolled proliferation

A

cancer cells lack or fail to respond to normal mechanisms that control cell division or growth

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3
Q

what are some cellular changes of cancer

A

loss of some or all of their differentiation characteristics
some changes to chromosomes, proteins, enzymes
can’t perform ntended functions of origin tissue

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4
Q

solid tumors are classified by

A

their tissue of origin

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5
Q

carcinomas originated in

A

surface epithelium

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6
Q

adenocarcinomas originated in

A

glandular (epithelial) tissue

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7
Q

osteosarcoma originated in

A

bone (connective tissue)

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8
Q

rhabdomyosarcoma originated in

A

striated muscle (connective tissue)

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9
Q

leiomyosarcoma originated in

A

smooth muscle (connective tissue)

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10
Q

glioblastomas originate in

A

glial tissue (neural)

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11
Q

astrocytomas originate in

A

astrocytes (neural)

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12
Q

melanomas originate in

A

melanocytes (dermal tissue)

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13
Q

germinomas originate in

A

germ cells (gonadal tissues)

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14
Q

liquid or hematologic malignancies are classified based on ____ and further divided based on ________

A

cell origin
pathology/cell lineage and presentation

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15
Q

leukemia cell of origin

A

hematopoetic cells

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16
Q

lymphoma cell of origin

A

lymphoid tissue cells

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17
Q

multiple myeloma cell of origin

A

plasma cells

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18
Q

carcinogenesis 4 steps

A

initiation
promotion
conversion
progression

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19
Q

initiation is

A

genetic alteration / exposure to carcinogen

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20
Q

promotion is

A

carcinogens or other things changes the environment to favor the growth of the changed cell pp

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21
Q

conversion/ transformation is

A

the altered cells become cancerous

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22
Q

progression is

A

further genetic alterations that result in increased proliferation of cancerous cells

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23
Q

T or F: germline mutation is inherited and present in all cells

A

T

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24
Q

T or F: somatic gene mutation is acquired and only in some cells

A

T

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25
Q

a gene that has the potential to cause cancer

A

oncogene

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26
Q

oncogenes begin as ______ and are upregulated through mutations to oncogenes

A

protooncogenes

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27
Q

an activated oncogene leads to

A

excessive production of genetic product (cell signals/ products) = dysregulation

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28
Q

T or F: protooncogenes are normal and are still regulators of normal cellular function

A

T

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29
Q

the mutation that takes a protooncogene to an oncogene is usually

A

acquired

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30
Q

what regulates and inhibits inappropriate cellular growth and proliferation

A

tumor suppressor genes

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31
Q

damage to DNA repair genes results in

A

errors in DNA not corrected, leading to activation of oncogenes or deactivation of tumor suppressor genes

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32
Q

6 hallmarks of cancer

A
  1. sustained proliferative signaling
  2. replicative immortality
  3. resisting cell death
  4. evading growth suppressors
  5. inducing angiogenesis
  6. activating invasion and metastasis
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33
Q

T or F: cancer cells are differentiated

A

F- and can’t perform function of origin tissue

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34
Q

local metastasis generally invade the

A

lymphatic system

35
Q

distant metastasis commonly involve the

A

brain, lungs, bone, liver

36
Q

metastasis retain the characteristics of the ________________

A

primary cancer

37
Q

cancer’s 7 warning signs (referral)

A
  1. changing bowel/ bladder habits
  2. lump in breasts
  3. unusual bleed or discharge
  4. diff swallowing/ indigestion
  5. obvious changes in wart or mole
  6. chronic cough or hoarseness
38
Q

radiation therapy kills cancer cells or slows their growth by

A

damaging the DNA
(once DNA is damaged beyond repair = die)

39
Q

3 ways that surgery can treat cancer

A

removal of primary tumor
removal of lymph nodes
reduce metastases

40
Q

what therapy damages or kills dividing cells, targeting more rapidly reproducing cells

A

cytotoxic chemo

41
Q

what therapy impacts cell signaling or signal transduction within the cell by targeting specific gene mutations or cell surface receptors

A

targeted therapies

42
Q

immunotherapies MOA

A

influence the body’s immune response to malignant cells

43
Q

endocrine therapies MOA

A

manipulate hormone production or actions for cancers that are hormone dependent

44
Q

angiogenesis inhibitors MOA

A

impact cell signaling or processes that influences angiogenesis

45
Q

impetus for workup may include

A

palpation of a mass or nodule
routine lab tests
new or nonresolving sx
screening test results

46
Q

cancer pt workup includes

A

hx and physical exam (consider exposure to carcinogens)
lab tests (tumor markers if available)
imaging

47
Q

why is a pathologist dx essential

A

many benign tumors can mimic appearance of cancer

48
Q

tissue is obtained through a biopsy through

A

excision, core, or fine needle aspirate
(or surgical resection)

49
Q

what tests can be performed on tissues to characterize the maligancy

A

tumor classification
identify any biomarkers
determine tumor grade

50
Q

a tumor grade is assigned based on

A

histopathologic type
morphologic features
degree of differentiation

51
Q

`a higher tumor grade means

A

more aggressive tumor and worse prognosis

52
Q

indicative of pt survival independent of treatment received + indicator of innate tumor aggressiveness

A

prognostic biomarker

53
Q

indicative of therapeutic efficacy because there is an interaction between the biomarker and therapy on pt outcome

A

predictive biomarker

54
Q

identification and documentation of the structure of a specific DNA, RNA, or protein molecule for purpose of dx or characterization of a genetic disorder

A

molecular profiling

55
Q

what can summarize the somatic mutations present

A

molecular profiling

56
Q

testing samples of tissue (cancer) to look for changes in the chromosomes of the cells

A

cytogenetics

57
Q

gene mutation screening assays include

A

fluorescence in situ hybridization
PCR
next gen sequencing

58
Q

4 types of mutations

A

insertion
deletion
translocation
insertion

59
Q

trade of DNA pieces between chromosomes

A

translocation

60
Q

ki-67 measures

A

growth rate or doubling time
is a protein in dividing cells

61
Q

ki-67 is measured by

A

immunohistochemsitry

62
Q

ki-67 could be a _______ biomarker and provide insight into

A

prognostic
aggressiveness + response to chemo

63
Q

TNM system for staging solid tumors stands for

A

T- size of primary tumor
N- lymph node involvement
M- presence of metastases
S- serum markers (only for testicular cancer)

64
Q

cancer staging signifies the extent of disease for

A

solid tumors

65
Q

the higher the stage, the _____ the cancer

A

worse (0-4)

66
Q

define neoadjuvant chemo

A

use of chemo prior to local treatment
usually to increase effectiveness of later treatment by reducing tumor bruden

67
Q

define adjuvant therapy

A

use of a treatment after local treatment
may be to destroy residual or undetectable tumor cells/ reduce risk of recurrance

68
Q

palliative therapy is

A

use of a treatment to alleviate/ reduce sx, stabilize disease/ slow progression, improve/ maintain quality of life

69
Q

define induction therapy

A

giving chemo to induce remission

70
Q

define consolidation

A

after induction, given to keep pt in remission

71
Q

define maintenance after induction and consolidation

A

to hold remission

72
Q

considerations when choosing pharm for cancer

A

age, ECOG, comorbidities. cancer type/ stage/ grade, molecular profiling, tx goals

73
Q

what is the ECOG

A

a performance scale on 0-5 and informs how the disease is impacting a pt’s daily living abilities and inform tx decisions

74
Q

“cure” of cancer as a GOT is defined as _______________
and measured as ___________ in literature

A

pt is cancer free and expected to have a lifespan eq to general pop

literature/ trials = 5 yrs disease free survival

75
Q

for prolonging survival, antineoplastic pharmcol is measured in trials as

A

progression free survival = number/ proportion of pts that are still alive and free of disease progression

76
Q

what is median progression free survival

A

the time that 50% died/ progressed with cancer

77
Q

what is overall survival

A

proportion of pts that are still alive at any spec time
takes into account death of any cause- even from med toxicities

78
Q

antineoplastic agents often have a _____ therapeutic window

A

narrow

79
Q

dose limiting toxicity is

A

an agent’s specific toxicities that caps how much can be administered

80
Q

dosing can be based on

A

BSA
renal fxn
flat dosing
adj for organ fxn

81
Q

frequency for cytotoxic agents

A

given cyclically to give body time to recover

82
Q

frequency for targeted oral agents (small molecules_

A

many administered daily for several consecutive days followed by rest period

83
Q

freq for targeted IV therapies (monoclonal antibodies)

A

administered IV cyclically with chemo
v long half life

84
Q

concepts to max efficacy in combo therapies

A

each drug must have clinical activity against tumor alone
each drug should have a different MOA
combinations should be synergistic

444-Oncology and Neurology (22 decks)

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