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Oncology Class > Final exam > Flashcards

Final exam Flashcards

1
Q

What are opioid conversions?

A

Morphine - 10mgIV = 30mgPO
Oxycodone - 20mgPO
Hydromorphone - 1.5mgIV = 7.5mgPO

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2
Q

What is length time bias?

A

Asymptomatic patients are more likely to have less aggressive malignancies, so screening appears to increase survival time

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3
Q

What factors affect the number needed to screen?

A

Frequency of testing
Prevalence of disease
Duration of follow-up

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4
Q

Cervical cancer screening guidelines

A

<21: no screening
21-65: pap q3y OR pap/HPV q5y (age 30+)
>65: no screening unless high risk

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5
Q

Breast cancer screening guidelines

A

40-49: pt discussion
50-74: q2y mammo
>75: no mammo

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6
Q

Lung ca screening guidelines

A

50-80 AND >20py OR currently smoking OR smoking in last 15 yrs = q1y LDCT

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7
Q

Prostate ca screening guidelines

A

55-69: joint decision making
>70: no screening

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8
Q

Colon ca screening guidelines

A

45-75: q10y colonoscopy
76-85: pt discussion
>85: no screening

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9
Q

What is the difference between Sanger and NGS?

A

Sanger: sequences one fragment at a time, good for small analysis
NGS: sequences millions of fragments simultaneously

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10
Q

What is a diagnostic biomarker? Example?

A

Characteristic that indicates what disease the patient has. Melan-a

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11
Q

What is a prognostic biomarker? Example

A

A marker that indicates risk of disease recurrence. Oncotype DX DCIS score

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12
Q

What is a predictive biomarker? Example

A

marker that indicates what treatment will most likely benefit the patient. NGS for solid tumors

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13
Q

what is a pharmacokinetic biomarker? example?

A

marker that indicates what drug dose should be given to the patient. G6PD for rasburicase.

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14
Q

How do you treat MSI-high CRC?

A

PD-1 blockade (pembro)

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15
Q

What molecular markers should you check for stage IV CRC?

A

KRAS, NRAS, BRAF, MSI, HER2 (BRHNK mnemonic)

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16
Q

How do you treat BRAF V600E stage IV CRC?

A

BRAF/MEK (can lead to phenotype switch to MMR deficient)

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17
Q

How do you treat HER2 stage IV CRC?

A

trastuzumab + TKI (better than TKI alone)

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18
Q

Why has KRAS been considered undruggable?

A

binding pocket on GTPase is hard to access, approaches have had high toxicity

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19
Q

How do you treat KRAS+ stage IV CRC?

A

Can use adagrasib + chemo (cetuximab)

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20
Q

MOA enzalutamide, darolutamide, apalutamide

A

binds to the androgen receptor to prevent androgen signaling

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21
Q

MOA abiraterone

A

blocks 17alpha-hydroxylase, reduces production of T

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22
Q

docetaxel MOA

A

inhibits microtubule formation (S phase)

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23
Q

MOA PARPis

A

stabilizes single-stranded DNA breaks, this inhibition gives time for a double-stranded break to form and the cell to apoptose

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24
Q

when do you test for somatic/germline mutations in prostate cancer?

A

metastatic disease

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25
Q

what is the ideal ratio of basal:demand for PCA?

A

2:1 (1:2 if prominent incident pain)

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26
Q

how do you determine basal rate for PCA?

A

determine total opioid in 24hr, convert to IV hourly rate, put 75% in basal considering cross-tolerance

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27
Q

what are three common mutations in AML?

A

DNMT3A (enzyme that catalyzes DNA methylation)
FLT3 (TK cytokine receptor)
IDH1

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28
Q

How does DNMT3A cause cells to be pre-leukemic?

A

biases fate decisions toward self-renewal rather than differentiation

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29
Q

what is 7+3 treatment?

A

common treatment for AML
7days cytarabine, 3 days daunorubicin

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30
Q

what is CPX-351?

A

a capsule containing both cytarabine and daunorubicin, delivers drug into the intracellular space, maintains ratio, does not rely on transporters

31
Q

what is gemtuzimab? where does it bind?

A

a mab attached to chemotherapy (ozogamicin). binds CD33 –> brought into endosome, degraded by lysosome, chemo is released into the cytoplasm and can make its way to the nucleus

32
Q

what is venetoclax?

A

blocks Bcl2, leading to cell death
used in AML

33
Q

What is azacitidine

A

a hypomethylating agent (typically reserved for patients ineligible for induction

34
Q

What is quizartinib? AEs?

A

FLT3 blocker for AML, QT prolongation

35
Q

What is ivosidenib? AEs?

A

IDH1 blocker, differentiation syndrome

36
Q

what is differentiation syndrome?

A

increased cytokine release and rapid differentiation of myeloid precursor cells. leads to fever, weight gain, peripheral edema, hypotension, acute renal failure, interstitial pulmonary infiltrates

37
Q

what are the stages of multiple myeloma?

A

initiation –> MGUS –> smoldering myeloma –> MM (intramedullary to extramedullary)

38
Q

what is bortezomib?

A

treatment for MM
binds proteosome, prevents degradation of pro-apoptotic factors, leads to programmed cell death

39
Q

red flags for hereditary cancer

A

early age of diagnosis
same types of cancer in close relatives, multiple generations
less common cancers
multiple cancers associated with same gene
Ashkenazi Jewish

40
Q

when is radiation therapy necessary post-mastectomy?

A

> =4LNs+ OR >=5cm

41
Q

what patients are more likely to benefit from endocrine therapy than chemo?

A

lobular histology, low grade, strong ER expression, low oncotype score

42
Q

list 4 actionable mutations in breast cancer

A

BRCA1/2 - PARPi
ESR1 - elecestrant
PIK3CA - alpelisib
PI3K, PTEN, AKT1 - capivasertib

43
Q

what is pancreatic cancer association with depression?

A

tumors make IDO1, shunts tryptophan away from serotonin synthesis, instead makes kynurenine

44
Q

What do you have to keep in mind with fluoxetine, paroxetine, bupropion use?

A

CYP2D6 inhibitors, interfere with tamoxifen

45
Q

what are the four steps of pre-clinical drug discovery?

A

target identification
hit generation
lead generation
preclinical studies in animals

46
Q

What are four characteristics important to be a successful drug candidate?

A

high potency
favorable pharmocokinetics
developability
good toxicity profile

47
Q

How does a PROTAC work?

A

binding of E3 ligase to target protein, ubiquitination and destruction of protein

48
Q

which cancers have the most diverse somatic mutations?

A

lung adenocarcinoma, stomach, head and neck

49
Q

What mechanisms contribute to the mutational spectra of melanoma, GI tumors, lung cancer?

A

melanoma- w/ and w/o UV factors
GI tumors- w/ and w/o MMR
lung cancer- w/ and w/o exposure to environmental carcinogens (cigarette smoke)

50
Q

Why do BRAF inhibitors not work in CRC?

A

EGFR is upregulated at baseline, mediates MAPK signaling through RAS shortly after deactivation of BRAF

51
Q

What are the phases of CML?

A

Chronic (<10% blasts) - luekocytosis, hypercellular marrow
Advanced
Accelerated (10-19% blasts, basophils, platelets, splemomegaly)
Blast phase (<20% blasts)

52
Q

what is the most frequent gatekeeper mutation in CML?

A

T315I

53
Q

list mechanisms of acquired resistance to targeted therapy

A

gatekeeper mutations
bypass pathways
mutations in pathways downstream of oncogene
morphological change
persistence of cancer stem cells
changes in microenvironment

54
Q

three genes most commonly mutated in SCLC?

A

RB1, p53, KMT2d (small park)

55
Q

lung adenocarcinoma most common mutations

A

p53, EGFR, KRAS (peak-ras)

56
Q

lung SCC most common mutations

A

p53, CDKN2A, KMT2d (pecks)

57
Q

indications for immunotherapy in NSCLC

A

advanced: PDL1>50% pembro, PDL1<50% pembro+chemo, stage III, N2 and N3

58
Q

side effects of checkpoint inhibitors

A

pneumonitis, myocarditis, myositis, nephritis, colitis, hepatitis

59
Q

what is the warburg effect?

A

cancer cells replace normal oxygen respiration with fermentation of sugar

shunt pyruvate to lactate, foregoing the efficient oxidative phosphorylation for the quicker aerobic glycolysis

60
Q

how does obesity lead to higher risk for cancer?

A

obesity causes chronic inflammation (oncogenic)
tumors activate oncogenes that lead to inflammation, obese tissue is conducive
high leptin:adiponectin ratio in adipose tissue creates an environment conducive to cell proliferation

61
Q

how does estrogen drive ER+ breast cancer

A

ER dependent: binds to ER, acts as TF for genes including MYC, Bcl2, and FOXM1
ER independent: metabolism of estrogen in cytoplasm leads to metabolites with genotoxic effects

62
Q

what are effects of phytoestrogens on the estrogen receptor?

A

low concentrations in vitro: promote tumor growth
high concentrations in vitro: inhibit tumor growth

63
Q

what are the steps involved in metastasis?

A

development of metastatic cell
establishment of premetastatic niche
motility and invasion
intravasation
dissemination and transport
cellular arrest, vascular adhesion, extravasation
colonization

64
Q

name 3 ways surgery can induce inflammatory responses

A

immunosuppression (systemic)
NETs - associated with metastatic risk
neovascularization

65
Q

nonsynonymous mutation that leads to cancer?

A

PTEN

66
Q

common copy number variant?

A

HER2

67
Q

common in/del?

A

EGFR exon 19 del

68
Q

common frameshift mutation

A

PTEN c800delA (premature stop codon)

69
Q

common splice site mutation

A

KIT in GIST

70
Q

common structural variant

A

ALK fusion in NSCLC

71
Q

how is sanger sequencing used in cancer (specific example)?

A

1790T>G in BRAF

72
Q

primary goals of cancer phase I trials

A

identify DLT and MTD

73
Q
A

Oncology Class (1 decks)

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