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Oncology > Onc drugs (+ some genes) > Flashcards

Onc drugs (+ some genes) Flashcards

1
Q

Cyclophosamide MOA

A

MOA: alkylating agent –> DNA crosslinks

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2
Q

Cyclophosamide SE

A 
Hemorrhagic cystitis 2/2 acrolein excretion through kidneys, 
N/V, 
alopecia, 
BM suppression, 
fertility effects, 
2ndary malignancy
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3
Q

Cyclophosamide Indictaions

A

breast, bladder, lymphomas

also vasculitic dz w kidney involvement such as SLE and granylomatosis w/ polyangiitis

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4
Q

5-fluorouracil MOA

A

Pyrimidine analog w/ Fluorine in uracil: bioactivated to 5F-dUMP & complexes w/ folate → inhibits thymidylate synthase (which converts uracil to thymine) → ↓ dTMP → ↓ DNA and protein synthesis (because no thymine)

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5
Q

5-fluorouracil metabolism

A

80% broken down in liver by DPD

adjust dose for liver impairment (toxicity can occur in those w/ low levels of DPD)

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6
Q

5-fluoracil indications

A

colon, esophagus, anus, cervix

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7
Q

5-fluoracil SE

A

Myelosuppression (leukopenia, thrombocytopenia, anemia) Skin photosensitivity,

GI toxicity including mouth sores, ulcers, diarrhea–diarrhea can be life threatening

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8
Q

Methotrexate MOA

A

Binds dihydrofolate reductase (DHFR) and inhibits its action (which converts dihydrofolate to tetrahydrofolate) → thymidine can not be produced → inhibit DNA synthesis

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9
Q

Methotrexate metabolism

A

90% renal metabolism, must establish good renal function (GRF) before administering

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10
Q

Methotrexate indications

A 
Breast, head and neck, 
lymphoma, leukemia, 
trophoblastic neoplasms. 
Can be used in spinal fluid (not toxic to neural tissue)
Low dose = rheumatoid arthritis
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11
Q

Methotrexate special considerations

A

High dose must be given w/ leucovorin rescue to terminate toxic effects

Can accumulate in third spaces and delay elimination

Must monitor blood levels to help w/ leucovorin

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12
Q

Methotrexate SE

A

GI side effects (stomatitis) w/ ulceration, diarrhea

Bone marrow suppression w/ leukopenia, thrombocytopenia, anemia,

hepatotoxicity (cumulative dose related), can be fatal

serious dermatologic toxicity (epidermal necrolysis, stevens johnsons, necrosis, etc – recovery reported w/ tx discontinuation

Renally excreted = must have good kidney fnx

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13
Q

Cytosine arabinoside MOA

A

Converted to ara-CTP and incorporated into DNA to cause strand termination. Also inhibits DNA and RNA polymerase

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14
Q

Cytosine arabinoside indications

A

Mostly for acute leukemia; can be safely administered into CSF

given continuous IV because of short 1/2 life

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15
Q

Cytosine arabinoside SE

A

GI: stomatitis, sometimes w/ ulceration/diarrhea

BM suppression: leukopenia, thrombocytopenia, anemia

Neurologic toxicity: mild peripheral neuropathy to acute cerebral and cerebellar syndromes (potentially fatal)

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16
Q

Fludarabine MOA

A

inhibits DNA polymerase

Mostly cleared via kidneys

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17
Q

Fludarabine indications

A

progressive or refractory B cell chronic lymphocytic leukemia (CLL)

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18
Q

Fludarabine SE

A

GI: N/V, anorexia, diarrhea
BM suppression
neurotixicy ranging from mild to fatal at higher than recommended doses

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19
Q

Gemcitabine MOA

A

Converted to two forms:
Diphosphate blocks DNA synth by inhibiting ribonucleotide reductase,
triphosphate form incorporated into DNA to inhibit DNA polymerase

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20
Q

Gemcitabine indications

A

metastatic pancreatic cancer (also erlotinib)

breast, lung, ovarian

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21
Q

Gemcitabine SE

A

GI: N/V, anorexia, diarrhea, hepatotoxicity

BM suppression w/ sequelae

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22
Q

Vincristine MOA

A

vinca alkaloid

Bind to tubulin dimer to prevent incorporation into microtubules → blocks mitotic spindle

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23
Q

Vincristine metabolism

A

extensive hepatic metabolism through CYP3A4 – must be used w/ caution in pts w/ impaired liver fnx. 80% excreted in feces

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24
Q

Vincristine SE / CI

A

note that it does NOT cause BM suppression or N/V!
FATAL if given intrathecally
Neurotoxicity –> peripheral neuropathy, can lead to weakness in distal muscles

Autonomic NS – impaired gut motility / constipation (place puts on bowel regimen). Postural hypotension. Bladder atony

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25
Q

Cisplatin MOA

A

Platinum binds adjacent G’s on DNA,
bending strand and causing
HMG1, UBF, MSH-2 to bind and
cause apoptosis (crosslinks DNA)`

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26
Q

Cisplatin Indications

A

Lung
ovaries
esophagus
head and neck

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27
Q

Cisplatin SE

A

N/V – one of the worst.

Nephrotoxicity: renal tubules. dose-limiting toxicity– must aggressively hydrate w / diuresis to lower amt

Impaired electrolyte metabolism: low Mg, K, Ca

Neurotoxicity: peripheral neuropathy

Ototoxicity: bilateral hearing loss in about 20 %, worse in kids

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28
Q

Doxorubicin MOA

A

1) intercalates into DNA which inhibits transcription process
2) inhibits topoisomerase II (which normally simultaneously cuts both strands of DNA to manage supercoils) –> strand break can’t be re-ligated
3) Generates free radicals, can damage cellular components like DNA and cell membrane

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29
Q

Doxorubicin uses

A
  • solid tumors like breast cancer
  • ALL, AML (heme)
  • Part of “R-CHOP” for B cell lymphoma)
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30
Q

Doxorubicin SE

A

Irreversible cardiomyopathy (left ventricular dysfunction) – dose related
GI: N/V, stomatitis, diarrhea
BM suppression,
Alopecia,
2ndary malignancies (usually hematologic) like AML and MDS, which present 2-3 years post-therapy
Severe skin/soft tissue damage if exposed

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31
Q

Paclitaxel MOA

A

Microtubulin inhibitors → help stabilize the microtubules/interfere with normal breakdown of microtubules during cell division

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32
Q

Paclitaxel indications

A

Breast cancer
non small cell lung
ovarian

others

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33
Q

Paclitaxel SE

A

most common: peripheral neuropathy

Alopecia
BM suppression
GI w/ N/V, mucositis and diarrhea

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34
Q

Irinotecan MOA

A

Inhibits topoisomerase I →prevents DNA from re-ligating the strand breaks → ultimately leads to apoptosis

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35
Q

Irnotecan indications

A

metastatic colon cancer

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36
Q

Irnotecan SE

A

BM suppression
Diarrhea, potentially serious. Shortly after can be treated w/ atropine, if develops after 24 hours can be severe leading to electrolyte imbalance and potentially death. Treat aggressively w/ loperamide and fluid/electrolyte repletion

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37
Q

Etoposide MOA

A

Forms complex w/ DNA and topo II → prevents re-ligation of strand breaks → apoptosis

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38
Q

Etoposide indications

A

small cell lung cancer
testicular cancer
PTCL

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39
Q

Etoposide SE

A

N/V, BM suppression, alopecia, risk of 2ndary malignancy 2-3 years after tx

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40
Q

Bleomycin MOA

A

Abx isolated from strep verticillus, causes cell death through inducing DNA strand breaks (exact mechanism not totally known)

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41
Q

Bleomycin metabolism

A

many different tissues including liver, GI, skin, lungs kidneys. 50-70% of active drug excreted in urine.

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42
Q

Bleomycin indications

A

testicular, some lymphoma, some H&N

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43
Q

Bleomycin SE

A

Dose related pulmonary fibrosis (possibly through enhanced oxygen toxicity).

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44
Q

Bortezomib MOA

A

inhibits proteasome

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45
Q

Bortezomib Indications

A

Multiple myeloma

non-hodgkins Mantle Cell lymphoma

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46
Q

Bortezomib SE’s

A 
CYP2C19 and 3A4 metabolism
peripheral neuropathy in ~50% of pets
lower in those who receive it subQ vs IV
GI: n/v, diarrhea or constipation
BM suppression in ~1/3 of patients
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47
Q

Lenalidomide MOA

A

derivative of thalidomide
↓TNF-α and IL-6 → direct induction of apoptosis, anti-angiogenic
Dose dependent, G1 growth arrest
Enhances activity of dexamethasone

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48
Q

Lenalidomide metabolism

A

drug is excreted unchanged in kidney, dose adjustment in patients w/ renal dysfunction

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49
Q

Lenalidomide indications

A

MDS (5q), Multiple Myeloma (MM)

Bone marrow for MM patients shows increase in microvessel density which correlates w/ disease activities

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50
Q

Lenalidomide SE

A

GI: N/V, diarrhea or constipation

*BM suppression may be dose-limiting toxicity

Derm: pruritis and skin rashes
** Teratogenic (discovered because it was used for anti-emetic)
Increased risk for thrombosis (prophylactic anticoag is recommended)
Dose adjustment for renal dysfnx

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51
Q

Rituximab MOA

A

Anti-CD20 monoclonal antibodies expressed on lymphocytes of B-cell lineate → antibody dependent cytotoxicity and cell lysis via complement system

  • Direct lysis
  • Apoptosis
  • Complement binding
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52
Q

Rituximab indications

A

Hematological malignancies of cells that express CD20 (B cell lymphocytes)

Some rheumatologic disease

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53
Q

Rituximab SE

A
  • Infusion reactions esp after 1st tx: hypotension, bronchospasm, urticarial and cardiac arrhythmias
  • Hep B reactivation if latent
  • Rare: multifocal leukoencephalopathy
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54
Q

Trastuzumab MOA

A

aka Herceptin
Monoclonal Ab against HER-2, a tyrosine kinase EGF receptor → kills breast cancer cells that overexpress HER-2 via 3 mechanisms:
1. Blocks R dimerization → prevents cell signaling**
2. Ab-dependent cytotoxicity (ADCC)
3. Receptor down-regulation

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55
Q

Trastuzumab Indications

A

HER2+ breast cancer

gastric cancer

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56
Q

Trastuzumab SE

A

Reversible Cardiotoxicity → lowered LVEF
–> NEVER USE IN COMBO W/ DOXORUBICIN B/C ^RISK
“HEARTceptin damages the HEART.”
Infusion rxn w/ chills, fever, N/V, HA

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57
Q

Bevacizumab MOA

A

Monoclonal Ab against VEGF → inhibits angiogenesis

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58
Q

Bevacizumab indications

A

Metastatic colon cancer, metastatic cervical cancer, non-small cell lung cancer, RCC and GBM

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59
Q

Bevacizumab SE

A

HTN most common, hemorrhage/bleeding, thrombosis, impaired wound healing (contraindicated 3 weeks pre-surgery), GI perforation

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60
Q

Cetuximab MOA

A

Monoclonal Ab against extracellular domain of EGFR

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61
Q

Cetuximab Indications

A

Metastatic colon cancer w/ WT k-ras gene

squamous cell carcinoma

62
Q

Cetuximab SE

A

Acneiform skin rash → correlated w/ survival (if you have the rash it’s more likely it’s working). If you have a k-ras mutation, it will not work!
Infusion rxn in some pts

63
Q

Imatinib MOA

A

Small molecule inhibitor – sits in the TK spot and blocks it. –> Inhibits tyroxine kinase enzymes, notably fusion protein Bcr-Abl in chronic myelogenous leukemia and the c-kit molecule in GIST; prevents ATP phosphate transfer and blocks downstream signaling

64
Q

Imatinib indications

A

Hematological malignancies that have the t9:22 (“Philadelphia Chromosome”); includes most w/ CML and some with ALL. Also indicated for GIST that are c-kit+

“Philadelphia IMITates New York City”

65
Q

Imatinib SE

A

BM suppression, GI: N/V, diarrhea, fluid retention

Metabolized via CYP450, dose adjustments for liver dz

66
Q

Sorafenib MOA

A

Inhibits tyrosine kinases at VEGFR and Raf kinase

67
Q

Sorafenib Indications

A

advanced RCC, unresectable HCC and thyroid cancer

68
Q

Sorafenib SE

A

Dermatological: palmar-plantar erythrodysesthesia, alopecia, skin rashes
GI: diarrhea, abdominal pain, anorexia

69
Q

Erlotinib MOA

A

Reversible TKI which blocks ATP binding site on EGFR; has affinity for mutated EGFR

70
Q

Erlotinib Indications

A

Advanced metastatic non-small cell lung cancer, locally advanced or metastatic pancreatic cancer w/ gemcitabine

71
Q

Erlotinib SE

A

Dermatological: acneiform rash on face/neck
GI: anorexia & diarrhea

72
Q

Leuprolide MOA

A

GnRH agonist → causes downregulation of receptors and decreased LH/FSH secretion, T drops very low (after initial surge)

73
Q

Leuprolide Indications

A

prostate cancer

estrogen dependent breast cancer

74
Q

Leuprolide SE

A

Low T: Decreased libido and erectile dysfunction, loss of bone density
Due to initial LH/FSH surge, may cause tumor growth → bone pain, bladder obstruction, and spinal cord compression (for those w/ vertebral body mets)

75
Q

Bicalutamide MOA

A

Androgen Receptor Inhibitor → prevents stimulation and thus growth

76
Q

Bicalutamide indications

A

May be used as monotherapy or in combo w/ leuprolide to prevent tumor flare in metastatic prostate cancer

77
Q

Bicalutamide SE

A

Low T: decreased libido and sexual impotence

Hepatotoxicity

78
Q

Abiraterone MOA

A

Inhibits CYP-17 hydroxylase, (necessary precursor to T, DHEA and androstenedione), gets T levels to undetectable (prostate cell cancers themselves can make T)

79
Q

Abiraterone Indications

A

Metastatic prostate cancer (w/ prednisone)

80
Q

Abiraterone SE

A

Low T: decreased libido and sexual function

Decreased cortisol production, increased aldo → all patients need concomitant prednisone

81
Q

Tamoxifen MOA

A

Selective estrogen-R modulator (SERM) which binds Estrogen-R → SERM-ER complex has tissue-dependent treatment effects:

  • Breast = antagonist →blocked estrogen effect in tumor cells → no breast cell proliferation
  • Uterus & bone = agonist → activation & proliferation
82
Q

Tamoxifen Indications

A

5 year treatment of hormone-R+ BC (ER+/PR+ > ER-/PR+ > ER+/PR-)

Decreases recurrence by 50%

Can be used regardless of menopausal status (pre or post)

83
Q

Tamoxifen SE

A
  • ¬Slightly increased risk of endometrial cancer (1/1000)
  • Thromboembolic events aka DVT/PE (1/1000) similar to OCP
  • Cataracts
  • Vasomotor effects (hot flashes, night sweats)
84
Q

Anastrozole MOA

A

Aromatase Inhibitor → prevents conversion of testosterone into estradiol.

85
Q

Anastrozole Indications

A

Can only be used in postmenopausal women with hormone-R+ breast cancer

Lower recurrence than Tamoxifen in Kaplan-Meyer curve

86
Q

Anastrozole SE

A

Worsens bone mineral density → arthralgia, bone fractures (Contraindicated w/ hx of osteoporosis)
Other effects of low estrogen like hot flashes and vaginal dryness

87
Q

Tretinoin (ATRA) MOA

A

Trans Retinoic Acid – Differentiation agent. In PML, patients have t(15;17) w/ fused PML gene and retinoic acid receptor (RAR) gene. Fusion PML-RAR prevents maturation of precursor myeloid cells. Giving ATRA, co repressors dissociated from PML-RAR complex and inhibition of maturation is removed

88
Q

Tretinoin (ATRA) indications

A

Acute promyelocytic anemia (APL) with t(15;17) translocation

89
Q

Tretinoin (ATRA) SE

A

25% develop APL differentiation syndrome: fever, dyspnea, pericardial effusion, periph edema, kidney/liver failure. ½ cases are severe
40% develop rapid WBC increase→ treat w/ steroids
Elevated LFTs in ~1/2

90
Q

Filgrastim MOA

A

stimulates production/maturation of neutrophils

Hematopoietic growth factor: Analogue of G-CSF = glycoprotein that stimulates the bone marrow to produce granulocytes and stem cells and release them into the bloodstream

91
Q

Filgrastim indications

A

Reduce duration of leucopenia following intensive chemo and for mobilizing peripheral blood stem cells for harvesting prior to stem cell transplantation

92
Q

Filgrastim SE

A

Bone pain, splenic rupture (C/I in pts w/ splenomegaly)

93
Q

ipilimumab MOA

A

Anti-CTLA-4: Cytotoxic T Lymphocytes (CTLs) can recognize and destroy cancer cells. However, an evolutionary inhibitory mechanism that we have in place interrupts this destruction. Ipilimumab turns off this inhibitory mechanism and allows CTLs to go to town on the tumors.

(CTLA4 is found on the surface of T cells, and acts as an “off” switch when bound to CD80 or CD86 on the surface of antigen-presenting cells.)

94
Q

Ipilimumab indications

A

metastatic / late stage melanoma

95
Q

Ipilimumab SE

A

Severe and potentially fatal immunological adverse effects due to T cell activation/ proliferation. (e.g., ulcerative colitis, rash, diarrhea, hepatitis, adrenal insufficiency)

GI: stomach pain, bloating, constipation or diarrhea, but also fever, breathing or urinating problems

96
Q

Nivolumab MOA

A

Selectively inhibits programmed cell death-1 (PD-1R on T cell – apparently many tumors release PD1 and kill off the T cells that would otherwise attack it).

The neg PD-1 receptor signaling that regulates T cell activation is disrupted → release PD-1 mediated inhibition of immune response

97
Q

Nivolumab indications

A

metastatic head/neck cancer

98
Q

Nivolumab SE

A

GI probs, skin reactions like rash/itching, anemia, fever, stiff joints

99
Q

Arsenic Trioxide MOA

A

At higher concentration it induces apoptosis of the leukemic cells (blocks Bcl-2, a protein that, in high quantities, prevents apoptosis)

At lower concentration, it triggers differentiation with elevation of CD11b expression accompanied by morphologically partial differentiation.
In general: As2O3 causes degradation of PML-RAR alpha protein

100
Q

Arsenic Trioxide indications

A

Acute promyelocytic anemia (APL)

ATRA (tretinoin) + arsenic trioxide: ~90% cure rate

101
Q

Genetics of CML

A

t(9;22) - Involves genes BCR and Abl; Result is a chimeric protein with tyrosine kinase activity

102
Q

JAK2 V617F mutation

A

Polycythemia vera
Essential thrombocytosis
Primary myelofibrosis

103
Q

Acute myeloid leukemia genetics

A

Inv(16), t(8;21): These mutations are associated with a good prognosis and make it less likely that the patient will require a hematopoietic stem cell transplant

104
Q

Acute promyelocytic leukemia genetics

A

t(15;17): Involves genes RAR and PML

105
Q

Follicular lymphoma genetics

A

t(14;18): Results in activation of Bcl-2 gene which is anti-apoptotic

106
Q

Burkitt’s lymphoma genetics

A

t(8;14)- Chromosome 8 has myc proto-ongene; the translocation results in its activation
t(8;22) t(2;8)

107
Q

Meds for ALL

A

Methotrexate (folate antagonist)
Vincristine (microtubule inhibitor)
Doxorubicin (topo II inhibitor)
Cyclophosamide (alkylating agent)

(Asparaginase)
(Dexamethasone + Prenidsone_

108
Q

Meds for CLL

A

Rituximab (anti-CD20) – SUPER important
cyclophosamide (alkylating agent)
Fludaribine (inhibits DNA polymerase)
F+C+R is one tx regimen

109
Q

Meds for AML

A

Cytarabine (cytosine arabinoside) + anthracycline (like doxorubicin) -

110
Q

Meds for testicular cancer

A

Cisplatin
Etoposide
Bleomycin

111
Q

Meds for hepatocellular

A

Sorafenib - Inhibits tyrosine kinases at VEGFR and Raf kinase

only works in setting of metastatic disease, not for adjuvant therapy

112
Q

Meds for APL (acute promyelocytic anemia)

A

Tretinoin (ATRA), disinhibits maturation

Arsenic trioxide

113
Q

Meds for MDS syndrome

A

EPO and Filgrastim (G-CSF- stimulate blood production)

MDS w/ -5q = lenalidomide

114
Q

Meds for CML

A

Imatinib - inhibits Brc-Abl tyrosine kinase (CML) and c-kit in GIST; prevents ATP phosphate transfer and blocks downstream signaling

115
Q

Meds/tx for Polycythemia Vera (PV)

A

Phlebotomy
if iron deficient w/ phleb, tx with interferon alpha 40 but prob don’t need to know that.

Low dose aspirin to prevent thrombosis

116
Q

Meds/tx for Essential Thrombocytosis (ET)

A

Low dose aspirin for low risk (

117
Q

Meds/tx for Myelofibrosis (MF)

A

Supportive: EPO, transfusions, hydroxyurea to control WBC count, splenectomy

Active: SC transplant (potential cure), thalidomide/steroids, JAK inhibitors

118
Q

Meds/tx for CLL

A

Cyclophosamide
Fludarabine (progressive or refractory)
Rituximab - super important

119
Q

Meds/tx for Follicular Lymphoma

A

watch/wait (incurable)

Rituximab sometimes

120
Q

Meds/tx for DLBCL

A 
R-CHOP:
Rituximab
Cyclophosamide
Doxorubicin (H)
Vincristine (O)
Prednisone
121
Q

Meds/tx for Burkitt’s Lymphoma

A

CODOX-M/IVAC regimen (cyclophosphamide, vincristine, doxorubicin, high-dose methotrexate / ifosfamide, etoposide, high-dose cytarabine

122
Q

Meds/tx for Mantle Cell Lymphoma

A

Bortezomib: proteasome inhibitor

SE: peripheral neuropathy

123
Q

Waldenstrom’s tx/meds

A

Plasmapheresis to get rid of excess IgM

124
Q

Meds for PTCL

A

Etoposide

transplant at first remission

125
Q

Meds for ATLL (Adult T Cell Leukemia/Lymphoma)

A 
subtype of PTCL
treat w/ EPOCH:
Etoposide
Prednisone
Vincristine (Oncovin)
Cyclophosamide
Doxorubicin Hydrochloride (H)
126
Q

Meds for Hodgkin’s

A 
“ABVD” is standard of care
Doxorubicin (Adriamycin) 
Bleomycin
Vinblastine/Vincristine
Decarbazine (alkylating agent)

relapse treated w/ salvage chemo

127
Q

Meds for Multiple Myeloma

A

Step 1: Transplant if candidate
Step 2: Lenalidomide & Bortezomib

If bone disease complications:
Add bisphosphonates (be aware of ONJ - dental check first)
Kyphoplasty – put cement in the bone hole?

128
Q

Pancreatic cancer Meds

A

Gemcitabine - blocks DNA synth by inhibiting DNA polymerase and ribonucleotide reductase

Erlotinib - reversible TKI for EGFR

129
Q

Erythropoietin indications

A

MDS, PM

130
Q

Meds for prostate cancer

A

Leuprolide (GnRH agonist, downregulates)
Bicalutamide (androgen receptor inhib)
Abiraterone (metastatic, tx also w/ prednisone)

131
Q

H&N meds

A

5FU (SE: stomatitis, diarrhea)
Cisplatin (SE: Nausea, renal & ototoxicity)
Paclitaxel (SE: peripheral neuropathy)
Cetuximab (SE: acneiform rash)

Newer: Nivolumab (PD-1 disinhibition of T cells)

132
Q

Metastatic H and N

A

Cetuximab

133
Q

Melanoma meds

A

Ipilimumab

Nivolumab – much more tolerable that ipi

If PD1 low, IPI + Nivo is best, if PD1 high, nivo alone works just fine – doing this to prevent toxicity of dual therapy because diarrhea is bad :(

134
Q

GIST meds

A

Imatinib - Imatinib blocks Tyrosine Kinase (BCR-Abl), and stops it from adding phosphate groups. As a result, cells stop growing and die via apoptosis.

(c-kit mutation)

135
Q

Retinoblatoma gene mutation

A

Inactivating mutations in Rb in hereditary and sporadic forms

136
Q

Lung cancer gene mutations

A

EGFR mutations are both predictive and prognostic (these pts do better – also respond to Erlotinib)

EML4-ALK fusion gene

137
Q

Colon cancer genes

A

Activating mutations in k-ras

Inactivating mutations in APC

Inactivating mutations in the DNA “spell-checking” genes (MLH1, MSH2, MSH6, PMS2) in Lynch’s syndrome and sporadic cases

138
Q

Pancreatic cancer gene mutations

A

Activating k-ras in 90% of cases

139
Q

GIST gene mutation

A

c-kit – constitutive activation of the TK function of c-kit leads to uncontrolled cell prolif.

140
Q

Rhabdomyosarcoma gene mutation

A

PAX-FKHR gene fusion (alveolar – has better prognosis than embryonal)

141
Q

Ewing’s sarcoma gene mutation

A

EWS-FLI1 gene fusion

142
Q

Malignant melanoma gene mutations

A

BRAFV-600E
MEK1

MEK1 is next step so we have to block both to prevent resistance to meds

143
Q

Biliary cancer meds

A

gemcitabine + cisplatin

it’s rare so think genetics for BC – could be FAP, BRCA2, and APC syndromes

144
Q

Cervical cancer meds

A

Cisplatin

metastatic: palliative; cisplatin, paclitax, bevacizumab. poor prog

145
Q

3 drugs that cause 2ndary heme malignancy as a side effect

A

Cyclophosamide
Etoposide
Doxorubicin

146
Q

Meds for uterine/endometrial cancer

A

Cisplatin
Doxorubicin
Paclitaxel

147
Q

Meds for ovarian cancer

A

Cisplatin + Paclitaxel

148
Q

Meds for ovarian cancer

A

Cisplatin
Paclitaxel

For recurrent can also try others

149
Q

Meds/tx for small cell lung cancer

A

Cisplatin – platinum doublets
Etoposide

Concurrent w/ radiotherapy = better than sequential

PCI - prophylactic cranial irradiation to prevent brain metastasis

150
Q

Meds/tx for non-small cell lung cancer

A

Cisplatin + other agent like gemcitabine or taxane

Erlotinib in pt’s with activating EGFR mutation (this is the one w/ acneiform rash, makes sense cause “epidermal” growth factor) –> good prognosis for these pts

151
Q

Meds for esophageal cancer

A

Unresectable: 5-fluorouracil, Cisplatin, Paclitaxel

Also irnotecan

Trastuzumab (herceptin) For ErbB2+ esophageal/gastric cancer

152
Q

Meds for stomach cancer

A

Chemo w/ 5-Fluorouracil & Leucovorin

Herceptin for ErbB2+

Oncology (1 decks)

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