Onc drugs (+ some genes) Flashcards
1
Q
Cyclophosamide MOA
A
MOA: alkylating agent –> DNA crosslinks
2
Q
Cyclophosamide SE
A
Hemorrhagic cystitis 2/2 acrolein excretion through kidneys, N/V, alopecia, BM suppression, fertility effects, 2ndary malignancy
3
Q
Cyclophosamide Indictaions
A
breast, bladder, lymphomas
also vasculitic dz w kidney involvement such as SLE and granylomatosis w/ polyangiitis
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)
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)
6
Q
5-fluoracil indications
A
colon, esophagus, anus, cervix
7
Q
5-fluoracil SE
A
Myelosuppression (leukopenia, thrombocytopenia, anemia) Skin photosensitivity,
GI toxicity including mouth sores, ulcers, diarrhea–diarrhea can be life threatening
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
9
Q
Methotrexate metabolism
A
90% renal metabolism, must establish good renal function (GRF) before administering
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
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
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
13
Q
Cytosine arabinoside MOA
A
Converted to ara-CTP and incorporated into DNA to cause strand termination. Also inhibits DNA and RNA polymerase
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
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)
16
Q
Fludarabine MOA
A
inhibits DNA polymerase
Mostly cleared via kidneys
17
Q
Fludarabine indications
A
progressive or refractory B cell chronic lymphocytic leukemia (CLL)
18
Q
Fludarabine SE
A
GI: N/V, anorexia, diarrhea
BM suppression
neurotixicy ranging from mild to fatal at higher than recommended doses
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
20
Q
Gemcitabine indications
A
metastatic pancreatic cancer (also erlotinib)
breast, lung, ovarian
21
Q
Gemcitabine SE
A
GI: N/V, anorexia, diarrhea, hepatotoxicity
BM suppression w/ sequelae
22
Q
Vincristine MOA
A
vinca alkaloid
Bind to tubulin dimer to prevent incorporation into microtubules → blocks mitotic spindle
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
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
25
Cisplatin MOA
Platinum binds adjacent G's on DNA,
bending strand and causing
HMG1, UBF, MSH-2 to bind and
cause apoptosis (crosslinks DNA)`
26
Cisplatin Indications
Lung
ovaries
esophagus
head and neck
27
Cisplatin SE
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
28
Doxorubicin MOA
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
29
Doxorubicin uses
- solid tumors like breast cancer
- ALL, AML (heme)
- Part of "R-CHOP" for B cell lymphoma)
30
Doxorubicin SE
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
31
Paclitaxel MOA
Microtubulin inhibitors → help stabilize the microtubules/interfere with normal breakdown of microtubules during cell division
32
Paclitaxel indications
Breast cancer
non small cell lung
ovarian
others
33
Paclitaxel SE
most common: peripheral neuropathy
Alopecia
BM suppression
GI w/ N/V, mucositis and diarrhea
34
Irinotecan MOA
Inhibits topoisomerase I →prevents DNA from re-ligating the strand breaks → ultimately leads to apoptosis
35
Irnotecan indications
metastatic colon cancer
36
Irnotecan SE
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
37
Etoposide MOA
Forms complex w/ DNA and topo II → prevents re-ligation of strand breaks → apoptosis
38
Etoposide indications
small cell lung cancer
testicular cancer
PTCL
39
Etoposide SE
N/V, BM suppression, alopecia, risk of 2ndary malignancy 2-3 years after tx
40
Bleomycin MOA
Abx isolated from strep verticillus, causes cell death through inducing DNA strand breaks (exact mechanism not totally known)
41
Bleomycin metabolism
many different tissues including liver, GI, skin, lungs kidneys. 50-70% of active drug excreted in urine.
42
Bleomycin indications
testicular, some lymphoma, some H&N
43
Bleomycin SE
Dose related pulmonary fibrosis (possibly through enhanced oxygen toxicity).
44
Bortezomib MOA
inhibits proteasome
45
Bortezomib Indications
Multiple myeloma
| non-hodgkins Mantle Cell lymphoma
46
Bortezomib SE's
```
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
```
47
Lenalidomide MOA
derivative of thalidomide
↓TNF-α and IL-6 → direct induction of apoptosis, anti-angiogenic
Dose dependent, G1 growth arrest
Enhances activity of dexamethasone
48
Lenalidomide metabolism
drug is excreted unchanged in kidney, dose adjustment in patients w/ renal dysfunction
49
Lenalidomide indications
MDS (5q), Multiple Myeloma (MM)
| Bone marrow for MM patients shows increase in microvessel density which correlates w/ disease activities
50
Lenalidomide SE
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
51
Rituximab MOA
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
52
Rituximab indications
Hematological malignancies of cells that express CD20 (B cell lymphocytes)
Some rheumatologic disease
53
Rituximab SE
- Infusion reactions esp after 1st tx: hypotension, bronchospasm, urticarial and cardiac arrhythmias
- Hep B reactivation if latent
- Rare: multifocal leukoencephalopathy
54
Trastuzumab MOA
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
55
Trastuzumab Indications
HER2+ breast cancer
| gastric cancer
56
Trastuzumab SE
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
57
Bevacizumab MOA
Monoclonal Ab against VEGF → inhibits angiogenesis
58
Bevacizumab indications
Metastatic colon cancer, metastatic cervical cancer, non-small cell lung cancer, RCC and GBM
59
Bevacizumab SE
HTN most common, hemorrhage/bleeding, thrombosis, impaired wound healing (contraindicated 3 weeks pre-surgery), GI perforation
60
Cetuximab MOA
Monoclonal Ab against extracellular domain of EGFR
61
Cetuximab Indications
Metastatic colon cancer w/ WT k-ras gene
| squamous cell carcinoma
62
Cetuximab SE
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
Imatinib MOA
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
Imatinib indications
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
Imatinib SE
BM suppression, GI: N/V, diarrhea, fluid retention
| Metabolized via CYP450, dose adjustments for liver dz
66
Sorafenib MOA
Inhibits tyrosine kinases at VEGFR and Raf kinase
67
Sorafenib Indications
advanced RCC, unresectable HCC and thyroid cancer
68
Sorafenib SE
Dermatological: palmar-plantar erythrodysesthesia, alopecia, skin rashes
GI: diarrhea, abdominal pain, anorexia
69
Erlotinib MOA
Reversible TKI which blocks ATP binding site on EGFR; has affinity for mutated EGFR
70
Erlotinib Indications
Advanced metastatic non-small cell lung cancer, locally advanced or metastatic pancreatic cancer w/ gemcitabine
71
Erlotinib SE
Dermatological: acneiform rash on face/neck
GI: anorexia & diarrhea
72
Leuprolide MOA
GnRH agonist → causes downregulation of receptors and decreased LH/FSH secretion, T drops very low (after initial surge)
73
Leuprolide Indications
prostate cancer
| estrogen dependent breast cancer
74
Leuprolide SE
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
Bicalutamide MOA
Androgen Receptor Inhibitor → prevents stimulation and thus growth
76
Bicalutamide indications
May be used as monotherapy or in combo w/ leuprolide to prevent tumor flare in metastatic prostate cancer
77
Bicalutamide SE
Low T: decreased libido and sexual impotence
| Hepatotoxicity
78
Abiraterone MOA
Inhibits CYP-17 hydroxylase, (necessary precursor to T, DHEA and androstenedione), gets T levels to undetectable (prostate cell cancers themselves can make T)
79
Abiraterone Indications
Metastatic prostate cancer (w/ prednisone)
80
Abiraterone SE
Low T: decreased libido and sexual function
| Decreased cortisol production, increased aldo → all patients need concomitant prednisone
81
Tamoxifen MOA
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
Tamoxifen Indications
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
Tamoxifen SE
- ¬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
Anastrozole MOA
Aromatase Inhibitor → prevents conversion of testosterone into estradiol.
85
Anastrozole Indications
Can only be used in postmenopausal women with hormone-R+ breast cancer
Lower recurrence than Tamoxifen in Kaplan-Meyer curve
86
Anastrozole SE
Worsens bone mineral density → arthralgia, bone fractures (Contraindicated w/ hx of osteoporosis)
Other effects of low estrogen like hot flashes and vaginal dryness
87
Tretinoin (ATRA) MOA
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
Tretinoin (ATRA) indications
Acute promyelocytic anemia (APL) with t(15;17) translocation
89
Tretinoin (ATRA) SE
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
Filgrastim MOA
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
Filgrastim indications
Reduce duration of leucopenia following intensive chemo and for mobilizing peripheral blood stem cells for harvesting prior to stem cell transplantation
92
Filgrastim SE
Bone pain, splenic rupture (C/I in pts w/ splenomegaly)
93
ipilimumab MOA
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
Ipilimumab indications
metastatic / late stage melanoma
95
Ipilimumab SE
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
Nivolumab MOA
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
Nivolumab indications
metastatic head/neck cancer
98
Nivolumab SE
GI probs, skin reactions like rash/itching, anemia, fever, stiff joints
99
Arsenic Trioxide MOA
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
Arsenic Trioxide indications
Acute promyelocytic anemia (APL)
| ATRA (tretinoin) + arsenic trioxide: ~90% cure rate
101
Genetics of CML
t(9;22) - Involves genes BCR and Abl; Result is a chimeric protein with tyrosine kinase activity
102
JAK2 V617F mutation
Polycythemia vera
Essential thrombocytosis
Primary myelofibrosis
103
Acute myeloid leukemia genetics
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
Acute promyelocytic leukemia genetics
t(15;17): Involves genes RAR and PML
105
Follicular lymphoma genetics
t(14;18): Results in activation of Bcl-2 gene which is anti-apoptotic
106
Burkitt's lymphoma genetics
t(8;14)- Chromosome 8 has myc proto-ongene; the translocation results in its activation
t(8;22) t(2;8)
107
Meds for ALL
Methotrexate (folate antagonist)
Vincristine (microtubule inhibitor)
Doxorubicin (topo II inhibitor)
Cyclophosamide (alkylating agent)
(Asparaginase)
(Dexamethasone + Prenidsone_
108
Meds for CLL
Rituximab (anti-CD20) -- SUPER important
cyclophosamide (alkylating agent)
Fludaribine (inhibits DNA polymerase)
F+C+R is one tx regimen
109
Meds for AML
Cytarabine (cytosine arabinoside) + anthracycline (like doxorubicin) -
110
Meds for testicular cancer
Cisplatin
Etoposide
Bleomycin
111
Meds for hepatocellular
Sorafenib - Inhibits tyrosine kinases at VEGFR and Raf kinase
only works in setting of metastatic disease, not for adjuvant therapy
112
Meds for APL (acute promyelocytic anemia)
Tretinoin (ATRA), disinhibits maturation
| Arsenic trioxide
113
Meds for MDS syndrome
EPO and Filgrastim (G-CSF- stimulate blood production)
| MDS w/ -5q = lenalidomide
114
Meds for CML
Imatinib - inhibits Brc-Abl tyrosine kinase (CML) and c-kit in GIST; prevents ATP phosphate transfer and blocks downstream signaling
115
Meds/tx for Polycythemia Vera (PV)
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
Meds/tx for Essential Thrombocytosis (ET)
Low dose aspirin for low risk (
117
Meds/tx for Myelofibrosis (MF)
Supportive: EPO, transfusions, hydroxyurea to control WBC count, splenectomy
Active: SC transplant (potential cure), thalidomide/steroids, JAK inhibitors
118
Meds/tx for CLL
Cyclophosamide
Fludarabine (progressive or refractory)
Rituximab - super important
119
Meds/tx for Follicular Lymphoma
watch/wait (incurable)
| Rituximab sometimes
120
Meds/tx for DLBCL
```
R-CHOP:
Rituximab
Cyclophosamide
Doxorubicin (H)
Vincristine (O)
Prednisone
```
121
Meds/tx for Burkitt's Lymphoma
CODOX-M/IVAC regimen (cyclophosphamide, vincristine, doxorubicin, high-dose methotrexate / ifosfamide, etoposide, high-dose cytarabine
122
Meds/tx for Mantle Cell Lymphoma
Bortezomib: proteasome inhibitor
SE: peripheral neuropathy
123
Waldenstrom's tx/meds
Plasmapheresis to get rid of excess IgM
124
Meds for PTCL
Etoposide
| transplant at first remission
125
Meds for ATLL (Adult T Cell Leukemia/Lymphoma)
```
subtype of PTCL
treat w/ EPOCH:
Etoposide
Prednisone
Vincristine (Oncovin)
Cyclophosamide
Doxorubicin Hydrochloride (H)
```
126
Meds for Hodgkin's
```
“ABVD” is standard of care
Doxorubicin (Adriamycin)
Bleomycin
Vinblastine/Vincristine
Decarbazine (alkylating agent)
```
relapse treated w/ salvage chemo
127
Meds for Multiple Myeloma
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
Pancreatic cancer Meds
Gemcitabine - blocks DNA synth by inhibiting DNA polymerase and ribonucleotide reductase
Erlotinib - reversible TKI for EGFR
129
Erythropoietin indications
MDS, PM
130
Meds for prostate cancer
Leuprolide (GnRH agonist, downregulates)
Bicalutamide (androgen receptor inhib)
Abiraterone (metastatic, tx also w/ prednisone)
131
H&N meds
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
Metastatic H and N
Cetuximab
133
Melanoma meds
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
GIST meds
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
Retinoblatoma gene mutation
Inactivating mutations in Rb in hereditary and sporadic forms
136
Lung cancer gene mutations
EGFR mutations are both predictive and prognostic (these pts do better -- also respond to Erlotinib)
EML4-ALK fusion gene
137
Colon cancer genes
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
Pancreatic cancer gene mutations
Activating k-ras in 90% of cases
139
GIST gene mutation
c-kit -- constitutive activation of the TK function of c-kit leads to uncontrolled cell prolif.
140
Rhabdomyosarcoma gene mutation
PAX-FKHR gene fusion (alveolar -- has better prognosis than embryonal)
141
Ewing's sarcoma gene mutation
EWS-FLI1 gene fusion
142
Malignant melanoma gene mutations
BRAFV-600E
MEK1
MEK1 is next step so we have to block both to prevent resistance to meds
143
Biliary cancer meds
gemcitabine + cisplatin
| it's rare so think genetics for BC -- could be FAP, BRCA2, and APC syndromes
144
Cervical cancer meds
Cisplatin
metastatic: palliative; cisplatin, paclitax, bevacizumab. poor prog
145
3 drugs that cause 2ndary heme malignancy as a side effect
Cyclophosamide
Etoposide
Doxorubicin
146
Meds for uterine/endometrial cancer
Cisplatin
Doxorubicin
Paclitaxel
147
Meds for ovarian cancer
Cisplatin + Paclitaxel
148
Meds for ovarian cancer
Cisplatin
Paclitaxel
For recurrent can also try others
149
Meds/tx for small cell lung cancer
Cisplatin -- platinum doublets
Etoposide
Concurrent w/ radiotherapy = better than sequential
PCI - prophylactic cranial irradiation to prevent brain metastasis
150
Meds/tx for non-small cell lung cancer
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
Meds for esophageal cancer
Unresectable: 5-fluorouracil, Cisplatin, Paclitaxel
Also irnotecan
Trastuzumab (herceptin) For ErbB2+ esophageal/gastric cancer
152
Meds for stomach cancer
Chemo w/ 5-Fluorouracil & Leucovorin
| Herceptin for ErbB2+
