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Flashcards in cancer Deck (138)
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1
Q

Atezolizumab

A

binds to PD-L1 (program death ligand) and blocks its interaction with PD-1
used in treatment of locally advanced or metastatic urothelial carcinoma
exclusions: autoimmune disease and medical conditions requiring immunosuppression

2
Q

Brentuximab

A

anti CD30 antibody conjugated to monomethyl auristatin E (MMAE) - so toxic it cannot be used alone
Reed-Sternberg cells express CD30
conjugation to the antibody targets the compound to the lymphoma cells

3
Q

Ipilimumab

A

CTL (cytotoxic T lymphocyes) will recognize and destroy malignant tumor cells - CTLA-4 is normally inhibitory of this action
binds to the CTLA-4 receptor and reverses CTL inhibition
used to treat advanced metatstatic melanoma

4
Q

Pembrolizumab and Nivolumab

A

binds to PD-1 (program death-1) receptor and blocks its interaction with PD-Ligand 1 and 2 (PD-L1 and PD-L2)
blockade of PD-1 prevents inhibitory signaling withing T-cells leading to enhanced tumor cell killing
treatment of metastatic melanoma following treatment with Ipilimumab and (if BRAF V600 mutation positive) a BRAF inhibitor
also approved for NSCLC if the patients tumor biopsy tests + for PD-L1

5
Q

Blinatumomab

A

bispecific T-cell engaging antibody (BiTE)
redirects T cells to lyse CD-19 positive malignant and nonmalignant B-cells
idea is to physically bring an activated T-cell into proximity with the tumor cell
the activated T-cell will then lyse the tumor cells
treatment of B-cell leukemia

6
Q

Sipucel-T

A

recombinant human protein (PAP) linked to an immune cell activator (GM-CSF)
APCs collected from a patient, activated ex vivo with PAP-GM-CSF and then reinfused into that individual patient
stimulates patients own immune system to attack cancer
treatment of minimally symptomatic metastatic hormone-refractory prostate cancer

7
Q

naming antibodies

A

mouse = ___omab
chimeric = ___ximab
humanized = ___zumab
fully humab = ___umab

8
Q

Aldesleukin

A

IL-2 recombinant protein
primary action is to stimulate proliferation of activated T cells bearing IL-2 receptors - enhances lymphocyte mitogenesis and cytotoxicity, also activated NK cells

9
Q

interferon-a

A

produced by a variety of cells
biological properties: immunomodulatory effects, antiviral effects, inhibition of cell proliferation, inhibition of angiogenesis, regulation of cell differentiation, and enhancement of specific antigen expression
therapeutic benefits multifactoral - antiproliferative, enhanced host immune response
excellent response rate in: newly diagnosed CML and cutaneous T cell lymphoma, hairy cell leukemia, superficial bladder cancer

10
Q

afilbercept

A

fusion protein consisting of vascular endothelial growth factor (VEGF) receptors 1 and 2 to the Fc portion of human IgG1
used in combination with 5FU, levocovorin, irinotecan for patients with metastatic colorectal cancer that is resistant to or has progressed following an oxaliplatin-contaning regimen

11
Q

romidepsin

A
inhibits HDACs (histone deacetylases) and promotes euchromatin leading to reexpression of tumor suppressor genes and tumor cell death
treatment of cutaneous and peripheral T-cell lymphoma in patients who have received at least 1 prior therapy
12
Q

vorinostat

A

HDAC inhibitor
treatment of patient with cutaneous T-cell lymphoma who have progressive, persistent or recurrent disease on or following two systemic therapies

13
Q

belinostat

A

HDAC inhibitor

treatment of patients with relapsed or refractory peripheral T-cell lymphoma (PTCL)

14
Q

azacytidine

A

DNMT inhibitor that results in the reactivation of tumor suppressor genes
treatment of patients with myelodysplastic syndrome (MDS)
AEs: leukopenia, thrombocytopenia, neutropenia

15
Q

decitabine

A

treatment of myelodysplastic syndrome (MDS)

16
Q

tretinoin

A

also known as all trans retinoic acid receptor (ATRA)
binds to retinoic acid receptor (RAR)
promotes differentiation and inhibits proliferation
studied as cancer prevention, also used topically to treat acne
success in treatment of acute promyelocytic leukemia (APL) where RAR has undergone a fusion with the PML gene
ATRA converts PML-RAR into a transcriptional activator and induces differentiation of leukemic cells and subsequent complete remission in a high % of patients

17
Q

bexarotene

A

agonists for retinoid X receptors (RXRs)
treatment of T-cell lymphoma
RXRs for heterodimers with other receptor partners and once activated function as transcription factors that regulate the expression of genes that increase cellular differentiation, inhibit proliferation and induce apoptosis

18
Q

thalidomide

A

anti-angiogenic activity - blocks bFGF and VEGF
treatment of multiple myeloma in combination with dexamethasone
toxicity - potent teratogen!!

19
Q

pomalidomide

A

analog of thalidomide
treatment of multiple myeloma
REMS

20
Q

lenalidomide

A
analog of thalidomide
multiple myeloma (MM), myeloplastic syndrome (MDS) , mantle cell lymphoma
21
Q

caflizomib and bortezomib

A

inhibitors of proteasome activity - disruption of protein homeostasis leads to cell death
treatment of multple myeloma (a B-cell malignancy)
bortezomib is reversible, carflizomib is irreversible
carflizomib lacks the neuropathy SEs of bortezomib

22
Q

visemodebig and sonidegib

A

treatment of basal cell carcinomas
hedgehog binds to patched and inhibition on smoothened and leads to nuclear translocation of GLI1 - 90% of basal cell carcinomas have mutations in either patched or smoothen activating pathway

23
Q

venetoclax

A

BCL-2 inhibitor that drives cell death via apoptosis
BCL-2 is anti-apoptotic protein overexpressed in several tumor cells - leads to apoptotic resistance
treatment of chronic lymphocytic leukemia

24
Q

oxemacetaxine

A

inhibits protein translocation
inhibits initial elongation step of protein synthesis and prevents the correct positioning of AA side chains of incoming tRNAs
CML patients who have failed 2 or more BCR-Abl inhibitors

25
Q

asparginase

A

administration degrades circulating asparagine and depletes pools - leukemic cells are “starved”
induction therapy in childhood acute lymphoblastic leukemia

26
Q

denosumab

A

binds RANKL and prevents its interaction with RANK on osteoclasts
interrupts this “viscous cycle” if bone remodeling that is associated with bone metastasis
treatment of multiple myeloma and advanced breast and prostate cancer

27
Q

bisphosphonates

A

for metastatic bone disease
analogs of pyrophosphate, attach to bone surface, released during resorption, taken up by osteoclasts and inhibit bone resorption
inhibits vicious cycle of abnormal bone remodeling that occurs in metastatic cancer

28
Q

allopurinol

A

modulator of treatment-induced toxicity
completitively inhibits xanthine oxidase - important step in metabolism of purines to uric acid
important adjuvant drug for induction therapy in leukemias and lymphomas

29
Q

rasburicase

A

recombinant urate oxidase
breaks down uric acid to allantoin which can be excreted by the kidney
higher order mammals do not naturally express this protein
used for prevention and treatment of hyperuricemia in subjects receiving chemo

30
Q

netupitant and palonosetron

A

fixed combo of NK1 antagonist and 5-HT3 antagonist
chemo produces NV by stimulating enterchromaffin cells on small intestine
palonostron prevents NV during acute phase, netupiant prevents NV during the acute and delayed phase after chemo
indicated for prevention of acute and delayed NV associated with initial and repeat courses of chemo

31
Q

neupogen

A

stimulating factors
promotes proliferation and differentiation of granulocyte progenitors
reduces period of neutropenia following myelosuppressive chemo
indications include both prophylaxis and treatment of chemotherapy induced granulocytopenia

32
Q

sargramostim

A

stimulating factor
promotes growth and differentiation of granulocyte progenitors
reduces period of neutropenia following myelosuppressive chemo
indications: following induction of chemo in acute myelogenous leukemia (AML), mobilization of progenitors prior to harvesting cells for bone marrow transplant, myeloid reconstitution following bone marrow transplant

33
Q

oprelvekin

A

stimulating factor
stimulates proliferation of stem cells and megakaryocyte progenitors - increases production of platelets
reduces period of thrombocytopenia following myelosuppressive chemo
alternative to platelet transfusions

34
Q

epoetin

A

stimulating factor
recombinant human erythropoietin
stimulates proliferation and differentiation of erythroid progenitors - increases production of erythocytes, enhances oxygen carrying capacity
indications: treatment of anemia secondary to chronic renal failure, treatment of chemo-induced anemia in non-myeloid malignancies, treatment of malignancy-induced anemia (MM)

35
Q

olaparib

A

poly ADP ribose polymerase (PARP) inhibitor

treatment of breast cancer with BRCA 1 or 2 mutation

36
Q

relevant tumor sizes

A

over 10^9 if detected by standard imaging
10^10 before symptomatic
10^12 is considered lethal

37
Q

palbociclib

A

Crk4/6 kinase inhibitor

recently approved for breast cancer

38
Q

cell response to DNA damage

A

when normal cells are exposed to chemo, DNA is damaged - cells halt in G1 until DNA is repaired - if cells proceed to S without repairing DNA, they apoptose
when cancer cells that lost G1/S checkpoint control are exposed to chemo, DNA is damaged - cell will try to replicate DNA and could trigger apoptosis - if cells do manage to replicate DNA, cell may have acquired lethal genetic insults that can cause it to die

39
Q

mechanisms of chemoresistance

A

decreased drug accumulation in the cell
changes in drug target or function
physiological changes that promote resistance
cell cycle changes

40
Q

electrophilic v nucleophilic

A
eletrophilic = electron deficient
nucleophilic = electron rich
41
Q

bendamusine, chlorambucil, melphalan

A

mechlorethamine derivates - alkylating agents
2 strategies to reduce reactivity and increase selectivity of nitrogen mustards
1) decrease nucleophilicity of nitrogen by adding aryl groups
2) prodrug strategy

42
Q

cyclophosphamide and ifosfamide

A

most useful alkylating agent currently available

side effects milk compared to most alkylating agents

43
Q

mesna

A

charged thiol - does not penetrate cells
drug accumulates in urine and inactivates reactive intermediates in unire
cyclophosphamide is toxic to bladder - reactive metabolites accumulate in urine and damage mucosa
mesna reacts with and inactivates cyclophosphamide metabolites in urine
administered with cyclophosphamide to block hemorrhagic cystitis

44
Q

carmustine and lomustine

A

nitrosoureas
non-enzymatic conversion to diazonium ion occurs - highly electrophilic and has extremely short t1/2 - conversion must take place in tumor cell
readily cross BBB - used to treat glioblastoma multiforme and other brain tumors
significant bone marrow toxicity - requires longer interval between doses than other agents

45
Q

bisulfan

A

alkyl sulfonates
given in high doses with cyclophosphamide before bone marrow transplant
pulmonary fibrosis - “bisulfan lung”

46
Q

dicarbazine

A

nonclassical alkylating agent
monoalkylating agent - does not crosslink DNA
requires activation via N-demthylation - N-demethylated intermediate is unstable and has a short t1/2 - methyldiazonium ion is highly reactive methylating agent
can be combined w other alkylating agents
typical SEs but generally less severe

47
Q

temozolide

A

nonclassical alkylating agent
doesnt require liver activation
100% bioavailable
readily crosses BBB

48
Q

cisplatin

A

platinum drug
highly effective agent for many solid tumors
side effect profile different than alkylating agents
-dose limiting nephrotoxicity
- severe NV
-minimal bone marrow toxicity
-peripheral neuropathy

49
Q

carboplatin and oxaliplatin

A

MOA and therapeutic profile similar to cisplatin
major differences are in dose-limiting toxicites
carboplatin: bone marrow toxicity significant and typical of other alkylating agents
oxaplatin: acute sensory neuropathy is dose-limiting, chronic peripheral neuropathy related to cumulative dose

50
Q

drug resistance of alkylating agents

A

increase expression of DNA repair enzyme
increased intracellular concentration of non-protein thiols, especially glutathione - thiols intercept reactive intermediates of alkylating agents
increased expression of cellular glutatione S-transferase (GST)

51
Q

mytomycin C

A

similarities to nitrogen mustards
functions as an alkylating agent and DNA alkylator but with different toxicites
myelosuppression is dose-limiting
can form monoadducts and bifunctional adducts

52
Q

radium 223 dichloride

A

absorbed selectively into bone

treats bone metastases

53
Q

procarbazine

A

unclear MOA
inhibits DNA, RNA and protein synthesis
not cross resistant w other alkylating agents

54
Q

5FU

A

fluorinated uracil analog
2-step transformation to FdUMP
with folates, FdUMP inhibitsthymidylate synthase
FuDMP-enzyme-folate ternary complex
-arrests synthesis of thymidine monophosphate (TMP)
-TMP depletion results in inhibition of DNA synthesis - “thymineless death”
5-FU can also be converted to FUMP and then to FUTP
FUTP incorporated into RNA - intereferes w RNA processing and fxn and polyadenylation (affects stability)
resistance
DIs:
thymidine: 5FU then thymidine - decreased cytotoxic effect, thymidine then 5FU - increased cytotoxic
leucovorate - increases 5FU efficacy
5% of population has polymorphisms which break down 5FU - life-threatening

55
Q

fluorodeoxyuridine

A

FUdR
deoxyribonucleoside version of 5FU
similar in most aspects to 5FU

56
Q

capecitabine

A

orally active prodrug of 5FU
multi-step conversion to 5FU in tissues
prodrug strategy generates higher levels of 5FU selectively within some tumors

57
Q

cytosine arabinoside

A

cytosine analog - inhibit DNA synth
converted to Ara-CTP - comp inhib of DNA polymerase a, incorperated into DNA and further inhibits synthesos
cytidine deaminase converts Ara-C to non-toxic uracil arabinoside
low levels of cytidine deaminase in CNS makes cytosine arabinoside a good treatment for meningeal leukemia and lymphoma
multiple resistance mechanisms

58
Q

gemcitabine

A

cytosine analog
phosphorylated to dFdCDP and dFdCTP intracellularly
dFdCDP inhibits ribonucleotide reductase which inhibits the synthesis of deoxyribonucleotides from ribonucleotides and inhibits DNA synthesis
dFdCTP is incorporated into DNA but halts any further chain elongation
greater potency that Ara-C

59
Q

6-mercaptopurine

A

purine analog
inhibits multiple enzymes in the de novo purine biosynthesis pathway - blocks synthesis of purine nucleotides
resistance is due to loss of HGPRT - the activating enzyme
hematogenic toxicity arises from TPMT polymorphism
heterozygous? 65% std dose
homosygous? 10% of std dose
allopurinol are at risk for toxicity bc 6MP is broken down by xanthine oxidase

60
Q

6-thioguanine

A
thio analog of guanine
similar activity to 6-MP
also rapidly converted to ribonucleoside by HGPRT - cross resistance
also metabolized by TPMT
allopurinal does NOT block breakdown
61
Q

fludarabine, nelarabine, cladribine

A

arabino adenosine analogs
interferes w DNA polymerase and ribonucleotide reductase
inhibits both DNA replication, as well as transcription - not cell cycle dependent

62
Q

folic acid

A

inhibits DNA synthesis
inhibits RNA and protein synthesis and DNA repair
binds to and inhibits DHFR

63
Q

methotrexate

A

binds to and inhibits DHFR - inhibits DNA synthesis

resistance

64
Q

pralatrexate

A

inhibits DHFR - designed to accumulate preferentially in tumor cells

65
Q

premetrexed

A

inhibits DHFR, thymidylate synthase and glycinamide ribonucleotide formyltransferase
decreased risk of resistance

66
Q

levcovorin

A

used to “rescue” normal tissues from the toxic effects of high-dose MTX
also used to enhance activity of 5FU and capecitabine

67
Q

hydroxyurea

A

decreases prouction of deoxyribonucleotides

inhibits DNA synthesis in S phase

68
Q

actinomycin C

A

binds DNA and inhibits transcription by RNA polymerase
also inhibits DNA replication
not cell-cycle specific

69
Q

camptothecin

A

potent Topo I inhibitor
low solubility
severe and unpredictable toxicity
not used

70
Q

topotecan

A

water soluble camptothecin
potent Topo I inhibitor
reduced toxicity and increased therapeutic effects

71
Q

irinotecan

A

water soluble camptothecin
potent Topo I inhibitor
reduced toxicity and increased therapeutic effects
~10% of pop has polymorphism predicting low UGT1A1 leading to increased toxicity

72
Q

daunorubicin

A

original anthracycline - inhibits Top2

cardiotoxicity

73
Q

doxorubicin

A

incraesed therapeutic index compared to daunorubicin
most widely used and best understood anthracycline
cardiotoxicity - dependent on cumulative dose
severe local tissue damage if extravasated
“red death” or “red devil”

74
Q

epirubicin

A

cardiotoxicity less severe than with doxorubicin - faster elimination

75
Q

idarubicin

A

increased fat solubility and cellular uptake

76
Q

doxrazoxane

A

cyclic analog of EDTA - metal chelating agent
binds to iron and block iron-oxygen induced toxicities
cardiotoxicity of doxorubicin and daunomycin believed to be caused by iron-catalyzed free radical formation
dexrazoxane protects against anthracycline-induced cadiotoxicity without affecting chemo properties

77
Q

mitoxantrone

A

not an anthracycline, but similar structure and mechanism

still shows cardiotoxicity - less than doxorubicin

78
Q

etoposide and teniposide

A

epipodophyllotoxins
inhibits religation of dsDNA breaks induced by Topo2
G2 specific

79
Q

bleomycin

A

2 essential parts
bis(thiazole) charged side chain intercalates with DNA
iron oxygen species generates DNA free radical
radical intermediate leads to DNA ss and ds breaks
toxicity: pulmonary is dose limiting and cumulative - inflammation progresses to fibrosis
myelosuppression is minimal

80
Q

vinca alkaloids

A

bind to tubulin and inhibit microtubule assembly - leads to metaphase and mitotic arrest
peripheral neuropathy

81
Q

vincristine

A

vinca alkaloid

toxicity: severe local inflammation
- neurotoxicity - dose dependent, limiting and cumulative

82
Q

vinblastine

A

vinca alkaloid
myelosppression dose limiting
neurotoxicity less severe the vincristine

83
Q

vinorelbine

A

vinca alkaloid
myelosppression dose limiting
neurotoxicity mild

84
Q

erubulin

A

prevents microtubule elongation

low rate of neurotoxicity

85
Q

taxanes - paclitaxel, docetaxel, cabitaxel

A

bind tubulin and leads to mitotic arrest
paclitaxel and docetaxel myelosuppression is dose-limiting
cabazitaxel shows efficacy in multi drug resistant tumors

86
Q

metaplasia

A

subsitiution

87
Q

desmoplasia

A

formation and proliferation of connective tissue

88
Q

carcinoma

A

malignant neoplasm of epithelial origin

89
Q

adenoma

A

derived from glandular tissue

90
Q

hallmarks of cancer

A
resist cell death
induce angiogenesis
sustain proliferative signaling
enable replicative immortality
evade growth suppressors
activate invasion and metastasis
91
Q

hormone dependent cancers

A

breast, endometrium, prostate

92
Q

tamoxifen

A

both pre and post menopause
use is for resected ER+/PR+ breast cancer (3-5 yrs) and metastatic ER+/PR+ breast cancer
approved for prevention

93
Q

raloxifene

A

decreases bone resporption - developed as SERM for osteoporosis
76% as effective as tamoxifen
NO ENDOMETRIAL HYPERPLASIA

94
Q

fulvestrant

A

SERD
rapid receptor degradation
treatment of ER+ metatstatic breast cancer in postmenopausal women who have progressed on other antiestrogen therapy

95
Q

anastrozole and letrozole

A

non-steroidal aromatase inihbitors
treatment of breast cancer in POSTmenopausal women
effective as first line or 3-5 years of tamoxifen

96
Q

exemestane

A

steroidal aromatase inhibitor
“suicide inhibitor”
treatment of estrogen-responsive breast cancer in POStmenopausal women who have progressed on antiestrogen therapy

97
Q

medroxyprogesterone

A

progesterone analog/agonist
inhibits adrenal steroid production
prevention of endometrial cancer in POSTmenopausal women

98
Q

leuprolide and goselerin in women

A

LHRH analogs
treatment of breast cancer in PREmenopausal women
“flare effect”
acute admin causes “surge” of LH and FSH but chronic downregulates LHRH receptors - severe loss of estrogen

99
Q

leuprolife and goselerin in men

A

palliative treatment of advanced prostate cancer
“flare effect”
3-4 weeks = chemical castration

100
Q

abarelix and degarelix

A

GnRH antagonists

treatment of prostate cancer

101
Q

flutamide

A
angrogen antagonist
blocks DHT binding
treatment of metastatic prostate cancer 
-freq used in combo w LHRH analogs
dosed TID
acute hepatotoxicity - rare but fatal - monitor serum transaminases monthly for 4 months
102
Q

biclutamide

A

androgen antagonist
treatment of metastatic prostate cancer - used in combo w LHRH analog
significantly reduced hepatotoxicity compared to flutamide
QD

103
Q

nilutamide

A

androgen antagonist
similar to biclutamide
impairs night vision

104
Q

enzalutamide

A

androgen antagonist
5x higher binding affinity for AR than biclutamide
inhibits AR binding to DNA

105
Q

abiraterone

A

androgen antagonist
inhibits CYP17 lyase 0 no conversion of pregnoolone and progesterone to DHEA and androstenedione
MUCH high step in hormone synthesis

106
Q

gefitinib and erlotinib

A

treatment of patients with metastatic NSCLC whose tumors have EGFR exon 19 or 21 mutation

107
Q

afatinib

A

treatment of EGFR mutant NSCLC with EGFR mutations

108
Q

osimertinib

A

treatment of metastatic NSCLC that has progressed on other EGFR inhibitor therapy and tests postitive for the T790M mutation

109
Q

lapatinib

A

treatment of advanced metastatic breast cancer in patients who have progressed on other therapies

110
Q

crizotinib and cabozantinib

A

inhibit cMET - receptor for HGF (hepatocyte growth factor)

111
Q

imatinib

A

inhibitor of Abl is Bcr-Abl protein

treatment of chronic myelocytic leukemia and GI stromal tumor (GIST)

112
Q

nilotinib

A

similar to imatinib but can inhibit some BCR-Abl mutants that are resistant to imatinib

113
Q

ponatinib

A

BCR-Abl inhibitor

effective against major mutant forms of BCR_Abl including “gatekeeper” mutation T315I

114
Q

dasatinib and bosutinib

A

BCR-Abl mutant CML

115
Q

crizotinib

A

inhibits ALK in ELM4-ALK in NSCLC patients (generally younger, nonsmokers)
requires diagnostic tests

116
Q

sorafenib

A

advanced renal cell carcinoma, unresected hepatocellular carcinoma

117
Q

vemurafenib

A

inhibits mutant MRAF having V600E
treatment of metastatic melanoma in patients with mutation
requires diagnostic test for BRAF mutation

118
Q

dabrafenib

A

BRAF V600 inhibitor

in combination with trametinib for treatment of BRAF V600E/K mutant resistant metastatic melenoma

119
Q

trametinib

A

inhibits kinase activity of MEK1 and MEK2
used in combo w dabrafenib
dont use if received prior BRAF inhibitor therapy
RASH

120
Q

Idelalisib

A

PI3K inhibitor
relapsed chronic lymphocytic leukemia
relapsed follicular B-call non-Hodgkin lymphoma and relapsed lymphocytic lymphoma
use in patients who have received 2 proir therapirs

121
Q

ibrutinib

A

indicated for Bcell leukemia

122
Q

sunitinib

A

inhibits VEGFR

advanced renal cell carcinoma and gastrointestnal stromal tumor (GIST)

123
Q

PAZOPANIB

A

advanced renal cell carcinoma and soft tissue sarcoma

124
Q

cabozantinib

A

metastatic thyroid cancer

125
Q

vanetanib

A

VEGFR, EGFR, RET

metastatic thyroid cancer

126
Q

sirolimus

A

inhibits mTOR amd blocks IL-2 transduction

127
Q

temsirolimus

A

renal cell carcinoma

128
Q

everolimus

A

also used in organ transplant

advanced renal carcinoma in patients who have failed sorafenib or sunitinib

129
Q

trastuzumab

A

humanized monoclonal AB for ErbB2/HER2/Neu

treatment of breast cancer that overexpresses HER2

130
Q

pertuzumab

A

binds HER2 and inhibits dimerization

used in combo w transtuzumab

131
Q

cetuximab

A

binds EGF receptor

colorectal and head and neck cancers

132
Q

panitumumab

A

binds to EGF receptor

treatment of colorectal cancers

133
Q

rituximab

A

CD20

B-cell non-hodgkin’s lymphoma

134
Q

ofatumumab

A

CD20

chronic lymphocytic leukemia (CLL)

135
Q

obinutuzumab

A

CD 20

CLL

136
Q

bevacizumab

A

VEGF
no efficacy alone
first-life metatstatic colorectal cancer

137
Q

ramucirumab

A

VEGF-R2
metastatic colorectal cancer whose disease has progressed on a first line bevacizumab, oxaliplatin, fluoropyrimidine regimen

138
Q

trastuzumab - emtansine

A

inhibits microtubule assay

treatment of HER2 positive metatstatic breast cancer that has failed other treatments