|
1
|
Siegel R, Naishadham D and Jemal A: Cancer
statistics, 2013. CA Cancer J Clin. 63:11–30. 2013. View Article : Google Scholar
|
|
2
|
Jilaveanu LB, Aziz SA and Kluger HM:
Chemotherapy and biologic therapies for melanoma: do they work?
Clin Dermatol. 27:614–625. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
3
|
Davies H, Bignell GR, Cox C, et al:
Mutations of the BRAF gene in human cancer. Nature. 417:949–954.
2002. View Article : Google Scholar : PubMed/NCBI
|
|
4
|
Flaherty KT, Puzanov I, Kim KB, et al:
Inhibition of mutated, activated BRAF in metastatic melanoma. N
Engl J Med. 363:809–819. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
5
|
Chapman PB, Hauschild A, Robert C, et al:
Improved survival with vemurafenib in melanoma with BRAF V600E
mutation. N Engl J Med. 364:2507–2516. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
6
|
Hauschild A, Grob JJ, Demidov LV, et al:
Dabrafenib in BRAF-mutated metastatic melanoma: a multicentre,
open-label, phase 3 randomised controlled trial. Lancet.
380:358–365. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
7
|
Flaherty KT, Robert C, Hersey P, et al:
Improved survival with MEK inhibition in BRAF-mutated melanoma. N
Engl J Med. 367:107–114. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
8
|
Sosman JA, Kim KB, Schuchter L, et al:
Survival in BRAF V600-mutant advanced melanoma treated with
vemurafenib. N Engl J Med. 366:707–714. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
9
|
Aplin AE, Kaplan FM and Shao Y: Mechanisms
of resistance to RAF inhibitors in melanoma. J Invest Dermatol.
131:1817–1820. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
10
|
Lito P, Rosen N and Solit DB: Tumor
adaptation and resistance to RAF inhibitors. Nat Med. 19:1401–1409.
2013. View Article : Google Scholar : PubMed/NCBI
|
|
11
|
Nikolaou VA, Stratigos AJ, Flaherty KT and
Tsao H: Melanoma: new insights and new therapies. J Invest
Dermatol. 132:854–863. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
12
|
Cragg MS, Jansen ES, Cook M, Harris C,
Strasser A and Scott CL: Treatment of B-RAF mutant human tumor
cells with a MEK inhibitor requires Bim and is enhanced by a BH3
mimetic. J Clin Invest. 118:3651–3659. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
13
|
Jiang CC, Lai F, Tay KH, et al: Apoptosis
of human melanoma cells induced by inhibition of B-RAFV600E
involves preferential splicing of bimS. Cell Death Dis. 1:e692010.
View Article : Google Scholar : PubMed/NCBI
|
|
14
|
Eberle J, Fecker LF, Hossini AM, Kurbanov
BM and Fechner H: Apoptosis pathways and oncolytic adenoviral
vectors: promising targets and tools to overcome therapy resistance
of malignant melanoma. Exp Dermatol. 17:1–11. 2008. View Article : Google Scholar
|
|
15
|
Wang X: The expanding role of mitochondria
in apoptosis. Genes Dev. 15:2922–2933. 2001.PubMed/NCBI
|
|
16
|
Guicciardi ME and Gores GJ: Life and death
by death receptors. FASEB J. 23:1625–1637. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
17
|
LaCasse EC, Mahoney DJ, Cheung HH,
Plenchette S, Baird S and Korneluk RG: IAP-targeted therapies for
cancer. Oncogene. 27:6252–6275. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
18
|
Santarpia L, Lippman SM and El-Naggar AK:
Targeting the MAPK-RAS-RAF signaling pathway in cancer therapy.
Expert Opin Ther Targets. 16:103–119. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
19
|
Liu P, Cheng H, Roberts TM and Zhao JJ:
Targeting the phosphoinositide 3-kinase pathway in cancer. Nat Rev
Drug Discov. 8:627–644. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
20
|
Pickup M, Novitskiy S and Moses HL: The
roles of TGFbeta in the tumour microenvironment. Nat Rev Cancer.
13:788–799. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
21
|
Ara T and Declerck YA: Interleukin-6 in
bone metastasis and cancer progression. Eur J Cancer. 46:1223–1231.
2010. View Article : Google Scholar : PubMed/NCBI
|
|
22
|
Crowe DL and Shuler CF: Regulation of
tumor cell invasion by extracellular matrix. Histol Histopathol.
14:665–671. 1999.PubMed/NCBI
|
|
23
|
Fedorenko IV, Gibney GT and Smalley KS:
NRAS mutant melanoma: biological behavior and future strategies for
therapeutic management. Oncogene. 32:3009–3018. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
24
|
Shi H, Hong A, Kong X, et al: A novel AKT1
mutant amplifies an adaptive melanoma response to BRAF inhibition.
Cancer Discov. 4:69–79. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
25
|
Davies MA, Stemke-Hale K, Tellez C, et al:
A novel AKT3 mutation in melanoma tumours and cell lines. Br J
Cancer. 99:1265–1268. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
26
|
Aguissa-Toure AH and Li G: Genetic
alterations of PTEN in human melanoma. Cell Mol Life Sci.
69:1475–1491. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
27
|
McCubrey JA, Steelman LS, Kempf CR, et al:
Therapeutic resistance resulting from mutations in Raf/MEK/ERK and
PI3K/PTEN/Akt/mTOR signaling pathways. J Cell Physiol.
226:2762–2781. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
28
|
Easty DJ, Gray SG, O’Byrne KJ, O’Donnell D
and Bennett DC: Receptor tyrosine kinases and their activation in
melanoma. Pigment Cell Melanoma Res. 24:446–461. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
29
|
Straussman R, Morikawa T, Shee K, et al:
Tumour micro-environment elicits innate resistance to RAF
inhibitors through HGF secretion. Nature. 487:500–504. 2012.
View Article : Google Scholar : PubMed/NCBI
|
|
30
|
Lippitz BE: Cytokine patterns in patients
with cancer: a systematic review. Lancet Oncol. 14:e218–228. 2013.
View Article : Google Scholar : PubMed/NCBI
|
|
31
|
Downward J: Targeting RAS signalling
pathways in cancer therapy. Nat Rev Cancer. 3:11–22. 2003.
View Article : Google Scholar : PubMed/NCBI
|
|
32
|
Populo H, Lopes JM and Soares P: The mTOR
signalling pathway in human cancer. Int J Mol Sci. 13:1886–1918.
2012. View Article : Google Scholar
|
|
33
|
Mendoza MC, Er EE and Blenis J: The
Ras-ERK and PI3K-mTOR pathways: cross-talk and compensation. Trends
Biochem Sci. 36:320–328. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
34
|
Shi H, Kong X, Ribas A and Lo RS:
Combinatorial treatments that overcome PDGFRbeta-driven resistance
of melanoma cells to V600EB-RAF inhibition. Cancer Res.
71:5067–5074. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
35
|
Britten CD: PI3K and MEK inhibitor
combinations: examining the evidence in selected tumor types.
Cancer Chemother Pharmacol. 71:1395–1409. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
36
|
Bjornsti MA and Houghton PJ: The TOR
pathway: a target for cancer therapy. Nat Rev Cancer. 4:335–348.
2004. View Article : Google Scholar : PubMed/NCBI
|
|
37
|
Hay N: The Akt-mTOR tango and its
relevance to cancer. Cancer Cell. 8:179–183. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
38
|
Aziz SA, Jilaveanu LB, Zito C, et al:
Vertical targeting of the phosphatidylinositol-3 kinase pathway as
a strategy for treating melanoma. Clin Cancer Res. 16:6029–6039.
2010. View Article : Google Scholar : PubMed/NCBI
|
|
39
|
Werzowa J, Cejka D, Fuereder T, et al:
Suppression of mTOR complex 2-dependent AKT phosphorylation in
melanoma cells by combined treatment with rapamycin and LY294002.
Br J Dermatol. 160:955–964. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
40
|
Marone R, Erhart D, Mertz AC, et al:
Targeting melanoma with dual phosphoinositide 3-kinase/mammalian
target of rapamycin inhibitors. Mol Cancer Res. 7:601–613. 2009.
View Article : Google Scholar : PubMed/NCBI
|
|
41
|
Babchia N, Calipel A, Mouriaux F, Faussat
AM and Mascarelli F: The PI3K/Akt and mTOR/P70S6K signaling
pathways in human uveal melanoma cells: interaction with B-Raf/ERK.
Invest Ophthalmol Vis Sci. 51:421–429. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
42
|
Werzowa J, Koehrer S, Strommer S, et al:
Vertical inhibition of the mTORC1/mTORC2/PI3K pathway shows
synergistic effects against melanoma in vitro and in vivo. J Invest
Dermatol. 131:495–503. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
43
|
Smalley KS: Understanding melanoma
signaling networks as the basis for molecular targeted therapy. J
Invest Dermatol. 130:28–37. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
44
|
Emery CM, Vijayendran KG, Zipser MC, et
al: MEK1 mutations confer resistance to MEK and B-RAF inhibition.
Proc Natl Acad Sci USA. 106:20411–20416. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
45
|
Mitsiades N, Chew SA, He B, et al:
Genotype-dependent sensitivity of uveal melanoma cell lines to
inhibition of B-Raf, MEK, and Akt kinases: rationale for
personalized therapy. Invest Ophthalmol Vis Sci. 52:7248–7255.
2011. View Article : Google Scholar : PubMed/NCBI
|
|
46
|
Shao Y and Aplin AE: BH3-only protein
silencing contributes to acquired resistance to PLX4720 in human
melanoma. Cell Death Differ. 19:2029–2039. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
47
|
Carlino MS, Gowrishankar K, Saunders CA,
et al: Antiproliferative effects of continued mitogen-activated
protein kinase pathway inhibition following acquired resistance to
BRAF and/or MEK inhibition in melanoma. Mol Cancer Ther.
12:1332–1342. 2013. View Article : Google Scholar
|
|
48
|
King AJ, Arnone MR, Bleam MR, et al:
Dabrafenib; preclinical characterization, increased efficacy when
combined with trametinib, while BRAF/MEK tool combination reduced
skin lesions. PLoS One. 8:e675832013. View Article : Google Scholar
|
|
49
|
Greger JG, Eastman SD, Zhang V, et al:
Combinations of BRAF, MEK, and PI3K/mTOR inhibitors overcome
acquired resistance to the BRAF inhibitor GSK2118436 dabrafenib,
mediated by NRAS or MEK mutations. Mol Cancer Ther. 11:909–920.
2012. View Article : Google Scholar : PubMed/NCBI
|
|
50
|
Gadiot J, Hooijkaas AI, Deken MA and Blank
CU: Synchronous BRAF(V600E) and MEK inhibition leads to superior
control of murine melanoma by limiting MEK inhibitor induced skin
toxicity. Onco Targets Ther. 6:1649–1658. 2013.PubMed/NCBI
|
|
51
|
Su F, Bradley WD, Wang Q, et al:
Resistance to selective BRAF inhibition can be mediated by modest
upstream pathway activation. Cancer Res. 72:969–978. 2012.
View Article : Google Scholar : PubMed/NCBI
|
|
52
|
Park SJ, Hong SW, Moon JH, et al: The
MEK1/2 inhibitor AS703026 circumvents resistance to the BRAF
inhibitor PLX4032 in human malignant melanoma cells. Am J Med Sci.
346:494–498. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
53
|
Nakamura A, Arita T, Tsuchiya S, et al:
Antitumor activity of the selective pan-RAF inhibitor TAK-632 in
BRAF inhibitor-resistant melanoma. Cancer Res. 73:7043–7055. 2013.
View Article : Google Scholar : PubMed/NCBI
|
|
54
|
Niessner H, Beck D, Sinnberg T, et al: The
farnesyl transferase inhibitor lonafarnib inhibits mTOR signaling
and enforces sorafenib-induced apoptosis in melanoma cells. J
Invest Dermatol. 131:468–479. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
55
|
Baudy AR, Dogan T, Flores-Mercado JE, et
al: FDG-PET is a good biomarker of both early response and acquired
resistance in BRAFV600 mutant melanomas treated with vemurafenib
and the MEK inhibitor GDC-0973. EJNMMI Res. 2:22–31. 2012.
View Article : Google Scholar : PubMed/NCBI
|
|
56
|
Carracedo A, Ma L, Teruya-Feldstein J, et
al: Inhibition of mTORC1 leads to MAPK pathway activation through a
PI3K-dependent feedback loop in human cancer. J Clin Invest.
118:3065–3074. 2008.PubMed/NCBI
|
|
57
|
Kinkade CW, Castillo-Martin M, Puzio-Kuter
A, et al: Targeting AKT/mTOR and ERK MAPK signaling inhibits
hormone-refractory prostate cancer in a preclinical mouse model. J
Clin Invest. 118:3051–3064. 2008.PubMed/NCBI
|
|
58
|
Roberts PJ, Usary JE, Darr DB, et al:
Combined PI3K/mTOR and MEK inhibition provides broad antitumor
activity in faithful murine cancer models. Clin Cancer Res.
18:5290–5303. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
59
|
Ho AL, Musi E, Ambrosini G, et al: Impact
of combined mTOR and MEK inhibition in uveal melanoma is driven by
tumor genotype. PLoS One. 7:e404392012. View Article : Google Scholar : PubMed/NCBI
|
|
60
|
Gopal YN, Deng W, Woodman SE, et al: Basal
and treatment-induced activation of AKT mediates resistance to cell
death by AZD6244 (ARRY-142886) in Braf-mutant human cutaneous
melanoma cells. Cancer Res. 70:8736–8747. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
61
|
Atefi M, von Euw E, Attar N, et al:
Reversing melanoma cross-resistance to BRAF and MEK inhibitors by
co-targeting the AKT/mTOR pathway. PLoS One. 6:e289732011.
View Article : Google Scholar : PubMed/NCBI
|
|
62
|
Ambrosini G, Musi E, Ho AL, de Stanchina E
and Schwartz GK: Inhibition of mutant GNAQ signaling in uveal
melanoma induces AMPK-dependent autophagic cell death. Mol Cancer
Ther. 12:768–776. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
63
|
Fowles JS, Denton CL and Gustafson DL:
Comparative analysis of MAPK and PI3K/AKT pathway activation and
inhibition in human and canine melanoma. Vet Comp Oncol. Jun
7–2013.(Epub ahead of print).
|
|
64
|
Meier F, Busch S, Lasithiotakis K, et al:
Combined targeting of MAPK and AKT signalling pathways is a
promising strategy for melanoma treatment. Br J Dermatol.
156:1204–1213. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
65
|
Lasithiotakis KG, Sinnberg TW, Schittek B,
et al: Combined inhibition of MAPK and mTOR signaling inhibits
growth, induces cell death, and abrogates invasive growth of
melanoma cells. J Invest Dermatol. 128:2013–2023. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
66
|
Dankort D, Curley DP, Cartlidge RA, et al:
Braf(V600E) cooperates with Pten loss to induce metastatic
melanoma. Nat Genet. 41:544–552. 2009. View
Article : Google Scholar : PubMed/NCBI
|
|
67
|
Hoeflich KP, Merchant M, Orr C, et al:
Intermittent administration of MEK inhibitor GDC-0973 plus PI3K
inhibitor GDC-0941 triggers robust apoptosis and tumor growth
inhibition. Cancer Res. 72:210–219. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
68
|
Tassi E, Zanon M, Vegetti C, et al: Role
of Apollon in human melanoma resistance to antitumor agents that
activate the intrinsic or the extrinsic apoptosis pathways. Clin
Cancer Res. 18:3316–3327. 2012. View Article : Google Scholar
|
|
69
|
Byron SA, Loch DC, Wellens CL, et al:
Sensitivity to the MEK inhibitor E6201 in melanoma cells is
associated with mutant BRAF and wildtype PTEN status. Mol Cancer.
11:75–89. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
70
|
Khalili JS, Yu X, Wang J, et al:
Combination small molecule MEK and PI3K inhibition enhances uveal
melanoma cell death in a mutant GNAQ- and GNA11-dependent manner.
Clin Cancer Res. 18:4345–4355. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
71
|
Choo EF, Ng CM, Berry L, et al: PK-PD
modeling of combination efficacy effect from administration of the
MEK inhibitor GDC-0973 and PI3K inhibitor GDC-0941 in A2058
xenografts. Cancer Chemother Pharmacol. 71:133–143. 2013.
View Article : Google Scholar : PubMed/NCBI
|
|
72
|
Posch C, Moslehi H, Feeney L, et al:
Combined targeting of MEK and PI3K/mTOR effector pathways is
necessary to effectively inhibit NRAS mutant melanoma in vitro and
in vivo. Proc Natl Acad Sci USA. 110:4015–4020. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
73
|
Ciuffreda L, Di Sanza C, Cesta Incani U,
et al: The mitogen-activated protein kinase (MAPK) cascade controls
phosphatase and tensin homolog (PTEN) expression through multiple
mechanisms. J Mol Med (Berl). 90:667–679. 2012. View Article : Google Scholar
|
|
74
|
Bedogni B, O’Neill MS, Welford SM, et al:
Topical treatment with inhibitors of the phosphatidylinositol
3′-kinase/Akt and Raf/mitogen-activated protein kinase
kinase/extracellular signal-regulated kinase pathways reduces
melanoma development in severe combined immunodeficient mice.
Cancer Res. 64:2552–2560. 2004.
|
|
75
|
Bedogni B, Welford SM, Kwan AC,
Ranger-Moore J, Saboda K and Powell MB: Inhibition of
phosphatidylinositol-3-kinase and mitogen-activated protein kinase
kinase 1/2 prevents melanoma development and promotes melanoma
regression in the transgenic TPRas mouse model. Mol Cancer Ther.
5:3071–3077. 2006. View Article : Google Scholar
|
|
76
|
Smalley KS, Haass NK, Brafford PA, Lioni
M, Flaherty KT and Herlyn M: Multiple signaling pathways must be
targeted to overcome drug resistance in cell lines derived from
melanoma metastases. Mol Cancer Ther. 5:1136–1144. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
77
|
Deng W, Gopal YN, Scott A, Chen G, Woodman
SE and Davies MA: Role and therapeutic potential of PI3K-mTOR
signaling in de novo resistance to BRAF inhibition. Pigment Cell
Melanoma Res. 25:248–258. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
78
|
Jiang CC, Lai F, Thorne RF, et al:
MEK-independent survival of B-RAFV600E melanoma cells selected for
resistance to apoptosis induced by the RAF inhibitor PLX4720. Clin
Cancer Res. 17:721–730. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
79
|
Molhoek KR, Brautigan DL and Slingluff CL
Jr: Synergistic inhibition of human melanoma proliferation by
combination treatment with B-Raf inhibitor BAY43-9006 and mTOR
inhibitor Rapamycin. J Transl Med. 3:39–49. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
80
|
Held MA, Langdon CG, Platt JT, et al:
Genotype-selective combination therapies for melanoma identified by
high-throughput drug screening. Cancer Discov. 3:52–67. 2013.
View Article : Google Scholar : PubMed/NCBI
|
|
81
|
Boisvert-Adamo K and Aplin AE: B-RAF and
PI-3 kinase signaling protect melanoma cells from anoikis.
Oncogene. 25:4848–4856. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
82
|
Villanueva J, Infante JR, Krepler C, et
al: Concurrent MEK2 mutation and BRAF amplification confer
resistance to BRAF and MEK inhibitors in melanoma. Cell Rep.
4:1090–1099. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
83
|
Curtin JA, Busam K, Pinkel D and Bastian
BC: Somatic activation of KIT in distinct subtypes of melanoma. J
Clin Oncol. 24:4340–4346. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
84
|
Ashida A, Takata M, Murata H, Kido K and
Saida T: Pathological activation of KIT in metastatic tumors of
acral and mucosal melanomas. Int J Cancer. 124:862–868. 2009.
View Article : Google Scholar : PubMed/NCBI
|
|
85
|
Thomas RK, Baker AC, Debiasi RM, et al:
High-throughput oncogene mutation profiling in human cancer. Nat
Genet. 39:347–351. 2007. View
Article : Google Scholar : PubMed/NCBI
|
|
86
|
Prickett TD, Agrawal NS, Wei X, et al:
Analysis of the tyrosine kinome in melanoma reveals recurrent
mutations in ERBB4. Nat Genet. 41:1127–1132. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
87
|
Ruhe JE, Streit S, Hart S, et al: Genetic
alterations in the tyrosine kinase transcriptome of human cancer
cell lines. Cancer Res. 67:11368–11376. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
88
|
Gitay-Goren H, Halaban R and Neufeld G:
Human melanoma cells but not normal melanocytes express vascular
endothelial growth factor receptors. Biochem Biophys Res Commun.
190:702–708. 1993. View Article : Google Scholar
|
|
89
|
Barnhill RL, Xiao M, Graves D and
Antoniades HN: Expression of platelet-derived growth factor
(PDGF)-A, PDGF-B and the PDGF-alpha receptor, but not the PDGF-beta
receptor, in human malignant melanoma in vivo. Br J Dermatol.
135:898–904. 1996. View Article : Google Scholar : PubMed/NCBI
|
|
90
|
Metzner T, Bedeir A, Held G, et al:
Fibroblast growth factor receptors as therapeutic targets in human
melanoma: synergism with BRAF inhibition. J Invest Dermatol.
131:2087–2095. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
91
|
de Wit PE, Moretti S, Koenders PG, et al:
Increasing epidermal growth factor receptor expression in human
melanocytic tumor progression. J Invest Dermatol. 99:168–173.
1992.PubMed/NCBI
|
|
92
|
Rakosy Z, Vizkeleti L, Ecsedi S, et al:
EGFR gene copy number alterations in primary cutaneous malignant
melanomas are associated with poor prognosis. Int J Cancer.
121:1729–1737. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
93
|
Reschke M, Mihic-Probst D, van der Horst
EH, et al: HER3 is a determinant for poor prognosis in melanoma.
Clin Cancer Res. 14:5188–5197. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
94
|
Ugurel S, Rappl G, Tilgen W and Reinhold
U: Increased serum concentration of angiogenic factors in malignant
melanoma patients correlates with tumor progression and survival. J
Clin Oncol. 19:577–583. 2001.
|
|
95
|
Molhoek KR, Shada AL, Smolkin M, et al:
Comprehensive analysis of receptor tyrosine kinase activation in
human melanomas reveals autocrine signaling through IGF-1R.
Melanoma Res. 21:274–284. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
96
|
Mendel DB, Laird AD, Xin X, et al: In vivo
antitumor activity of SU11248, a novel tyrosine kinase inhibitor
targeting vascular endothelial growth factor and platelet-derived
growth factor receptors: determination of a
pharmacokinetic/pharmacodynamic relationship. Clin Cancer Res.
9:327–337. 2003.
|
|
97
|
Qin JZ, Ziffra J, Stennett L, et al:
Proteasome inhibitors trigger NOXA-mediated apoptosis in melanoma
and myeloma cells. Cancer Res. 65:6282–6293. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
98
|
Fernandez Y, Verhaegen M, Miller TP, et
al: Differential regulation of noxa in normal melanocytes and
melanoma cells by proteasome inhibition: therapeutic implications.
Cancer Res. 65:6294–6304. 2005. View Article : Google Scholar
|
|
99
|
Markovic SN, Geyer SM, Dawkins F, et al: A
phase II study of bortezomib in the treatment of metastatic
malignant melanoma. Cancer. 103:2584–2589. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
100
|
Yeramian A, Sorolla A, Velasco A, et al:
Inhibition of activated receptor tyrosine kinases by Sunitinib
induces growth arrest and sensitizes melanoma cells to Bortezomib
by blocking Akt pathway. Int J Cancer. 130:967–978. 2012.
View Article : Google Scholar : PubMed/NCBI
|
|
101
|
Li J, Rix U, Fang B, et al: A chemical and
phosphoproteomic characterization of dasatinib action in lung
cancer. Nat Chem Biol. 6:291–299. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
102
|
Dewaele B, Floris G, Finalet-Ferreiro J,
et al: Coactivated platelet-derived growth factor receptor {alpha}
and epidermal growth factor receptor are potential therapeutic
targets in intimal sarcoma. Cancer Res. 70:7304–7314. 2010.
View Article : Google Scholar
|
|
103
|
Vultur A, Villanueva J, Krepler C, et al:
MEK inhibition affects STAT3 signaling and invasion in human
melanoma cell lines. Oncogene. Apr 29–2013.(Epub ahead of
print).
|
|
104
|
Hamai A, Richon C, Meslin F, et al:
Imatinib enhances human melanoma cell susceptibility to
TRAIL-induced cell death: relationship to Bcl-2 family and caspase
activation. Oncogene. 25:7618–7634. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
105
|
Klosowska-Wardega A, Hasumi Y, Ahgren A,
Heldin CH and Hellberg C: Combination therapy using imatinib and
vatalanib improves the therapeutic efficiency of paclitaxel towards
a mouse melanoma tumor. Melanoma Res. 21:57–65. 2011. View Article : Google Scholar
|
|
106
|
Molhoek KR, Griesemann H, Shu J,
Gershenwald JE, Brautigan DL and Slingluff CL Jr: Human melanoma
cytolysis by combined inhibition of mammalian target of rapamycin
and vascular endothelial growth factor/vascular endothelial growth
factor receptor-2. Cancer Res. 68:4392–4397. 2008. View Article : Google Scholar
|
|
107
|
O’Reilly T, Lane HA, Wood JM, et al:
Everolimus and PTK/ZK show synergistic growth inhibition in the
orthotopic BL16/BL6 murine melanoma model. Cancer Chemother
Pharmacol. 67:193–200. 2011.PubMed/NCBI
|
|
108
|
Schicher N, Paulitschke V, Swoboda A, et
al: Erlotinib and bevacizumab have synergistic activity against
melanoma. Clin Cancer Res. 15:3495–3502. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
109
|
Vergani E, Vallacchi V, Frigerio S, et al:
Identification of MET and SRC activation in melanoma cell lines
showing primary resistance to PLX4032. Neoplasia. 13:1132–1142.
2011.PubMed/NCBI
|
|
110
|
Girotti MR, Pedersen M, Sanchez-Laorden B,
et al: Inhibiting EGF receptor or SRC family kinase signaling
overcomes BRAF inhibitor resistance in melanoma. Cancer Discov.
3:158–167. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
111
|
Abel EV, Basile KJ, Kugel CH III, et al:
Melanoma adapts to RAF/MEK inhibitors through FOXD3-mediated
upregulation of ERBB3. J Clin Invest. 123:2155–2168. 2013.
View Article : Google Scholar : PubMed/NCBI
|
|
112
|
Fattore L, Marra E, Pisanu ME, et al:
Activation of an early feedback survival loop involving
phospho-ErbB3 is a general response of melanoma cells to RAF/MEK
inhibition and is abrogated by anti-ErbB3 antibodies. J Transl Med.
11:180–190. 2013. View Article : Google Scholar
|
|
113
|
Karasic TB, Hei TK and Ivanov VN:
Disruption of IGF-1R signaling increases TRAIL-induced apoptosis: a
new potential therapy for the treatment of melanoma. Exp Cell Res.
316:1994–2007. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
114
|
Villanueva J, Vultur A, Lee JT, et al:
Acquired resistance to BRAF inhibitors mediated by a RAF kinase
switch in melanoma can be overcome by cotargeting MEK and
IGF-1R/PI3K. Cancer Cell. 18:683–695. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
115
|
Wehrli P, Viard I, Bullani R, Tschopp J
and French LE: Death receptors in cutaneous biology and disease. J
Invest Dermatol. 115:141–148. 2000. View Article : Google Scholar : PubMed/NCBI
|
|
116
|
Zhang XD, Franco A, Myers K, Gray C,
Nguyen T and Hersey P: Relation of TNF-related apoptosis-inducing
ligand (TRAIL) receptor and FLICE-inhibitory protein expression to
TRAIL-induced apoptosis of melanoma. Cancer Res. 59:2747–2753.
1999.
|
|
117
|
Micheau O, Shirley S and Dufour F: Death
receptors as targets in cancer. Br J Pharmacol. 169:1723–1744.
2013. View Article : Google Scholar : PubMed/NCBI
|
|
118
|
Roberts NJ, Zhou S, Diaz LA Jr and
Holdhoff M: Systemic use of tumor necrosis factor alpha as an
anticancer agent. Oncotarget. 2:739–751. 2011.PubMed/NCBI
|
|
119
|
Etter AL, Bassi I, Germain S, et al: The
combination of chemotherapy and intraperitoneal MegaFas ligand
improves treatment of ovarian carcinoma. Gynecol Oncol. 107:14–21.
2007. View Article : Google Scholar : PubMed/NCBI
|
|
120
|
Gajewski TF: On the TRAIL toward death
receptor-based cancer therapeutics. J Clin Oncol. 25:1305–1307.
2007. View Article : Google Scholar : PubMed/NCBI
|
|
121
|
Duiker EW, Mom CH, de Jong S, et al: The
clinical trail of TRAIL. Eur J Cancer. 42:2233–2240. 2006.
View Article : Google Scholar : PubMed/NCBI
|
|
122
|
Zhang XD, Borrow JM, Zhang XY, Nguyen T
and Hersey P: Activation of ERK1/2 protects melanoma cells from
TRAIL-induced apoptosis by inhibiting Smac/DIABLO release from
mitochondria. Oncogene. 22:2869–2881. 2003. View Article : Google Scholar : PubMed/NCBI
|
|
123
|
Berger A, Quast SA, Plotz M, Kuhn NF,
Trefzer U and Eberle J: RAF inhibition overcomes resistance to
TRAIL-induced apoptosis in melanoma cells. J Invest Dermatol.
134:430–440. 2014. View Article : Google Scholar : PubMed/NCBI
|
|
124
|
Quast SA, Berger A and Eberle J:
ROS-dependent phosphorylation of Bax by wortmannin sensitizes
melanoma cells for TRAIL-induced apoptosis. Cell Death Dis.
4:e8392013. View Article : Google Scholar : PubMed/NCBI
|
|
125
|
Phipps LE, Hino S and Muschel RJ:
Targeting cell spreading: a method of sensitizing metastatic tumor
cells to TRAIL-induced apoptosis. Mol Cancer Res. 9:249–258. 2011.
View Article : Google Scholar : PubMed/NCBI
|
|
126
|
Bolden JE, Peart MJ and Johnstone RW:
Anticancer activities of histone deacetylase inhibitors. Nat Rev
Drug Discov. 5:769–784. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
127
|
Zhang XD, Gillespie SK, Borrow JM and
Hersey P: The histone deacetylase inhibitor suberic bishydroxamate:
a potential sensitizer of melanoma to TNF-related
apoptosis-inducing ligand (TRAIL) induced apoptosis. Biochem
Pharmacol. 66:1537–1545. 2003. View Article : Google Scholar
|
|
128
|
Gillespie S, Borrow J, Zhang XD and Hersey
P: Bim plays a crucial role in synergistic induction of apoptosis
by the histone deacetylase inhibitor SBHA and TRAIL in melanoma
cells. Apoptosis. 11:2251–2265. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
129
|
Lillehammer T, Engesaeter BO, Prasmickaite
L, Maelandsmo GM, Fodstad O and Engebraaten O: Combined treatment
with Ad-hTRAIL and DTIC or SAHA is associated with increased
mitochondrial-mediated apoptosis in human melanoma cell lines. J
Gene Med. 9:440–451. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
130
|
Perotti V, Baldassari P, Bersani I, et al:
NFATc2 is a potential therapeutic target in human melanoma. J
Invest Dermatol. 132:2652–2660. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
131
|
Zimmerman ZF, Kulikauskas RM, Bomsztyk K,
Moon RT and Chien AJ: Activation of Wnt/beta-catenin signaling
increases apoptosis in melanoma cells treated with trail. PLoS One.
8:e695932013. View Article : Google Scholar : PubMed/NCBI
|
|
132
|
Berger A, Quast SA, Plotz M, Kammermeier A
and Eberle J: Sensitization of melanoma cells for TRAIL-induced
apoptosis by BMS-345541 correlates with altered phosphorylation and
activation of Bax. Cell Death Dis. 4:e4772013. View Article : Google Scholar : PubMed/NCBI
|
|
133
|
Lecis D, Drago C, Manzoni L, et al: Novel
SMAC-mimetics synergistically stimulate melanoma cell death in
combination with TRAIL and Bortezomib. Br J Cancer. 102:1707–1716.
2010. View Article : Google Scholar : PubMed/NCBI
|
|
134
|
Baritaki S, Yeung K, Palladino M, Berenson
J and Bonavida B: Pivotal roles of snail inhibition and RKIP
induction by the proteasome inhibitor NPI-0052 in tumor cell
chemoimmunosensitization. Cancer Res. 69:8376–8385. 2009.
View Article : Google Scholar : PubMed/NCBI
|
|
135
|
Chawla-Sarkar M, Bae SI, Reu FJ, Jacobs
BS, Lindner DJ and Borden EC: Downregulation of Bcl-2, FLIP or IAPs
(XIAP and survivin) by siRNAs sensitizes resistant melanoma cells
to Apo2L/TRAIL-induced apoptosis. Cell Death Differ. 11:915–923.
2004. View Article : Google Scholar : PubMed/NCBI
|
|
136
|
Engesaeter BO, Sathermugathevan M,
Hellenes T, et al: Targeting inhibitor of apoptosis proteins in
combination with dacarbazine or TRAIL in melanoma cells. Cancer
Biol Ther. 12:47–58. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
137
|
Chetoui N, Sylla K, Gagnon-Houde JV, et
al: Down-regulation of mcl-1 by small interfering RNA sensitizes
resistant melanoma cells to fas-mediated apoptosis. Mol Cancer Res.
6:42–52. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
138
|
Safa AR: c-FLIP, a master anti-apoptotic
regulator. Exp Oncol. 34:176–184. 2012.PubMed/NCBI
|
|
139
|
Geserick P, Drewniok C, Hupe M, et al:
Suppression of cFLIP is sufficient to sensitize human melanoma
cells to TRAIL- and CD95L-mediated apoptosis. Oncogene.
27:3211–3220. 2008. View Article : Google Scholar
|
|
140
|
Hartman ML and Czyz M: Anti-apoptotic
proteins on guard of melanoma cell survival. Cancer Lett.
331:24–34. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
141
|
Oltersdorf T, Elmore SW, Shoemaker AR, et
al: An inhibitor of Bcl-2 family proteins induces regression of
solid tumours. Nature. 435:677–681. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
142
|
Hann CL, Daniel VC, Sugar EA, et al:
Therapeutic efficacy of ABT-737, a selective inhibitor of BCL-2, in
small cell lung cancer. Cancer Res. 68:2321–2328. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
143
|
Wroblewski D, Mijatov B, Mohana-Kumaran N,
et al: The BH3-mimetic ABT-737 sensitizes human melanoma cells to
apoptosis induced by selective BRAF inhibitors but does not reverse
acquired resistance. Carcinogenesis. 34:237–247. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
144
|
VanBrocklin MW, Verhaegen M, Soengas MS
and Holmen SL: Mitogen-activated protein kinase inhibition induces
translocation of Bmf to promote apoptosis in melanoma. Cancer Res.
69:1985–1994. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
145
|
Tse C, Shoemaker AR, Adickes J, et al:
ABT-263: a potent and orally bioavailable Bcl-2 family inhibitor.
Cancer Res. 68:3421–3428. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
146
|
Sale MJ and Cook SJ: The BH3 mimetic
ABT-263 synergizes with the MEK1/2 inhibitor selumetinib/AZD6244 to
promote BIM-dependent tumour cell death and inhibit acquired
resistance. Biochem J. 450:285–294. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
147
|
Verhaegen M, Bauer JA, Martin de la Vega
C, et al: A novel BH3 mimetic reveals a mitogen-activated protein
kinase-dependent mechanism of melanoma cell death controlled by p53
and reactive oxygen species. Cancer Res. 66:11348–11359. 2006.
View Article : Google Scholar
|
|
148
|
Senft D, Berking C, Graf SA, Kammerbauer
C, Ruzicka T and Besch R: Selective induction of cell death in
melanoma cell lines through targeting of Mcl-1 and A1. PLoS One.
7:e308212012. View Article : Google Scholar : PubMed/NCBI
|
|
149
|
Haq R, Yokoyama S, Hawryluk EB, et al:
BCL2A1 is a lineage-specific antiapoptotic melanoma oncogene that
confers resistance to BRAF inhibition. Proc Natl Acad Sci USA.
110:4321–4326. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
150
|
Koul HK, Pal M and Koul S: Role of p38 MAP
kinase signal transduction in solid tumors. Genes Cancer.
4:342–359. 2013. View Article : Google Scholar : PubMed/NCBI
|
|
151
|
Keuling AM, Andrew SE and Tron VA:
Inhibition of p38 MAPK enhances ABT-737-induced cell death in
melanoma cell lines: novel regulation of PUMA. Pigment Cell
Melanoma Res. 23:430–440. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
152
|
Boyle GM, Martyn AC and Parsons PG:
Histone deacetylase inhibitors and malignant melanoma. Pigment Cell
Res. 18:160–166. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
153
|
Kortylewski M, Jove R and Yu H: Targeting
STAT3 affects melanoma on multiple fronts. Cancer Metastasis Rev.
24:315–327. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
154
|
Qin JZ, Xin H, Sitailo LA, Denning MF and
Nickoloff BJ: Enhanced killing of melanoma cells by simultaneously
targeting Mcl-1 and NOXA. Cancer Res. 66:9636–9645. 2006.
View Article : Google Scholar : PubMed/NCBI
|
|
155
|
Wolter KG, Verhaegen M, Fernandez Y, et
al: Therapeutic window for melanoma treatment provided by selective
effects of the proteasome on Bcl-2 proteins. Cell Death Differ.
14:1605–1616. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
156
|
Nguyen M, Marcellus RC, Roulston A, et al:
Small molecule obatoclax (GX15-070) antagonizes MCL-1 and overcomes
MCL-1-mediated resistance to apoptosis. Proc Natl Acad Sci USA.
104:19512–19517. 2007. View Article : Google Scholar : PubMed/NCBI
|
|
157
|
Freudlsperger C, Thies A, Pfuller U and
Schumacher U: The proteasome inhibitor bortezomib augments
anti-proliferative effects of mistletoe lectin-I and the PPAR-gamma
agonist rosiglitazone in human melanoma cells. Anticancer Res.
27:207–213. 2007.
|
|
158
|
Miller LA, Goldstein NB, Johannes WU, et
al: BH3 mimetic ABT-737 and a proteasome inhibitor synergistically
kill melanomas through Noxa-dependent apoptosis. J Invest Dermatol.
129:964–971. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
159
|
Reuland SN, Goldstein NB, Partyka KA, et
al: ABT-737 synergizes with Bortezomib to kill melanoma cells. Biol
Open. 1:92–100. 2011. View Article : Google Scholar
|
|
160
|
Mlynarczuk-Bialy I, Roeckmann H,
Kuckelkorn U, et al: Combined effect of proteasome and calpain
inhibition on cisplatin-resistant human melanoma cells. Cancer Res.
66:7598–7605. 2006. View Article : Google Scholar : PubMed/NCBI
|
|
161
|
Millward M, Price T, Townsend A, et al:
Phase 1 clinical trial of the novel proteasome inhibitor marizomib
with the histone deacetylase inhibitor vorinostat in patients with
melanoma, pancreatic and lung cancer based on in vitro assessments
of the combination. Invest New Drugs. 30:2303–2317. 2012.
View Article : Google Scholar
|
|
162
|
Lai F, Guo ST, Jin L, et al: Cotargeting
histone deacetylases and oncogenic BRAF synergistically kills human
melanoma cells by necrosis independently of RIPK1 and RIPK3. Cell
Death Dis. 4:e6552013. View Article : Google Scholar
|
|
163
|
Niu G, Wright KL, Huang M, et al:
Constitutive Stat3 activity up-regulates VEGF expression and tumor
angiogenesis. Oncogene. 21:2000–2008. 2002. View Article : Google Scholar : PubMed/NCBI
|
|
164
|
van Delft MF, Wei AH, Mason KD, et al: The
BH3 mimetic ABT-737 targets selective Bcl-2 proteins and
efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralized.
Cancer Cell. 10:389–399. 2006.PubMed/NCBI
|
|
165
|
Konopleva M, Contractor R, Tsao T, et al:
Mechanisms of apoptosis sensitivity and resistance to the BH3
mimetic ABT-737 in acute myeloid leukemia. Cancer Cell. 10:375–388.
2006. View Article : Google Scholar : PubMed/NCBI
|
|
166
|
Keuling AM, Felton KE, Parker AA, Akbari
M, Andrew SE and Tron VA: RNA silencing of Mcl-1 enhances
ABT-737-mediated apoptosis in melanoma: role for a
caspase-8-dependent pathway. PLoS One. 4:e66512009. View Article : Google Scholar : PubMed/NCBI
|
|
167
|
Lucas KM, Mohana-Kumaran N, Lau D, et al:
Modulation of NOXA and MCL-1 as a strategy for sensitizing melanoma
cells to the BH3-mimetic ABT-737. Clin Cancer Res. 18:783–795.
2012. View Article : Google Scholar : PubMed/NCBI
|
|
168
|
Pandey MK, Gowda K, Doi K, Sharma AK, Wang
HG and Amin S: Proteasomal degradation of Mcl-1 by maritoclax
induces apoptosis and enhances the efficacy of ABT-737 in melanoma
cells. PLoS One. 8:e785702013. View Article : Google Scholar : PubMed/NCBI
|
|
169
|
Davies MA, Fox PS, Papadopoulos NE, et al:
Phase I study of the combination of sorafenib and temsirolimus in
patients with metastatic melanoma. Clin Cancer Res. 18:1120–1128.
2012. View Article : Google Scholar : PubMed/NCBI
|
|
170
|
Margolin KA, Moon J, Flaherty LE, et al:
Randomized phase II trial of sorafenib with temsirolimus or
tipifarnib in untreated metastatic melanoma (S0438). Clin Cancer
Res. 18:1129–1137. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
171
|
Hong DS, Sebti SM, Newman RA, et al: Phase
I trial of a combination of the multikinase inhibitor sorafenib and
the farnesyltransferase inhibitor tipifarnib in advanced
malignancies. Clin Cancer Res. 15:7061–7068. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
172
|
Flaherty KT, Infante JR, Daud A, et al:
Combined BRAF and MEK inhibition in melanoma with BRAF V600
mutations. N Engl J Med. 367:1694–1703. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
173
|
Su F, Viros A, Milagre C, et al: RAS
mutations in cutaneous squamous-cell carcinomas in patients treated
with BRAF inhibitors. N Engl J Med. 366:207–215. 2012. View Article : Google Scholar : PubMed/NCBI
|
|
174
|
Hainsworth JD, Infante JR, Spigel DR, et
al: Bevacizumab and everolimus in the treatment of patients with
metastatic melanoma: a phase 2 trial of the Sarah Cannon Oncology
Research Consortium. Cancer. 116:4122–4129. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
175
|
Slingluff CL Jr, Petroni GR, Molhoek KR,
et al: Clinical activity and safety of combination therapy with
temsirolimus and bevacizumab for advanced melanoma: a phase II
trial (CTEP 7190/Mel47). Clin Cancer Res. 19:3611–3620. 2013.
View Article : Google Scholar : PubMed/NCBI
|
|
176
|
Vaishampayan UN, Burger AM, Sausville EA,
et al: Safety, efficacy, pharmacokinetics, and pharmacodynamics of
the combination of sorafenib and tanespimycin. Clin Cancer Res.
16:3795–3804. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
177
|
Vanneman M and Dranoff G: Combining
immunotherapy and targeted therapies in cancer treatment. Nat Rev
Cancer. 12:237–251. 2012. View Article : Google Scholar
|
|
178
|
Hodi FS, O’Day SJ, McDermott DF, et al:
Improved survival with ipilimumab in patients with metastatic
melanoma. N Engl J Med. 363:711–723. 2010. View Article : Google Scholar
|
|
179
|
Hamid O, Robert C, Daud A, et al: Safety
and tumor responses with lambrolizumab (anti-PD-1) in melanoma. N
Engl J Med. 369:134–144. 2013. View Article : Google Scholar : PubMed/NCBI
|