1
|
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.
|
2
|
Myers AP and Cantley LC: Targeting a
common collaborator in cancer development. Sci Transl Med.
2:48ps452010.
|
3
|
McCubrey JA, Steelman LS, Franklin RA, et
al: Targeting the RAF/MEK/ERK, PI3K/AKT and p53 pathways in
hematopoietic drug resistance. Adv Enzyme Regul. 47:64–103.
2007.
|
4
|
Vivanco I and Sawyers CL: The
phosphatidylinositol 3-kinase-AKT pathway in human cancer. Nat Rev
Cancer. 2:489–501. 2002.
|
5
|
Bhaskar PT and Hay N: The two TORCs and
Akt. Dev Cell. 12:487–502. 2007.
|
6
|
Lee DF and Hung MC: All roads lead to
mTOR: integrating inflammation and tumor angiogenesis. Cell Cycle.
6:3011–3014. 2007.
|
7
|
Pirker R, Pereira JR, Szczesna A, von
Pawel J, et al; FLEX study team. Cetuximab plus chemotherapy in
patients with advanced non-small-cell lung cancer (FLEX): an
open-label randomised phase III trial. Lancet. 373:1525–1531.
2009.
|
8
|
Tortora G, Ciardiello F and Gasparini G:
Combined targeting of EGFR-dependent and VEGF-dependent pathways:
rationale, preclinical studies and clinical applications. Nat Clin
Pract Oncol. 5:521–530. 2008.
|
9
|
Gridelli C, Maione P and Rossi A: The
potential role of mTOR inhibitors in non-small cell lung cancer.
Oncologist. 13:139–147. 2008.
|
10
|
Tokunaga C, Yoshino K and Yonezawa K: mTOR
integrates amino acid- and energy-sensing pathways. Biochem Biophys
Res Commun. 313:443–446. 2004.
|
11
|
Beevers CS, Li F, Liu L and Huang S:
Curcumin inhibits the mammalian target of rapamycin-mediated
signaling pathways in cancer cells. Int J Cancer. 119:757–764.
2006.
|
12
|
Huang S and Houghton PJ: Mechanisms of
resistance to rapamycins. Drug Resist Updat. 4:378–391. 2001.
|
13
|
Huang S, Bjornsti M and Houghton P:
Rapamycins: mechanism of action and cellular resistance. Cancer
Biol Ther. 2:222–232. 2003.
|
14
|
Lazaridis G, Lambaki S, Karayannopoulou G,
et al: Prognostic and predictive value of p-Akt, EGFR, and p-mTOR
in early breast cancer. Strahlenther Onkol. 190:636–638.
640–645
|
15
|
Wullschleger S, Loewith R and Hall MN: TOR
signaling in growth and metabolism. Cell. 124:471–484. 2006.
|
16
|
Betz C and Hall MN: Where is mTOR and what
is it doing there? J Cell Biol. 203:563–574. 2013.
|
17
|
Kim DH, Sarbassov DD, Ali SM, King JE,
Latek RR, Erdjument-Bromage H, Tempst P and Sabatini DM: mTOR
interacts with raptor to form a nutrient-sensitive complex that
signals to the cell growth machinery. Cell. 110:163–175. 2002.
|
18
|
Kim DH, Sarbassov DD, Ali SM, Latek RR,
Guntur KV, Erdjument-Bromage H, Tempst P and Sabatini DM: GbetaL, a
positive regulator of the rapamycin-sensitive pathway required for
the nutrient-sensitive interaction between raptor and mTOR. Mol
Cell. 11:895–904. 2003.
|
19
|
Fang Y, Vilella-Bach M, Bachmann R,
Flanigan A and Chen J: Phosphatidic acid-mediated mitogenic
activation of mTOR signaling. Science. 294:1942–1945. 2001.
|
20
|
Frias MA, Thoreen CC, Jaffe JD, Schroder
W, Sculley T, Carr SA and Sabatini DM: mSin1 is necessary for
Akt/PKB phosphorylation, and its isoforms define three distinct
mTORC2s. Curr Biol. 16:1865–1870. 2006.
|
21
|
Sarbassov DD, Ali SM, Kim DH, Guertin DA,
Latek RR, Erdjument-Bromage H, Tempst P and Sabatini DM: Rictor, a
novel binding partner of mTOR, defines a rapamycin-insensitive and
raptor-independent pathway that regulates the cytoskeleton. Curr
Biol. 14:1296–1302. 2004.
|
22
|
Betz C, Stracka D, Prescianotto-Baschong
C, Frieden M, Demaurex N and Hall MN: Feature Article: mTOR complex
2-Akt signaling at mitochondria-associated endoplasmic reticulum
membranes (MAM) regulates mitochondrial physiology. Proc Natl Acad
Sci USA. 110:12526–12534. 2013.
|
23
|
Sarbassov DD, Guertin DA, Ali SM and
Sabatini DM: Phosphorylation and regulation of Akt/PKB by the
rictor-mTOR complex. Science. 307:1098–1101. 2005.
|
24
|
Stephens L, Anderson K, Stokoe D,
Erdjument-Bromage H, Painter GF, Holmes AB, Gaffney PR, Reese CB,
McCormick F, Tempst P, Coadwell J and Hawkins PT: Protein kinase B
kinases that mediate phosphatidylinositol
3,4,5-trisphosphate-dependent activation of protein kinase B.
Science. 279:710–714. 1998.
|
25
|
Lamming DW, Ye L, Katajisto P, Goncalves
MD, Saitoh M, Stevens DM, Davis JG, Salmon AB, Richardson A, Ahima
RS, Guertin DA, Sabatini DM and Baur JA: Rapamycin-induced insulin
resistance is mediated by mTORC2 loss and uncoupled from longevity.
Science. 335:1638–1643. 2012.
|
26
|
Tang JM, He QY, Guo RX and Chang XJ:
Phosphorylated Akt overexpression and loss of PTEN expression in
non-small cell lung cancer confers poor prognosis. Lung Cancer.
51:181–191. 2006.
|
27
|
Dowling RJ, Topisirovic I, Fonseca BD and
Sonenberg N: Dissecting the role of mTOR: lessons from mTOR
inhibitors. Biochim Biophys Acta. 1804:433–439. 2010.
|
28
|
Dunlop EA and Tee AR: Mammalian target of
rapamycin complex 1: signalling inputs, substrates and feedback
mechanisms. Cell Signal. 21:827–835. 2009.
|
29
|
Wislez M, Spencer ML, Izzo JG, et al:
Inhibition of mammalian target of rapamycin reverses alveolar
epithelial neoplasia induced by oncogenic K-ras. Cancer Res.
65:3226–3235. 2005.
|
30
|
Balsara BR, Pei J, Mitsuuchi Y, Page R, et
al: Frequent activation of AKT in non-small cell lung carcinomas
and preneoplastic bronchial lesions. Carcinogenesis. 25:2053–2059.
2004.
|
31
|
Amado RG, Wolf M, Peeters M, et al:
Wild-type KRAS is required for panitumumab efficacy in patients
with metastatic colorectal cancer. J Clin Oncol. 26:1626–1634.
2008.
|
32
|
Sarosi V, Losonczy G, Francovszky E,
Tolnay E, Torok S, Galffy G, Hegedus B, Dome B and Ostoros G:
Effectiveness of erlotinib treatment in advanced KRAS
mutation-negative lung adenocarcinoma patients: Results of a
multicenter observational cohort study (MOTIVATE). Lung Cancer.
86:54–58. 2014.
|
33
|
Gridelli C, de Marinis F, Cappuzzo F, et
al: Treatment of advanced non-small-cell lung cancer with epidermal
growth factor receptor (EGFR) mutation or ALK gene rearrangement:
results of an international expert panel meeting of the Italian
Association of Thoracic Oncology. Clin Lung Cancer. 15:173–181.
2014.
|
34
|
Laurent-Puig P, Pekin D, Normand C,
Kotsopoulos SK, Nizard P, Perez Toralla K, Rowell R, Olson J,
Srinivasan P, Le Corre D, et al: Clinical relevance of KRAS-mutated
sub-clones detected with picodroplet digital PCR in advanced
colorectal cancer treated with anti-EGFR therapy. Clin Cancer Res.
Sep 23–2014.(Epub ahead of print).
|
35
|
Choughule A, Sharma R, Trivedi V,
Thavamani A, Noronha V, Joshi A, Desai S, Chandrani P, Sundaram P,
Utture S, et al: Coexistence of KRAS mutation with mutant but not
wild-type EGFR predicts response to tyrosine-kinase inhibitors in
human lung cancer. Br J Cancer. Aug 12–2014.(Epub ahead of
print).
|
36
|
Conde E, Angulo B, Tang M, et al:
Molecular context of the EGFR mutations: evidence for the
activation of mTOR/S6K signaling. Clin Cancer Res. 12:710–717.
2006.
|
37
|
Legrier ME, Yang CP, Yan HG, et al:
Targeting protein translation in human non small cell lung cancer
via combined MEK and mammalian target of rapamycin suppression.
Cancer Res. 67:11300–11308. 2007.
|
38
|
Buck E, Eyzaguirre A, Brown E, et al:
Rapamycin synergizes with the epidermal growth factor receptor
inhibitor erlotinib in non-small-cell lung, pancreatic, colon, and
breast tumors. Mol Cancer Ther. 5:2676–2684. 2006.
|
39
|
Glaysher S, Bolton LM, Johnson P, Torrance
C and Cree IA: Activity of EGFR, mTOR and PI3K inhibitors in an
isogenic breast cell line model. BMC Res Notes. 7:3972014.
|
40
|
Jänne PA, Cohen RB, Laird AD, et al: Phase
I safety and pharmacokinetic study of the PI3K/mTOR inhibitor
SAR245409 (XL765) in combination with erlotinib in patients with
advanced solid tumors. J Thorac Oncol. 9:316–323. 2014.
|
41
|
Wen PY, Chang SM, Lamborn KR, Kuhn JG,
Norden AD, Cloughesy TF, Robins HI, Lieberman FS, Gilbert MR, Mehta
MP, et al: Phase I/II study of erlotinib and temsirolimus for
patients with recurrent malignant gliomas: North American Brain
Tumor Consortium trial 04–02. Neuro Oncol. 16:567–578. 2014.
|
42
|
Wang Q, Wei F, Li C, Lv G, Wang G, Liu T,
Bellail AC and Hao C: Combination of mTOR and EGFR kinase
inhibitors blocks mTORC1 and mTORC2 kinase activity and suppresses
the progression of colorectal carcinoma. PLoS One.
8:e731752013.
|
43
|
Bauman JE, Arias-Pulido H, Lee SJ,
Fekrazad MH, Ozawa H, Fertig E, Howard J, Bishop J, Wang H, Olson
GT, et al: A phase II study of temsirolimus and erlotinib in
patients with recurrent and/or metastatic, platinum-refractory head
and neck squamous cell carcinoma. Oral Oncol. 49:461–467. 2013.
|
44
|
Papadimitrakopoulou VA, Soria JC, Jappe A,
Jehl V, Klimovsky J and Johnson BE: Everolimus and erlotinib as
second- or third-line therapy in patients with advanced
non-small-cell lung cancer. J Thorac Oncol. 7:1594–1601. 2012.
|
45
|
Bago-Horvath Z, Sieghart W, Grusch M,
Lackner A, Hayden H, Pirker C, Komina O, Węsierska-Gądek J, Haitel
A, Filipits M, et al: Synergistic effects of erlotinib and
everolimus on bronchial carcinoids and large-cell neuroendocrine
carcinomas with activated EGFR/AKT/mTOR pathway.
Neuroendocrinology. 96:228–237. 2012.
|
46
|
Matar P, Rojo F, Cassia R, et al: Combined
epidermal growth factor receptor targeting with the tyrosine kinase
inhibitor gefitinib (ZD1839) and the monoclonal antibody cetuximab
(IMC-C225): superiority over single-agent receptor targeting. Clin
Cancer Res. 10:6487–6501. 2004.
|
47
|
O’Donnell A1, Faivre S, Burris HA III, et
al: Phase I pharmacokinetic and pharmacodynamic study of the oral
mammalian target of rapamycin inhibitor everolimus in patients with
advanced solid tumors. J Clin Oncol. 26:1588–1595. 2008.
|
48
|
Besse B, Leighl N, Bennouna J, et al:
Phase II study of everolimus-erlotinib in previously treated
patients with advanced non-small-cell lung cancer. Ann Oncol.
25:409–415. 2014.
|
49
|
Owonikoko TK, Stoller RG, Petro D, et al:
Phase II study of RAD001 (Everolimus) in previously treated small
cell lung cancer (SCLC). J Clin Oncol. 26(Suppl 15): 190172008.
|
50
|
Pandya KJ, Dahlberg S, Hidalgo M, et al;
Eastern Cooperative Oncology Group (E1500). A randomized, phase II
trial of two dose levels of temsirolimus (CCI-779) in patients with
extensive-stage small-cell lung cancer who have responding or
stable disease after induction chemotherapy: a trial of the Eastern
Cooperative Oncology Group (E1500). J Thorac Oncol. 2:1036–1041.
2007.
|
51
|
Mita MM, Mita AC, Chu QS, et al: Phase I
trial of the novel mammalian target of rapamycin inhibitor
deforolimus (AP23573; MK-8669) administered intravenously daily for
5 days every 2 weeks to patients with advanced malignancies. J Clin
Oncol. 26:361–367. 2008.
|
52
|
Milton DT, Riely GJ, Azzoli CG, et al:
Phase 1 trial of everolimus and gefitinib in patients with advanced
nonsmall-cell lung cancer. Cancer. 110:599–605. 2007.
|
53
|
Riely GJ, Kris MG, Zhao B, et al:
Prospective assessment of discontinuation and reinitiation of
erlotinib or gefitinib in patients with acquired resistance to
erlotinib or gefitinib followed by the addition of everolimus. Clin
Cancer Res. 13:5150–5155. 2007.
|
54
|
Papadimitrakopoulou V, Blumenschein GR Jr,
Leighl NB, et al: A phase 1/2 study investigating the combination
of RAD0001 (everolimus) and erlotinib (E) as 2nd and 3rd line
therapy in patients (pts) with advanced non-small cell lung cancer
(NSCLC) previously treated with chemotherapy (C): phase 1 results.
J Clin Oncol. 26(Suppl 15): 80512008.
|