Transcript Slide 1

Potential Consequences of
EGFR Dysregulation
EGFR
 Invasion
P
PI3K
 Metastasis
Nucleus
MAPK
Signaling
Cascades
Gene Activation
Cell Cycle Progression
Myc
M
G1
G2
S
Fos
Jun
 Survival
 Angiogenesis
P
 Proliferation
 Apoptosis
MAPK = mitogen-activated protein kinase; P13K = phosphatidylinositol 3-kinase.
Roskoski R Jr. Biochem Biophys Res Commun. 2004;319:1. Rowinsky EK. Annu Rev Med. 2004;55:433.
ISEL Trial
No Survival Benefit with Gefitinib
Gefitinib Placebo
(n = 1129) (n = 563)
Probability of Survival
1.0
Overall median survival (mo)
1-year survival (%)
0.8
5.6
27
5.1
21
HR = 0.89 (95% CI, 0.77–1.02)*; P = .087†
0.6
0.4
Gefitinib
Placebo
0.2
0.0
0
2
4
6
8
10
12
Survival Time (Months)
*From Cox regression model
†From Log-rank test
Reprinted from Lancet, 2005;366:1527, with permission from Elsevier.
14
16
Phase III BR.21 Study Design
NSCLC
• Double-blind
• Stratified according to
– Center
RANDOMIZED
– EC0G performance
2:1
status (0/1 vs 2/3)
– Best response to prior (Erlotinib) (Placebo)
therapy
(C or PR vs SD vs PD)
– # prior regimens (1 vs 2)
– Exposure to prior
platinum Rx (Y/N)
Shepherd FA, et al. N Engl J Med. 2005;353:123.
Erlotinib
150 mg/d
Placebo
Phase III BR.21
Overall Survival Favors Erlotinib
42.5% Improvement in Median Survival
100
Erlotinib
Placebo
n = 488
n = 243
Median survival (months)
6.7
4.7
1-y survival (%)
31.2
21.5
Patients (%)
80
60
40
*HR = 0.73, P < .001
20
Erlotinib
Placebo
0
0
No. at Risk
Placebo
243
Erlotinib
488
6
107
255
12
Months
18
24
30
50
145
9
23
0
4
0
0
*HR and P-value adjusted for stratification factors at randomization and HER1/EGFR status
Adapted from Shepherd FA, et al. N Engl J Med, 353:123-132, Figure 1A. Copyright © 2005
Massachusetts Medical Society. All rights reserved.
BR.21
Survival Across Subgroups
Factors
Gender
Male
Female
Smoking status
Never smoked
Current/ex-smoker
Ethnicity
Caucasian
Asian
EGFR status
EGFR-positive
EGFR-negative
EGFR unmeasured
Performance status
0–1
2–3
Histology
Adenocarcinoma
Squamous cell carcinoma
Other histology
Prior regimens
1
>2
N
HR
95% CI
475
256
0.76
0.80
0.6–0.9
0.6–1.1
146
545
0.42
0.87
0.3–0.6
0.7–1.0
567
91
0.79
0.61
0.6–1.0
0.4–1.0
185
141
405
0.68
0.61
0.77
0.5–0.9
0.6–1.4
0.6–1.0
486
245
0.73
0.77
0.6–0.9
0.6–1.0
365
222
144
0.71
0.67
1.04
0.6–0.9
0.5–0.9
0.7–1.5
364
367
0.76
0.75
0.6–1.0
0.6–1.0
Adapted from Tarceva® (erlotinib) Product Information. Melville, NY:
OSI Pharmaceuticals, Inc, and Genentech, Inc; 2007.
Courtesy of Dr. A. Sandler, MD.
0.00
0.50
Decreased
risk of death
1.00
1.50
2.00
Increased
risk of death
EGFR Monoclonal Antibody
Cetuximab

IgG1 (chimerized antibody)

Exclusive for EGFR and its heterodimers

Prevents repair and survival of tumor cells damaged
by effects of chemotherapy and radiotherapy

–
Potentiates apoptosis
–
Inhibits cell-cycle progression
–
Decreases production of angiogenic factors
–
Inhibits invasion/metastasis
Recent FDA approvals for squamous cell carcinoma
of the head and neck and colorectal cancer
Cetuximab in Advanced NSCLC
Reference
Regimen
N
Overall
Response
Rate (%)
*Lilenbaum
ASCO 2005
Cetuximab
66
3.3
8.1
43
Thienelt
J Clin Oncol
2005
Carboplatin/paclitaxel/
cetuximab
31
26
11
40
Rosell
ASCO 2004
Cisplatin/vinorelbine/
cetuximab
Cisplatin/vinorelbine
43
35
8.3
32
43
28
7.0
26
Robert
J Clin Oncol
2005
Carboplatin/gemcitabine/
cetuximab
35
29
10.2
46
*Kim
ASCO 2003
Docetaxel/cetuximab
47
25
7.5
—
Kelly
ASCO 2006
Chemotherapy + cetuximab
Chemotherapy → cetuximab
106
119
37
25
10
9
49
43
*1 or more prior therapies
Median
Survival
(Mo)
1-Year
Survival
(%)
Other Targeted Agents

Mammalian target of rapamycin (mTOR)
inhibitors

Insulin growth factor receptor antagonists

Histone deacetylase inhibitors (HDACs)

Bortezomib

Next-generation EGFR tyrosine kinase
inhibitors
– HKI-272

Toll-like receptor (TLR) antagonists
Downstream Targets in the Tyrosine
Kinase Pathway
Receptor Tyrosine
Kinase
Ras
P13K
Raf
Akt
MEK
mTOR
ERK/MAP
kinase
P70S6K
CDKs
Apoptosis
Cell Cycle Progression
Proliferation
MAP = mitogen-activated protein; MEK = MAPK kinase; mTOR = mammalian target of rapamycin;
P13K = phosphatidylinositol 3-kinase.
Adapted from Cancer Control, 2003;10(2):125, with permission from H. Lee Moffitt Cancer Center and
Research Institute, Inc.
Examples of mTOR Inhibitors Under
Evaluation for Lung Cancer

Temsirolimus (CCI-779): ongoing phase II trial in
1st-line therapy of stage IIIB or IV NSCLC1
–

Recent FDA approval for advanced renal cell carcinoma
Everolimus (RAD 001): preliminary data from phase
I/II studies in combination with EGFR tyrosine kinase
inhibitors reported2,3; phase II studies ongoing
mTOR = mammalian target of rapamycin.
1. CCI-779 protocol available at: http://www.clinicaltrials.gov/ct/show/NCT00079235?order=1.
2. Milton DT, et al. J Clin Oncol. 2005;23(No. 16S):646s. Abstract 7104. 3. Kris MG, et al. J Clin Oncol.
2007;25(No. 18S). Abstract 7575.