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8s Breast Cancer—HER2/ER 504 Oral Abstract Session, Sun, 8:00 AM-11:00 AM Intrinsic subtype and its clinical significance in early node-negative breast cancer: Results from two randomized trials of adjuvant chemoendocrine therapy. Presenting Author: Ewan K. A. Millar, The Kinghorn Cancer Centre, Sydney, Australia Background: Gene expression profiling has identified four main intrinsic subtypes of breast cancer which have distinct clinical behaviours and responses to therapy. A simplified immunohistochemical (IHC) panel can provide meaningful discrimination and help guide patient management. Methods: Using tissue microarrays (TMA) created from two randomized trials of adjuvant chemoendocrine therapy in node negative early breast cancer (IBCSG VIII and IX,n� 1220) we assessed intrinsic subtype as follows: “luminal A” (LA): ER and/or PR present, Ki-67 low (�median: 19%), HER2-; “Luminal B” (LB): ER and/or PR present, Ki-67 high(��19% median) and/or HER2� (IHC 3� or FISH amplified); HER2 enriched: ER and PR negative, HER2 positive (IHC 3� or FISH amplified), Triple Negative (TNP): ER, PR and HER2 negative. p53� and high cyclin D1 expression were then assessed to determine if they provided any further additive discriminatory value. Results: The standard definitions of intrinsic subtype demonstrated a significant difference in disease-free survival between the subtypes in both trials VIII and IX (p� 0.02), but this was not significant in multivariate analysis. The discrimination between luminal A and B tumors could not be improved upon by the addition of p53 or cyclin D1 expression. The standard definitions demonstrated that TNP and HER2-enriched tumors benefited from the addition of chemotherapy to endocrine therapy, but LA and LB did not. p53� was associated with a poorer prognosis in ER� luminal tumors but improved prognosis in ERnon-luminal tumors (Interaction p � 0.002). Conclusions: Intrinsic subtyping using a panel of ER, PR, HER2 and Ki67 provides meaningful prognostic information to help guide patient management in early breast cancer. Whilst it predicts benefit from the addition of chemotherapy in TNP and HER2-enriched tumors it did not in this series do so for LB. Although p53 status did not improve the definition of luminal tumors, p53� appeared to have a divergent effect on outcome dependent on ER status. LBA506 Oral Abstract Session, Sun, 8:00 AM-11:00 AM Evaluation of lapatinib as a component of neoadjuvant therapy for HER2� operable breast cancer: NSABP protocol B-41. Presenting Author: Andre Robidoux, National Surgical Adjuvant Breast and Bowel Project and Centre Hospitalier de l’Universite de Montreal, Montreal, QC, Canada The full, final text of this abstract will be available at abstract.asco.org at 12:01 AM (EDT) on Sunday, June 3, 2012, and in the Annual Meeting Proceedings online supplement to the June 20, 2012, issue of Journal of Clinical Oncology. Onsite at the Meeting, this abstract will be printed in the Sunday edition of ASCO Daily News. 505 Oral Abstract Session, Sun, 8:00 AM-11:00 AM 13-gene signature to predict rapid development of brain metastases in patients with HER2-positive advanced breast cancer. Presenting Author: Renata Duchnowska, Military Institute of Medicine, Warsaw, Poland Background: Brain metastases (BM) of breast cancer constitute an important part of therapeutic failures and are associated with severe morbidity and mortality. The risk of BM is particularly high in HER2� advanced breast cancer pts. We earlier developed in this group a 13-gene signature strongly predicting for rapid development of BM (J Clin Oncol 2008; 26: 45s). Now, we validated these results in an independent group of pts and on culture model system. Methods: Discovery group included 87 samples analyzed using cDNA synthesis, annealing, selection, extension, ligation and array hybridization (DASL). Independent validation group included 75 samples analyzed using quantitative reverse-transcriptase PCR. 3D culture validation model system used immortal, non-tumorigenic human MCF10A breast epithelial cells with and without ectopic expression of HER-2 and RAD51, a DNA double strand break repair gene (one of the three genes of this group overexpressed in 13-gene signature). The number and morphology of breast acini were scored using indirect immunoflourescence and confocal microscopy. Results: Median brain metastasis-free survival (BMFS) in the discovery group for ‘high’ vs. ‘low’ expression signature tumors was 36 months and 66 months, respectively (P�0.0068), and in the validation group 54 and 86 months, respectively (P�0.032). Short BMFS was also associated with ER-negativity; BMFS in the cohort of ‘high’ 13-gene signature and ER- tumors vs. other 3 groups was 31 months and 66 months in discovery group, and 41 and 77 months in validation group (P�0.0001 and P�0.02, respectively). Overexpression of RAD51 in MCF-10A breast cells altered their three-dimensional acinar morphology and increased the percentage of invasive structures by 6.5 fold, both in the presence and absence of HER2 overexpression. Conclusions: 13-gene signature and ER-negativity predict rapid development of BM in HER� advanced breast cancer pts. RAD51 may promote aggressiveness in breast epithelial cells. These data may be useful in the design of BM preventive trials and may prompt new treatment strategies. 507 Clinical Science Symposium, Sat, 1:15 PM-2:45 PM Tumor PIK3CA mutations, lymphocyte infiltration, and recurrence-free survival (RFS) in early breast cancer (BC): Results from the FinHER trial. Presenting Author: Sherene Loi, Jules Bordet Institute, Brussels, Belgium Background: Tumor PIK3CA mutations (mts) and lymphocyte infiltration (LI) are prognostic in BC, but their importance is unknown in HER2positive (HER2�) BC treated with adjuvant trastuzumab (T). Methods: The FinHER trial randomized 1010 patients (pts) with pN� or high-risk pN- BC to 3 cycles of docetaxel (D) or vinorelbine, followed by 3 cycles of FEC. Pts with HER2� BC were further randomized to 9 weeks of T or no T (n�232). Pts treated with D and T had superior outcome in prior analyses. BC samples were subjected to somatic hotspot mt profiling (Sequenom) and quantification of percentage tumor LI using full-face H&E sections. RFS and interactions with T were explored with Kaplan-Meier and Cox regression analyses. Results: The median FU time was 62 months. 935 (92.6%) and 687 (68.1%) tumors underwent LI and mt analysis, respectively. Correlation of LI assessment between 2 pathologists was 0.78 (p�0.001). 54 mts detected in 13 genes were evaluated. PIK3CA mts (exons 1,2,9,13,18,20) was present in 25.3% (n�174) and ERBB2 mt in 4.5% (n�31) BCs. Only 1 AKT mt was found and none in KRAS, BRAF, NRAS or PTEN. In ER�/HER2-, HER2� and ER-/HER2- subtypes the prevalence of PIK3CA mts was 30.2%, 19.5% and 9.2%; ERBB2 mt 6.3%, 1.9% and 2.6%, respectively (both p�0.05). Neither PIK3CA nor ERBB2 mts were associated with RFS overall or within BC subgroups. No interaction was found for the benefit with T and presence of PIK3CA mt in HER2� BC (interaction p�0.17 T vs no T). Increasing LI was associated with favorable RFS in ER-/HER2- BC (continuous score adjusted p�0.032); 3-y RFS was 90% with extensive LI (�30% infiltrated) vs 66% with non-extensive LI (p�0.007). In HER2� BC, whilst there was no association with prognosis overall, there was a significant interaction with the benefit from T vs. no T and increasing LI (continuous score interaction p�0.042) with 3-yr RFS 96% vs 78% for extensive and non-extensive LI treated with T respectively (p�0.014). Conclusions: We report 3 clinically relevant findings from this large clinical trial dataset: 1) PIK3CA mts were not prognostic; 2) LI is a strong prognostic factor in ER-/HER2- BC and 3) for the first time that extensive LI predicts benefit from adjuvant T. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
508 Clinical Science Symposium, Sat, 1:15 PM-2:45 PM A phase I/IB dose-escalation study of BEZ235 in combination with trastuzumab in patients with PI3-kinase or PTEN altered HER2� metastatic breast cancer. Presenting Author: Ian E. Krop, Dana-Farber Cancer Institute, Boston, MA Background: Alterations in the PI3K/AKT/mTOR pathway have been implicated in resistance to trastuzumab (T) in HER2� breast cancer. BEZ235, a potent oral dual PI3K/mTORC1/2 inhibitor, has demonstrated growth inhibition and apoptosis in HER2� breast cancer models, including those harboring PI3K pathway alterations, and with T resistance. In a Phase I study, BEZ235 was well tolerated as a single agent in pts with advanced solid tumors. The aim of this study was to determine the MTD of BEZ235 in combination with T in pts with T-resistant HER2� metastatic breast cancer (mBC) with alterations of the PI3K pathway. Methods: Pts with T-resistant HER2� mBC (i.e. disease progression during adjuvant therapy or metastatic disease on therapy with T) received oral BEZ235 daily, with weekly T (2 mg/kg). Pts were eligible for enrollment if a tumor sample was demonstrated to contain a molecular alteration of PIK3CA and/or PTEN. Dose escalation was guided by a Bayesian logistic regression model with overdose control. Results: As of 23 Sep 2011, 15 of the 19 enrolled pts were evaluable for dose escalation analysis. BEZ235 was evaluated at 3 dose levels: (1) 400 mg/day (3 pts); (2) 600 mg/day (6 pts); (3) 800 mg/day (10 pts), administered either in capsule form (400 mg) or in sachet form (600 mg and 800 mg). The MTD of BEZ235 in combination with T was estimated to be 600 mg/day. Observed DLTs were G3 nausea at 600 mg/day (1 pt), and G3 nausea, G3 fatigue and G3 skin rash (1 pt each) at 800 mg/day. The most frequent G3/4 adverse events (CTCAE v3.0) suspected to be related to study treatment were diarrhea (4 pts) and nausea (2 pts). No deaths related to study treatment occurred. 1 pt with lung and brain metastases had a partial response. 4 pts had disease stabilization for �4 cycles (16 weeks), including 1 pt with liver metastases, in whom BEZ235/T treatment resulted in disease stabilization for more than 21 cycles (84 weeks). Conclusions: BEZ235in combination with T demonstrated an acceptable safety profile in pts with HER2� mBC and PI3K pathway alterations. Following the Bayesian model recommendation, the MTD for BEZ235 in combination with T was estimated to be 600 mg/day. The safety expansion arm is ongoing at the MTD. 510 Clinical Science Symposium, Sat, 1:15 PM-2:45 PM SU2C phase Ib study of pan-PI3K inhibitor BKM120 with letrozole in ER�/ HER2- metastatic breast cancer (MBC). Presenting Author: Ingrid A. Mayer, Vanderbilt-Ingram Cancer Center, Nashville, TN Background: Mutations in PIK3CA, the gene encoding the p110a subunit of PI3K, have been associated with antiestrogen resistance in ER� BC. In general, antiestrogen-resistant cancers retain ER and responsiveness to estradiol. This suggests that treatment of ER�/PI3K mutant BC should include PI3K inhibitors plus antiestrogens. Methods: We conducted a phase Ib trial of letrozole (2.5 mg/d) with the pan-PI3K inhibitor BKM120 in post-menopausal patients (pts) with ER�/HER2 MBC. BKM120 (100 mg/d) was given continuously (Arm A) or intermittently (5 on/2 off days; Arm B). Upon toxicity, BKM120 was reduced to 80 and 60 mg/d. Treatment continued until unacceptable toxicity or disease progression. Disease was assessed every 2 months. FDG-PET was done at baseline and at 2 weeks in all pts in Arm A. Results: Fifty-one pts were accrued; 49 had progressed on an AI previously. Median age was 56 years (range 34-77); 95% had bone and 70% visceral metastases. Toxicities and outcomes are summarized in the table. The only DLT* in Arm A and B were transaminitis and depression, respectively; both at 100 mg. Over 50% of Arm A pts had �25% reduction in their peak SUV at the 2-week FDG-PET. Pts who did not exhibit a metabolic response by FDG-PET progressed rapidly on therapy. Three pts in Arm A had a PI3K mutation; one of them has had stable disease on treatment for �12 months. Conclusions: The combination of letrozole/ BKM120 is safe in pts with AI-refractory ER�/HER2 MBC. Arm B is ongoing and will be updated at the meeting. All tumor biopsies will be analyzed for PI3K pathway alterations. FDG-PET at 2 weeks appears to be a useful pharmacodynamic biomarker of PI3K pathway inhibition in most patients. Its value in predicting treatment response remains to be determined. ArmA(N�20) Arm B (N�31) Grade (%) Grade (%) Toxicity 1 2 3 Total 1 2 3 Total Hyperglycemia 50 10 10 70 16 3 0 19 Nausea 55 10 0 65 12 0 0 12 Fatigue 25 40 5 70 9 3 0 12 Transaminitis 35 25 15* 75 16 6 6 16 Diarrhea 40 10 0 50 19 0 0 19 Anxiety 25 15 5 45 3 3 0 6 Depression 15 35 5 55 3 6 3* 12 Rash 30 0 5 35 3 0 0 3 Outcomes Arm A (N�20) Arm B (N�31) CR 1 0 PR 1 0 SD >4 months 9 4 PD 7 8 Non-evaluable 2 5 Still on treatment 1 17 Median TTP (months) 4 (2-11) N/A Discontinued due to toxicity 6 3 Treatment > 8 weeks without interruption 17 N/A Breast Cancer—HER2/ER 509 Clinical Science Symposium, Sat, 1:15 PM-2:45 PM PI3K pathway (PI3Kp) dysregulation and response to pan-PI3K/AKT/mTOR/ dual PI3K-mTOR inhibitors (PI3Kpi) in metastatic breast cancer (MBC) patients (pts). Presenting Author: Mafalda Oliveira, Breast Cancer Group, Vall d’Hebron University Hospital, Barcelona, Spain Background: The role of PI3Kp dysregulation as a predictor of sensitivity to PI3Kpi is unclear. We aimed to evaluate the efficacy of PI3Kpi in two cohorts of MBC pts with assessable PI3Kp status. Methods: MBC pts treated in �3rd line with PI3Kpi were reviewed. PI3Kp status: (a) No dysregulation: PIK3CA wt and PTEN normal; (b) PI3Kp dysregulation: PIK3CA mutation (PIK3CAmut) or PTEN low (HScore�50). Cohort A: pts treated with single agent PI3Kpi. Cohort B: pts treated with PI3Kpi in combination with hormonal therapy (HT), chemotherapy (CT) and/or trastuzumab (T). Results: Out of 232 MBC pts screened for PI3Kp alterations from Sep09 to Sep11, 32 were treated with PI3Kpi. Cohort A (n�17): HR�/HER2- 88%, HER2� 6%, triple negative 6%; median age 43, median MBC lines 4 (2-9); PIK3CAmut in 10/17 (58.8%; 6 exon9, 4 exon20), PTEN low 3/17 (17.6%), 1 pt both; PI3Kp dysregulation 12/17 pts. Cohort B (n�15): HR�/HER2- 40%, HER2� 60%; median age 49, median MBC lines 4 (2-13); PIK3CAmut 3/13 assessable (23.1%; all exon20), PTEN low 6/15 (40%), 1 pt both; PI3Kp dysregulation 8/15 pts. Time to progression to PI3Kpi (TTP), overall survival from MBC diagnosis (OSMBC) and OS from PI3Kpi beginning (OSPI3Kpi), according to PIK3CA status and PI3Kp dysregulation, are shown. No differences were found according to PTEN status. Conclusions: These results suggest that the best outcomes with PI3Kpi in PIK3CAmut MBC pts occur when they are used in combination with HT/CT/T. Activity of non selective PI3Kpi used as single agents seems to be limited, making results from prospective trials with selective PI3K� inhibitors and PI3Kpi in combinations eagerly awaited. Months Median (95%CI) Cohort A n�17 TTP OSMBC OSPI3Ki Cohort B n�15 TTP OSMBC OSPI3Ki PIK3CA PI3Kp dysregulation WT Mut p No Yes p n�7 n�10 n�5 n�12 7.4 (3.5-11.2) 95 (0-206.9) NR 1.4 (0-3.6) 47.1 (12.4-81.9) 8.5 (2.8-14.2) 0.026 0.217 0.048 4.9 (1.5-8.2) 95 (-) NR 1.4 (0-3.3) 47.1 (13.6-80.7) 5.7 (1.8-9.5) n�10 n�3 n�7 n�8 3.6 (1.2-6.1) NR NR 8.4 (-) NR NR 0.053 0.212 0.223 3.6 (0.7-6.6) 55.7 (53.5-57.8) 5.9 (2.6-9.2) 3.7 (2.2-5.2) NR NR 0.092 0.097 0.039 0.451 0.216 0.306 511 Poster Discussion Session (Board #1), Sat, 1:15 PM-5:15 PM and 4:45 PM-5:45 PM Randomized trial of marker-directed versus standard schedule zoledronic acid for bone metastases from breast cancer. Presenting Author: Robert Edward Coleman, CR-UK/YCR Sheffield Cancer Research Centre, Sheffield, United Kingdom Background: Zoledronic acid (ZOL) reduces skeletal morbidity associated with metastatic bone disease by 30-50%. Current recommendations are for indefinite administration of intravenous 3-4 weekly (w) ZOL 4mg. Over recent years it has become clear that the risk of skeletal morbidity is related to the rate of bone resorption. We have compared a marker directed schedule of ZOL (M-ZOL), using measurements of urinary n-telopeptide of type I collagen (NTX), to a standard treatment schedule (S-ZOL) in patients with bone metastases from breast cancer. Methods: The primary endpoint was skeletal related events (SRE). A non-inferiority study was designed with 80% power and (one-sided) 5% alpha to demonstrate that M-ZOL retained 67% of the efficacy of S-ZOL. This required 1500 patients, assuming a SRE rate of 0.7/year. Following minimisation for known prognostic factors, patients were randomised to receive S-ZOL 3-4 w or M-ZOL (15-16w; 8-9 w or 3-4w if NTX levels were �50, 50-100, �100 nmol/mmol creatinine respectively), with the schedule adjusted according to NTX measured every 16 weeks. The study duration was 24 months. Results: Due to lower than expected recruitment, the study closed in 2009 following recruitment of 289 patients. 90% of patients had received �4 cycles of ZOL or pamidronate prior to randomisation. The median number of ZOL infusions administered to S-ZOL patients was �2x that received on M-ZOL. 46 (32%) S-ZOL and 55 (38%) M-ZOL patients experienced an SRE. The numbers of SRE were 94 and 138 in the S-ZOL and M-ZOL arms, with the excess in SRE being largely due to more patients on M-ZOL experiencing �2 SRE. Multivariate analysis adjusting for key minimisation factors and baseline NTX for all SRE showed a hazard ratio for M-ZOL vs. S-ZOL of 1.41 (90%CI 0.98-2.02, p�.12). NTX levels were significantly higher at all time points in the M-ZOL treated patients. Osteonecrosis of the jaw was uncommon with 3 cases with S-ZOL and 1 with M-ZOL. Conclusions: The study is underpowered to demonstrate non-inferiority in SRE outcome between the treatment strategies. However, the results suggest that the adjustment of ZOL schedule based on NTX values alone may represent sub-optimal management. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information. 9s
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Author Index Note: Numerals refer t
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Alexanian, Raymond 8093 Alexeev, Bo
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Arkenau, Hendrik-Tobias 2540, 3000,
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Ballen, Karen K. 6606, 6617, 6618,
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Ben-Aharon, Irit 548, 2556, e13080
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Blancas, Isabel e11535, e11545, e21
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Brandes, Johann Christoph 7048, 106
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Cakir, Betul 9567 Calabek, Bernadet
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Ceraulo, Domenica 4017 Cerbone, Lin
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Chinen, Ludmilla T.D. e16046 Chinen
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Come, Steven E. 9071, 9100 Comis, S
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Dahlheimer, Tambra 2546 Dahmane, El
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DeLacure, Mark D. e16052 Delage, Ju
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Domingo, Gelenis 6568, 6575, 6588 D
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El Sherbeiny, Esam e15129 El-Deiry,
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Fayad, Luis 6501, 8067 Fayette, Jer
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Foroni, Chiara e11546 Foroni, Letiz
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Gang, Wu 7091, e14511 Gangaram, Anj
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Gimenez Capitan, Ana 4068, 10596, e
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Granowetter, Linda 9537 Grant, Barb
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Hainsworth, John D. 618, 1018, 1086
Page 746 and 747:
Heerschap, Arend e13111 Heersink, M
Page 748 and 749:
Hong, Seung-Mo 3568 Hong, Sook Hee
Page 750 and 751:
Im, Young-Hyuck 598^, 644, TPS649,
Page 752 and 753:
Ji, Yongling e17527 Jia, Jingquan e
Page 754 and 755:
Kaparelou, Maria 583 Kapaun, Christ
Page 756 and 757:
Kim, Chan Kyu e14688 Kim, Chang Won
Page 758 and 759:
Komatsu, Yoshihiro e14689 Komatsu,
Page 760 and 761:
Laack, Nadia N. 2032, e14507 Laadem
Page 762 and 763:
Lee, Ji-Hyun TPS3114, 6100 Lee, Jih
Page 764 and 765:
Lim, Kian-Huat e14584 Lim, Kiat Hon
Page 766 and 767:
Loupakis, Fotios 3518, 3540, 3546,
Page 768 and 769:
Man, Shan e11061, e15177^ Manaloor,
Page 770 and 771:
Mathieu-Nicot, Florence e19623 Math
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Mergenthaler, Hans-Guenther e15026
Page 774 and 775:
Molero, Xavier e21035 Moles-Moreau,
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Munoz-Sanchez, MM e19590 Munsell, M
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Ng, Daniel e15050 Ng, Dawn Marie e1
Page 780 and 781:
Oguri, Senri 5556 Oh, Do Youn 1003
Page 782 and 783:
Palassini, Elena 10026, 10053, 1006
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Peisker, Uwe 10600 Peker, Deniz e18
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Piwnica-Worms, Helen 3047 Pizzo, Fa
Page 788 and 789:
Rabinowits, Guilherme 5501, 5582, 9
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Reyes-Rivera, Irmarie CRA3503 Reyna
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Rose, Steven C. 3590 Rosell, Rafael
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Sakata, Shinya e18059 Sakata, Yuh 3
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Schenkein, David P. 6606 Schepp, Wo
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Sha, Dan 3564 Sha, Huifang e13528 S
Page 800 and 801:
Silva, Jose D. 5567 Silva, Milton J
Page 802 and 803:
Sousa, Carlos Eduardo Pires 643 Sou
Page 804 and 805:
Su, Xinying 4124 Su, Yu-Chieh e1600
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Tan, Chee Seng 1064, e19523 Tan, Ch
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Tillmanns, Todd D. 5014, e15514 Til
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Uchiyama, Tomotaka e21108 Udovitsa,
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Videtic, Gregory M.M. e14611, e1466
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Wang, Yuan e15124 Wang, Yunfei 547
Page 816 and 817:
Wischnewsky, Manfred 1078 Wischnik,
Page 818 and 819:
Yasuda, Hiromi e14029 Yasuda, Hiroy
Page 820:
Zhang, Xinmin e16022 Zhang, Xu Dong
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