Annual Meeting Proceedings Part 1 - American Society of Clinical ...

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22s Breast Cancer—HER2/ER 561 General Poster Session (Board #4D), Sat, 8:00 AM-12:00 PM Assessment of the prognostic and predictive utility of the breast cancer index (BCI): An NCIC CTG MA.14 study. Presenting Author: Dennis Sgroi, Massachusetts General Hospital, The Avon Foundation, Boston, MA Background: Breast Cancer Index (BCI), a continuous risk index, combines the ratio of HOXB13 to IL17BR (H/I) and the molecular grade index (MGI) (Jerevall et al., British J Cancer, 2011). Here, the prognostic and predictive performance of BCI for BC relapse in MA.14 trial was examined. Methods: MA.14 randomly assigned 667 hormone receptor positive (HR�) women to 5 years of tamoxifen (TAM) �/- 2 years of octreotide LAR (TAM-OCT). A representative subgroup of 299 patients was profiled by RT-PCR for BCI. The primary objective was to determine the prognostic performance of BCI based on relapse-free survival (RFS) with median 9.8 years follow-up. Association of BCI was assessed with step-wise forward stratified Cox regression. Pre-defined categories of low (L), intermediate (I) and high (H) BCI risk groups were used to provide adjusted 5- and 10-year RFS. Results: 292 of 299 patient samples passed internal analytical quality control. The 292 patients contained 49% LN� patients and had 19.9% BC relapses. Both continuous and pre-specified BCI risk groups were significant multivariate factors (p�0.0001; p�0.007) with higher BCI associated with shorter RFS. Adjusted univariate hazard ratios and 95% CI were 2.53 (1.36 – 4.71) for BCI-H vs -L and 1.28 (0.65 – 2.52) for BCI-I vs -L. With both LNand LN� included, BCI-L had 5- and 10-year RFS of 94.0% and 87.5%; -I, 91.8% and 83.9%; and -H, 81.5% and 74.7%. No significant difference in BCI’s ability to stratify patients into 3 risk groups was observed between LN-/no chemotherapy subgroup vs balance of MA.14 patients (p�0.26). Higher pathologic T-stage was multivariately associated with shorter RFS (p�0.01). Interactions between trial therapy and BCI was not significant (p�0.40). Conclusions: This study confirmed the strong prognostic effect of BCI on breast cancer recurrence. BCI was prognostic in both LN- and LN� patients. The lower 10-year RFS in the BCI-L group than in our previous studies reflected the mixed LN-/LN� population examined. Like the parent MA.14 trial, BCI did not predict benefit of adding OCT to TAM therapy (Pritchard et al., J Clin Oncol, 2011). This retrospective study is an independent validation of the prognostic performance of BCI within a prospective trial. 563 General Poster Session (Board #4F), Sat, 8:00 AM-12:00 PM Impact of exogenous female hormone use (EHU) on breast cancer (BC) recurrence as assessed by the 21-gene assay (Oncotype DX). Presenting Author: Wendy M. Ledesma, University of Wisconsin Carbone Cancer Center, Madison, WI Background: Observational studies suggest that EHU, such as oral contraceptive (OCPs) or postmenopausal hormone replacement therapy (HRT), increases the risk of developing BC. However, the prognosis of women taking EHU compared to nonusers remains controversial. The Oncotype Dx 21-gene assay RS predicts the distant recurrence risk for early stage, HR� BC. We assessed RS in patients (pts) on EHU at diagnosis (users) vs nonusers. Methods: Retrospective chart review was conducted on BC pts with a RS, diagnosed 2005–2010. Stage, grade, estrogen (ER), progesterone (PR) and HER2 receptor status were abstracted. Manual review of medications, as well as electronic data pull within �5yrs of diagnosis, defined users as pts on EHU within 1 yr of diagnosis for �1 yr. Nonusers had been on EHU � 5 yrs before diagnosis or never. Comparisons between EHU users and nonusers were made using two-sample tests; chi-square or Fisher’s exact test for discrete data such as stage and ER status and t-test or Wilcoxon rank sum test for continuous data such as RS. All tests were at a two-sided significance level of 0.05. Results: 495 pts had RS. EHU was documentable for 475, 77 were using exogenous hormone at diagnosis. Type of hormone use included systemic HRT (48%), OCPs (36%), other (4%), and unknown (12%). For users vs nonusers, mean RS was 17 vs 19, (p�0.007, t-test). See table for other predictors. Conclusions: Prior study shows21-gene assay predict distant recurrence risk for HR�BC. In our study, an association existed between EHU and lower RS, suggesting that BC developing on EHU may have less risk of recurrence. Prospective evaluation is warranted. Users at diagnosis versus nonusers. Nonusers N�398 Users N�77 P-value RS # 19 (9.2) 17 (6.3) 0.007* Age # 57 (10.3) 54 (9.4) 0.04* Stage I 280 (70%) 54 (70%) 0.8 ^ II 105 (26%) 18 (23%) Grade Unknown 1 13 (3%) 117 (29%) 5 (6%) 32 (42%) 0.013 ^ 2 217 (54%) 40 (52%) 3 57 (14%) 3 (4%) ER Unknown � 7 (2%) 386 (97%) 2 (3%) 74 (96%) 1 $ - 4 (1%) 0 PR Unknown � 8 (2%) 340 (85%) 3 (4%) 70 (91%) 0.11 ^ - 49 (12%) 4 (5%) HER2 Unknown � 9 (2%) 4 (1%) 3 (4%) 1 (1%) 0.6 $ - 368 (92%) 69 (90%) Unknown 26 (7%) 7 (9%) # Mean(SD);*t-test; ^ Chi-square test (excluding unknown); $ Fisher’s exact test (excludes unknown). 562 General Poster Session (Board #4E), Sat, 8:00 AM-12:00 PM Association of the phosphorylation of the estrogen receptor at serine 118 and 167 with prognosis in postmenopausal breast cancer patients. Presenting Author: Karin J. Beelen, Netherlands Cancer Institute, Amsterdam, Netherlands Background: The sensitivity of the estrogen receptor (ER�) to anti-estrogen therapy can be affected by phosphorylation events. In premenopausal breast cancer patients, phosphorylation of the ER� at serine 118 (ER�S118-p) is predictive for benefit from adjuvant tamoxifen. Since ER�S118-p represents the common hallmark of different signaling cascades that differ in E2 dependency, the resulting effect on estrogen sensitivity may differ between pre- and postmenopausal patients. Phosphorylation of serine 167 (ER�S167-p) has been associated with favorable disease outcome, but whether ER�S167-p can predict tamoxifen sensitivity is currently unknown. We tested the predictive value of both ER�S118-p and ER�S167-p for benefit from adjuvant tamoxifen in postmenopausal breast cancer patients. Methods: We collected primary tumor blocks from 563 ER� positive (stage I-III) postmenopausal patients who had been randomized between tamoxifen (1 to 3 years) vs. no adjuvant therapy (IKA trial). The median follow-up of patients without a recurrence event was 9.4 years. Immunohistochemistry was performed on a TMA using monoclonal antibodies for ER�S118-p and ER�S167-p. The percentage of positive nuclei was scored and a score of � 10 % was considered as positive. Multivariate Cox models were used to assess hazard ratios (HRs) for recurrence free interval and the interaction between these phosphorylations and tamoxifen treatment. Results: We did not find a significant interaction between either ER�S118-p (p�0.99) or ER�S167-p (p�0.44) and tamoxifen, suggesting that the relative benefit from adjuvant tamoxifen in postmenopausal patients is not dependent on the presence of one of these phosphorylations. Both tamoxifen treated patients as well as control patients had a better prognosis when their tumor was positive for ER�S118-p (adjusted HR 0.60 p�0.02) or ER�S167-p (adjusted HR 0.62, p�0.02) compared to patients whose tumor did not express these ER� phosphorylations. Conclusions: In postmenopausal patients ER�S118-p and ER�S167-p are both associated with better prognosis, but do not predict differential benefit from tamoxifen. 564 General Poster Session (Board #4G), Sat, 8:00 AM-12:00 PM Effect of MDV3100, an androgen receptor signaling inhibitor, on tumor growth of estrogen and androgen receptor-positive (ER�/AR�) breast cancer xenografts. Presenting Author: Anthony D. Elias, University of Colorado Anschutz Medical Campus, Aurora, CO Background: The androgen receptor (AR) is detected by immunohistochemistry in approximately 75% of all invasive breast cancer; with ~88% of ER� tumors expressing AR. Potent inhibition of AR activity could be a therapeutic strategy in ER�/AR� breast cancer. MDV3100 is an androgen receptor signaling inhibitor (ARSI), which inhibits AR activity via three mechanisms: inhibition of androgen binding to AR, inhibition of AR nuclear translocation, and inhibition of nuclear AR-DNA binding. MDV3100 has demonstrated an overall survival benefit in men with post-docetaxel prostate cancer. Methods: Two ER�/AR� breast cancer cell lines, MCF7 and BCK4 (recently derived from a pleurocentesis), were used to assess the proliferative effect of dihydrotestosterone (DHT) and estradiol (E2). The efficacy of MDV3100 at blocking DHT-mediated proliferation was compared to bicalutamide in ER�/AR� breast cancer cells. MCF7 xenograft studies were performed to determine if MDV3100 can affect DHT or E2 mediated proliferation in vivo. Results: Both bicalutamide and MDV3100 inhibited DHT-mediated proliferation of ER�/AR� cell lines. Although MDV3100 binds AR very effectively and does not bind ER, it also uniquely inhibited E2-mediated proliferation, while bicalutamide slightly enhanced E2 mediated proliferation. Results presented here demonstrate that MDV3100 inhibited E2-stimulated tumor growth of MCF7 mammary xenografts as effectively as tamoxifen. Conclusions: MDV3100 blocked both DHT- and E2-mediated growth of breast cancer cells, whereas bicalutamide enhanced E2-mediated proliferation. MDV3100 may have unique therapeutic utility in patients with AR� breast cancer, regardless of ER status. Funding: DOD Breast Cancer Program Idea Award BC074403, Avon Foundation for Women, and University of Colorado Cancer Center pilot project funds to JKR. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
565 General Poster Session (Board #4H), Sat, 8:00 AM-12:00 PM Prognostic factor Ki67 for breast cancer patients in each subgroup. Presenting Author: Naoki Niikura, Tokai University School of Medicine, Isehara Kanagawa, Japan Background: Immunohistochemical (IHC) Ki67 has described it as a prognostic and predictive marker for breast cancer. The St. Gallen Consensus Meeting determined that Ki67 labeling index is chiefly important for distinguishing between “Luminal A” and “Luminal B (HER2 negative)” subtypes and is a predictive marker for chemotherapeutic efficacy. However, the high and low cutoff points remain controversial. Our objective is to compare survival in patients with low, intermediate, and high Ki67 levels in each subgroup. Methods: We retrospectively identified all the patients in the Tokai University breast cancer database for whom IHC Ki67 data were available between January 1, 2000, and December 31, 2010. Ki67 was defined as low if �10% Ki67 was detected, as Intermediate if 10–20% Ki67 was detected, and as high if �20% Ki67 was detected. To assess Ki67 levels and survival outcomes, survival curves were calculated using the Kaplan–Meier method and compared using the log-rank test. Results: We identified 1331 primary breast cancer patients without metastasis, of whom 686 received neoadjuvant or adjuvant chemotherapy. Patients with high Ki67 had poorer relapse-free survival (RFS) than patients with intermediate (p � 0.009) and low Ki67 (p � 0.001). Patients with intermediate Ki67 had poorer RFS than patients with low Ki67 (p � 0.001). In ER-positive cases (n � 1059), patients with high and intermediate Ki67 had poorer RFS than patients with low Ki67 (p � 0.001 and p � 0.002, respectively). In HER2-positive and ER-negative cases (n � 103), patients with high Ki67 had poorer RFS than patients with low Ki67 (p � 0.002). In triple-negative cases (n � 164), patients with high Ki67 tended to have poorer RFS than patients with low Ki67 (p � 0.064). Conclusions: Our data demonstrated that low, intermediate, and high Ki67 levels may be used to differentiate prognosis in ER-positive cancer patients as well as HER2-positive and triple-negative cancer patients. 567 General Poster Session (Board #5B), Sat, 8:00 AM-12:00 PM Characterization of the overall survival benefit in ENCORE 301, a randomized placebo-controlled phase II study of exemestane with and without entinostat in ER� postmenopausal women with metastatic breast cancer. Presenting Author: Pamela Klein, PMK Consulting, San Mateo, CA Background: Histone deacetylase inhibitors (HDACi) prevent the emergence of drug tolerant clones and sensitize cells to a variety of anti-cancer therapies. We previously reported ENCORE 301, a randomized placebo controlled phase 2 study comparing exemestane with (EE) and without (EP) the HDACi entinostat met its primary endpoint of prolonging progression free survival (PFS) (4.3 months vs 2.3 months) and extending overall survival (OS) benefit (26.9 vs 19.8 months). In order to characterize and better understand the OS benefit, exploratory analyses were conducted. Methods: Hazard ratios (HR) for treatment were estimated from the Cox proportional hazards model, with EP serving as the reference treatment in the calculations. Inferential comparisons between treatment groups were made using the log-rank test. Results: Analysis of OS across multiple subsets of interest demonstrated a consistent benefit in EE group versus EP. Sensitivity analysis of baseline characteristics potentially impacting OS did not identify any factors that influenced the effect of EE on OS. Examination of treatments received during follow-up after discontinuation of EE and EP demonstrated balance between treatment group for patients receiving chemotherapy (48% EE: 44% EP), hormone therapy (37% EE: 35% EP), bisphosphonates (2% EE; 0% EP), radiation (6% EE; 5%EP), and surgery (0% EE: 2% EP). Compared to EP, OS was longer in EE group for patients whose first subsequent treatment was a hormone therapy (EE median not reached vs EP median 20.5 months; HR 0.65 [95% CI 0.26, 1.58]) or chemotherapy (EE median 26.9 months vs EP median 17.6 months; HR 0.51 [95% CI 0.25, 1.04]). Updated PFS and OS data will also be presented along with correlation analysis of PFS and OS. Conclusions: Analyses of baseline characteristics, subsequent treatment and subsets of prognostic factors in ENCORE 301 did not identify any contributing factors that account for the extended OS benefit in the EE treatment group. Long lasting effects of entinostat on progenitor cells, emergence of drug tolerant cells and or priming to subsequent therapies cannot be ruled out. Breast Cancer—HER2/ER 23s 566 General Poster Session (Board #5A), Sat, 8:00 AM-12:00 PM Prognostic significance of PI3K pathway (PI3Kp) dysregulation in metastatic breast cancer (MBC) patients (pts). Presenting Author: Alejandro Navarro, Medical Oncology Department, Vall d’Hebron University Hospital, Barcelona, Spain Background: PI3Kp dysregulation represents a potential target for therapies that are currently being tested in clinical trials. This observational retrospective study aims to evaluate the prognostic implications of PI3Kp dysregulation in MBC. Methods: MBC pts with PI3Kp status assessment from Sep09 to Sep11 were reviewed. PIK3CA mutation status analyzed in paraffin-embedded tissue by DxS PI3K Mutation Test Kit or Sequenom MassARRAY. PTEN status determined by IHC. PI3Kp status: (a) No dysregulation: PIK3CA wt and PTEN normal; (b) PI3Kp dysregulation: PIK3CA mutation (PIK3CAmut) or PTEN low (HScore�50). Results: 232 MBC pts screened, median age 49.8 (22.9-83.1) and median MBC lines 4 (1-15). Distribution: HR�/HER2- 99 (43%), HER2� 52 (22%), triple negative 35 (15%), unclassified 46 (20%). Sites of metastasis: visceral 173 (75%), only skin 10 (4%), only bone 49 (21%). PIK3CA status assessed in 174 pts, 53 (22.8%) bearing a mutation (21 exon9, 32 exon20). PTEN status assessed in 229 pts, PTEN low 61 (26.6%). PI3Kp dysregulation in 103/185 pts (55.6%). Time to progression to first line MBC treatment (TTP) and overall survival after MBC diagnosis (OS) are shown. Disease free survival (DFS) and distant-disease free survival (DDFS) in pts initially diagnosed with early breast cancer (n�193) has also been calculated. Conclusions: These results suggest that PI3Kp dysregulation, either by PIK3CA mutation or PTEN low, does not seem to have impact on disease recurrence, response to first line MBC treatment or overall MBC survival. PIK3CA PTEN PI3Kp dysregulation Median (95%CI) WT Mut Normal Low No Yes n�174 n�229 n�185 n�121 n�53 n�168 n�61 n�82 n�103 TTP (m) 12.0 11.8 13.0 11.5 12.3 11.8 (10.3-13.8) (9.6-14.0) (11.4-14.6) (7.4-15.6) (10.0-14.5) (9.1-14.5) p�0.780 p�0.891 p�0.516 OS (y) 5.5 5.0 5.6 5.1 5.5 5.0 (4.1-6.9) (3.3-6.7) (4.9-6.3) (3.0-7.3) (3.9-7.1) (3.5-6.5) p�0.882 p� 0.460 p�0.443 n�158 n�189 n�167 n�107 n�51 n�132 n�57 n�69 n�98 DFS (m) 45.0 36.6 38.6 49.6 36.0 46.0 (35.6-54.4) (28.6-44.6) (32.2-45.1) (42.6-56.5) (24.3-47.7) (38.5-53.4) p� 0.476 p�0.071 p�0.163 DDFS (m) 51.0 44.6 46.3 57.1 40.0 49.6 (43.1-58.8) (32.5-56.7) (35.8-56.8) (44.3-69.9) (22.5-57.5) (39.7-59.4) p� 0.505 p� 0.289 p� 0.254 568^ General Poster Session (Board #5C), Sat, 8:00 AM-12:00 PM Prospective study of the impact of using the 21-gene recurrence score assay on clinical decision making in women with estrogen receptorpositive, HER2-negative, early-stage breast cancer in France. Presenting Author: Joseph Gligorov, APHP Tenon APREC, CancerEst, University Paris VI, Paris, France Background: The 21-gene Oncotype DX Recurrence Score (RS) is a validated assay to help inform the appropriate treatment of estrogen receptor-positive (ER�), early stage breast cancer in the adjuvant setting. Treatment traditions regarding choice of adjuvant treatment vary significantly in different countries. This prospective multicenter study is the first to assess the impact of using the Oncotype DX assay in the French clinical setting. Methods: A total of 100 consecutive patients with ER�, HER2negative, node negative or pN1 (mi) breast cancer were enrolled. Overall treatment recommendation change, change from chemoendocrine to endocrine alone and change from endocrine alone to chemoendocrine treatment were recorded. Medical oncologists completed questionnaires regarding their confidence in their recommendation before and after knowing the patient’s RS. A preliminary analysis was conducted on the first 92 evaluable patients with data available at the time of abstract submission. Final data will be presented at the meeting. Results: Prior to Oncotype DX 49% of patients were recommended chemoendocrine treatment and 51% endocrine treatment alone. After having the RS, 26% were recommended chemoendocrine treatment and 74% endocrine treatment alone. The overall reduction in chemotherapy recommendation from 49% to 26% was significant (p�0.001). Of patients originally recommended chemoendocrine treatment, 58% were changed to endocrine treatment alone after having the RS. Of patients originally recommended endocrine treatment, 11% were changed to chemoendocrine treatment after receiving the RS. There was a significant improvement in physician confidence in treatment recommendations (p�0.002) when using Oncotype DX. Conclusions: These are the first prospective data regarding the impact of using Oncotype DX in France. Using Oncotype DX was associated with a significant change in treatment decisions and an overall reduction in chemotherapy use. The data are consistent with those presented from Germany, Spain, the UK and the US. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
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Author Index Note: Numerals refer t
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Alexanian, Raymond 8093 Alexeev, Bo
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Ballen, Karen K. 6606, 6617, 6618,
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Blancas, Isabel e11535, e11545, e21
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Ceraulo, Domenica 4017 Cerbone, Lin
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Domingo, Gelenis 6568, 6575, 6588 D
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El Sherbeiny, Esam e15129 El-Deiry,
Page 734 and 735:
Fayad, Luis 6501, 8067 Fayette, Jer
Page 736 and 737:
Foroni, Chiara e11546 Foroni, Letiz
Page 738 and 739:
Gang, Wu 7091, e14511 Gangaram, Anj
Page 740 and 741:
Gimenez Capitan, Ana 4068, 10596, e
Page 742 and 743:
Granowetter, Linda 9537 Grant, Barb
Page 744 and 745:
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
Page 772 and 773:
Mergenthaler, Hans-Guenther e15026
Page 774 and 775:
Molero, Xavier e21035 Moles-Moreau,
Page 776 and 777:
Munoz-Sanchez, MM e19590 Munsell, M
Page 778 and 779:
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
Page 784 and 785:
Peisker, Uwe 10600 Peker, Deniz e18
Page 786 and 787:
Piwnica-Worms, Helen 3047 Pizzo, Fa
Page 788 and 789:
Rabinowits, Guilherme 5501, 5582, 9
Page 790 and 791:
Reyes-Rivera, Irmarie CRA3503 Reyna
Page 792 and 793:
Rose, Steven C. 3590 Rosell, Rafael
Page 794 and 795:
Sakata, Shinya e18059 Sakata, Yuh 3
Page 796 and 797:
Schenkein, David P. 6606 Schepp, Wo
Page 798 and 799:
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
Page 806 and 807:
Tan, Chee Seng 1064, e19523 Tan, Ch
Page 808 and 809:
Tillmanns, Todd D. 5014, e15514 Til
Page 810 and 811:
Uchiyama, Tomotaka e21108 Udovitsa,
Page 812 and 813:
Videtic, Gregory M.M. e14611, e1466
Page 814 and 815:
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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