GENERAL SESSION 1
WEBCAST (registration required)
View the 2020 SABCS Abstracts
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O'Shaughnessy JA, Johnston S, Harbeck N, et al. |
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The authors conclude that: At the primary outcome analysis, with a median follow-up of approximately 19 months, abemaciclib combined with ET continued to demonstrate a clinically meaningful improvement in IDFS in patients with HR+, HER2-, node-positive, high risk, EBC with a statistically significant improvement in IDFS in patients with central Ki-67 ≥20%. ClinicalTrials.gov: NCT03155997 Table 1: PrimaryOutcome Efficacy
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Loibl S, Marmé F, Martin M, Untch M, et al. |
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The authors conclude that: PENELOPE-B evaluates the effect of palbociclib for 1 year compared to placebo in addition to endocrine therapy in high-risk primary breast cancer patients. The database was locked with 308 events on September 25th 2020. After breaking the blind for analysis, top line results will be available as of mid October 2020. Results of the final iDFS analysis will be presented at the meeting.
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[GS1-03] Discussant |
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Ruth O'Regan, MD |
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Prat A, Chaudhury A, Solovieff N, et al. |
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The authors conclude that: This is the largest analysis evaluating the correlation of intrinsic ABC subtype with efficacy outcomes in patients treated with CDK4/6 inhibitors. Patients with HER2E, LumA, LumB, and normal-like subtypes all exhibited a consistent PFS benefit with RIB treatment, while patients with basal-like ABC (RIB: 2%; PBO: 3%) did not. The HER2E subtype (RIB: 14%; PBO: 11%) exhibited the greatest relative reduction in risk of progression or death (61%) with RIB plus ET.
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[GS1-05] Hotspot ESR1 mutations rewire cell-cell adhesome to facilitate breast cancer metastasis |
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Li Z, Wu Y, Bahreini A, et al. |
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The authors conclude that: Hotspot ESR1 mutations induce expression of multiple desmosome and gap junction genes and confer increased cell-cell adhesion, which facilitate breast cancer metastasis via increased CTCs clustering propensity. These findings might guide approaches to test potential repurpose of drugs targeting gap junction in ER mutant tumors.
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[GS1-06] FGFR1 associates with gene promoters and regulates gene transcription: Implications for endocrine resistance in ER+/FGFR1-amplified breast cancer |
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Servetto A, Kollipara R, Formisano L, et al. |
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The authors conclude that: We have demonstrated a role for nuclear FGFR1 in transcriptional regulation in breast cancer. FGFR1-induced gene expression contributes to endocrine resistance and is not affected by FGFR TKIs. These findings provide a rationale for developing treatment strategies to inhibit nuclear FGFR1 in ER+/FGFR1-amplified breast cancer.
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Dhimolea E, De Matos Simoes R, Kansara D, et al. |
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The authors conclude that: Overall, our study shows that breast tumors dynamically co-opt the stress survival mechanism of embryonic diapause to persist during treatment, and reveals an unexpected role of Myc as regulator of cancer cell entry into transient drug-refractory dormancy. The diapause-like persister organoid cancer models provide ex vivo tractability for studying the otherwise elusive, dormant, drug-refractory residual tumors, with potential implications in personalized medicine and drug discovery.
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Lee JV, Housley F, Yau C, et al. |
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The authors conclude that: Our data suggest MYC is an indicator of whether a breast cancer patient will respond to immunotherapy. Analysis of the MYC gene signature as a predictor of patient response to pembrolizumab in combination with paclitaxel followed by AC in the neoadjuvant I-SPY 2 trial is on-going and will be presented. Our study is the first to describe oncogenic MYC downregulation of MHC-I in a TNBC model of breast cancer and to demonstrate translatable approaches to overcome MYC orchestrated immune evasion.
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Thomas "Trey" Westbrook, PhD |
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Simons JM, v Nijnatten TJA, Koppert LB, et al. The authors conclude that: This prospective multicenter validation trial shows that the RISAS procedure/Targeted Axillary Dissection is most suitable in terms of identification rate and accuracy to replace ALND for axillary staging after NAC in cN+ patients. The trial was funded by the Dutch Cancer Society (KWF, grant number 2015-8023). |
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