GENERAL SESSION 2

Alle Vortragsfolien

 

[GS2-01] High levels of interferon-response gene signatures are associated with de novo and acquired resistance to CDK4/6 inhibitors in ER+ breast cancer

 

 

De Angelis C, Fu X, Cataldo ML, Nardone A, et al.

 

 

 

The authors conclude that: Aberrant IFN-signaling predicts resistance to CDK4/6i in both ER+/HER2- BC cell lines and in primary BCs from neoadjuvant clinical trials. Experimentally, acquired resistance to Palbo is associated with activation of the IFN-pathway suggesting its involvement in resistance to CDK4/6i. Future studies are warranted to provide mechanistic insights into the association of IFN-signaling with response to CDK4/6i. 

 

 

 

[GS2-02] Acquired activating mutations in RTKs confer endocrine resistance in ER+ metastatic breast cancer through ER-reprogramming, MAPK signaling, and an induced stem-like cell state

 

 

Cohen O, Mao P, Nayar U, Buendia-Bue JE, et al.

 

 

 

The authors conclude that: This study demonstrated that activating RTKs constitute of prevalent modality of acquired resistance to endocrine therapies, inducing a distinct state with clinical implications - suggesting the potential benefit of combination therapies with specific TKIs over CDK4/6i. The common MAPK activity and our preliminary results - suggests the potential of convergence-node targeting strategy with added MEK or SHP2 inhibition.

 

 

 

[GS2-03] The androgen receptor is a tumour suppressor in estrogen receptor positive breast cancer

 

 

Lim E, Hickey TA, Selth LA, Chia KM, et al.

 

 

 

The authors conclude that: Collectively, these findings provide compelling evidence that AR has a tumour suppressor role in ER+ breast cancer and advocate an AR agonist strategy for treatment, even in the context of therapy-resistant, ESR1 mutant disease, and should dispel widespread confusion over the role of AR in ER-driven breast cancer, an issue that currently hinders progress in leveraging modern AR-targeted therapies, including available SARMs that lack the undesirable side-effects of androgens, for clinical benefit.

 

 

 

[GS2-04] Improvements in long-term outcome for women with estrogen receptor positive (ER+) early stage breast cancer treated with 5 years of endocrine therapy: Analyses of 82,598 women in the Early Breast Cancer Trialists’ Collaborative Group (EBCTCG) database

 

 

Pan H, Braybrooke J, Gray R, Peto R, et al.

 

 

 

The authors conclude that: The risk of DR at 20 years after diagnosis for women with node-negative ER+ early stage breast cancer, who discontinue endocrine therapy at 5 years is likely to be about a third lower now than in our previous report. However, long-term follow-up of patients diagnosed more recently is required to accurately characterize long-term recurrence risks.

 

 

 

[GS2-05]Microscaled proteogenomic methods for precision oncology

 

 

Satpathy S, Jaehnig E, Karsten K, Kim B-J, et al.

 

 

 

The authors conclude that: In summary, we have developed a robust proteogenomics pipeline well suited for large-scale cancer clinical studies to identify potential resistance mechanism in patients. We conclude that microscaled cancer proteogenomics could improve diagnostic precision in the clinical setting.

 

 

 

[GS2-06] Primary results of SOLTI-1402/CORALLEEN phase 2 trial of neoadjuvant ribociclib plus letrozole versus chemotherapy in PAM50 Luminal B early breast cancer: An open-label, multicenter, two-arm, randomized study

 

 

Gavilá J, Saura C, Pascual T, Hernando C, et al.

 

 

 

The authors conclude that: Neoadjuvant ribociclib and letrozole in high-risk Luminal B breast cancer achieves similar rates of ROR-low disease at surgery as multi-agent chemotherapy. Future studies in high-risk early breast cancer evaluating the survival outcomes and quality of life of this combination in the absence of cytotoxic therapy are justified.

 

 

 

[GS2-07]Results from PEARL study (GEICAM/2013-02_CECOG/BC.1.3.006): A phase 3 trial of Palbociclib (PAL) in combination with endocrine therapy (ET) versus Capecitabine (CAPE) in hormonal receptor (HR)-positive/human epidermal growth factor receptor (HER) 2-negative metastatic breast cancer (MBC) patients (pts) whose disease progressed on aromatase inhibitors (AIs)

 

 

Martín M, Zielinski C, Ruíz-Borrego M, Carrasco E, Ciruelos E, et al.

 

 

 

The authors conclude that: The PEARL study did not show a statistically superiority in PFS for PAL+ET vs CAPE in MBC pts progressing to AIs. No superiority of PAL+ET was observed in the luminal subgroup either. Treatment with PAL+ET was generally better tolerated than CAPE.

 

 

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