Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

E-Poster Display

335P - Resistance to CDK4/6 inhibitors: Clinical practice use of liquid biopsy to identify KRAS-mutations in ctDNA and overexpression of CDK9 in plasma derived exosomes

Date

17 Sep 2020

Session

E-Poster Display

Topics

Tumour Site

Breast Cancer

Presenters

Lucrezia Raimondi

Citation

Annals of Oncology (2020) 31 (suppl_4): S348-S395. 10.1016/annonc/annonc268

Authors

L. Raimondi1, M. Pietranera2, G.P. Spinelli3

Author affiliations

  • 1 Department Of Medical-surgical Sciences And Biotechnologies, UOC Territorial Oncology - Aprilia (LT) – ASL Latina, University of Rome “Sapienza”, 04100 - Latina/IT
  • 2 Centro Medico Diagnostico, Salus, 00053 - Civitavecchia/IT
  • 3 Department Of Medical-surgical Sciences And Biotechnologies, Sapienza University Of Rome, ., UOC Territorial Oncology- Aprilia (LT) – ASL Latina, University of Rome “Sapienza”, Latina/IT

Resources

Login to get immediate access to this content.

If you do not have an ESMO account, please create one for free.

Abstract 335P

Background

Despite therapeutic improvements, all patients (pts) sooner or later acquire resistance to CDK4/6 inhibitors. Mutations in KRAS have been thought to be the main cause of resistance in several cancers, but have not been analysed extensively in breast cancer in the era of Palbociclib+Fulvestrant (P+F). In our study, using liquid biopsy, we correlated the emerging KRAS-mutated ctDNA and overexpression of CDK9 with resistance to P+F as first line metastatic treatment in HR+/HER2-Metastatic Breast Cancer (MBC).

Methods

A total of 948 blood samples were collected from 106 pts with HR+/HER2-MBC treated with P+F as first-line metastatic therapy (Dec17-Mar20). KRAS ctDNA levels in plasma were determined with Bio-Rad QX200 ddPCR system; we used exoRNeasy kit to analyze CDK4/9 expression.

Results

KRAS mutations were detected in ctDNA of 54% (57pts) of pts before starting P+F treatment: detection of KRAS ctDNA was significantly associated with resistance, recurrence and prognosis (p<0.001). At 18-month follow up [1-NA], pts with KRAS-mutated ctDNAand overexpression of CDK9 had a median PFS of 3 months [1-6months,95%CI 0.8-3.6] contrary to ones with no detection of KRAS ctDNA whose PFS had not yet been reached (p<0.001). We demonstrated the association between circulating number of copies/ml of KRAS-mutated ctDNA and tumoral burden: hgher number of metastatic sites correlated with higher mutant ctDNA copy number (p<0.0001). Moreover, lower LMr (<5.0) was associated with progression disease within 12months (p<0.001).

Conclusions

Despite the study’s limitations, our findings suggest detection of KRAS ctDNA levels, which correlates with overexpression of CDK9, enables to predict the onset of resistance to P+F treatment. Monitoring KRAS status with liquid biopsy, we could predict who will take advantage from P+F, offering highly individualized treatment plans. With a careful treatment selection, we could decrease wastes of resources ensuring the best pts’ quality of life.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

ASL Latina - University of Rome \"Sapienza\".

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.