Dr. Kornblum on Impact of PrECOG 0102 Trial for HR+/HER2- Breast Cancer

Noah S. Kornblum, MD
Published: Thursday, Dec 08, 2016



Noah S. Kornblum, MD, assistant professor of medicine, Albert Einstein College of Medicine, and attending physician of medicine, Montefiore-Einstein Center for Cancer Care, discusses the phase II PrECOG 0102 trial, which explored the addition of everolimus (Afinitor) to fulvestrant (Faslodex) as a treatment for patients with metastatic hormone receptor (HR)–positive, HER2-negative breast cancer.

PrECOG 0102 was a randomized, double-blind, phase II study. Here, the everolimus/fulvestrant combination doubled median progression-free survival rates compared with fulvestrant alone, from 5.1 months on fulvestrant to 10.4 months with the combination (HR, 0.60; 95% CI, 0.40-0.92; P = .02).

The PI3k/Akt/mTOR pathway is usually a variant in aromatase inhibitor or endocrine resistant breast cancer in multiple ways, Kornblum explains. The logic behind the investigative regimen was to target the mTOR pathway with a mTOR inhibitor in combination with an established endocrine backbone, such as fulvestrant. Fulvestrant was chosen as it has more potent estrogen receptor-inhibitory activity than an agent such as exemestane.

<<< View more from the 2016 San Antonio Breast Cancer Symposium



Noah S. Kornblum, MD, assistant professor of medicine, Albert Einstein College of Medicine, and attending physician of medicine, Montefiore-Einstein Center for Cancer Care, discusses the phase II PrECOG 0102 trial, which explored the addition of everolimus (Afinitor) to fulvestrant (Faslodex) as a treatment for patients with metastatic hormone receptor (HR)–positive, HER2-negative breast cancer.

PrECOG 0102 was a randomized, double-blind, phase II study. Here, the everolimus/fulvestrant combination doubled median progression-free survival rates compared with fulvestrant alone, from 5.1 months on fulvestrant to 10.4 months with the combination (HR, 0.60; 95% CI, 0.40-0.92; P = .02).

The PI3k/Akt/mTOR pathway is usually a variant in aromatase inhibitor or endocrine resistant breast cancer in multiple ways, Kornblum explains. The logic behind the investigative regimen was to target the mTOR pathway with a mTOR inhibitor in combination with an established endocrine backbone, such as fulvestrant. Fulvestrant was chosen as it has more potent estrogen receptor-inhibitory activity than an agent such as exemestane.

<<< View more from the 2016 San Antonio Breast Cancer Symposium


View Conference Coverage
Online CME Activities
TitleExpiration DateCME Credits
Medical Crossfire®: Key Questions for the Use of Immunotherapy Throughout the Disease Continuum for NSCLC in an Era of Rapid DevelopmentSep 29, 20181.5
Provider and Caregiver Connection™: Addressing Patient Concerns While Managing GlioblastomaSep 29, 20182.0
Publication Bottom Border
Border Publication
x