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Natalia Baran: GD3 Synthase Drives Resistance to p53-Induced Apoptosis in Breast Cancer by Modulating Mitochondrial Function
May 21, 2025, 05:49

Natalia Baran: GD3 Synthase Drives Resistance to p53-Induced Apoptosis in Breast Cancer by Modulating Mitochondrial Function

Natalia Baran, Leading Attending and Assistant Professor at the University Hospital Department of Hematology at Insel Group, posted on LinkedIn:

“I am thrilled to share groundbreaking insights from our latest research into the molecular drivers of breast cancer progression. I feel incredibly grateful to have been part of this collaborative effort led by Dr Vivek Anand, Ph.D. and supervised by Prof. V. Lokesh Battula, which has just been published in Oncogene Springer Nature!

This study dives deep into the vital role of the tumor suppressor p53—particularly how its mutations, common in triple-negative breast cancer (TNBC), are linked to poor prognosis and limited treatment success. We explore the fascinating interplay between mutant p53 and GD3 synthase (GD3S), an enzyme critical for cancer stem cell maintenance and tumor growth.

By examining how different p53 mutations—loss- or gain-of-function—affect GD3S activity, and how this interaction influences tumor initiation and progression, our research uncovers potential new vulnerabilities. Using patient data and cell models, we highlight promising therapeutic targets that could revolutionize how we approach hard-to-treat breast cancers.

In essence, our findings reveal that GD3S drives tumor growth—especially in cells with gain-of-function p53 mutations—by supporting mitochondrial function and preventing apoptosis. This opens up exciting new possibilities for targeted therapy!”

Title: GD3 synthase drives resistance to p53-induced apoptosis in breast cancer by modulating mitochondrial function

Authors: Vivek Anand, Fouad El-Dana, Natalia Baran, Jenny Borgman, Zheng Yin, Hong Zhao, Stephen T. Wong, Michael Andreeff and V. Lokesh Battula

Read The Full Article at Oncogene.

Natalia Baran: GD3 Synthase Drives Resistance to p53-Induced Apoptosis in Breast Cancer by Modulating Mitochondrial Function

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