New path to treat advanced triple-negative breast cancer

Date:
February 2, 2022
Source:
Yale University
Summary:
A new study shows inhibition of the CECR2 gene prevents
triple-negative breast cancer from advancing or metastasizing.



FULL STORY ==========================================================================
A new study by researchers at Yale Cancer Center shows inhibition of
the CECR2 gene prevents triple-negative breast cancer from advancing
or metastasizing.

The discovery is an early step in finding new therapeutics for
triple-negative breast cancer (TNBC), one of the most difficult disease sub-types to treat. The findings are published online today in the
journal Science Translational Medicine.


========================================================================== "These study results are very encouraging as there are few effective
treatments for triple-negative breast cancer once it has metastasized,"
said senior study author Qin Yan, PhD, Associate Professor of Pathology
and Director of Center for Epigenetics and Biomarkers in the Department
of Pathology at Yale School of Medicine, co-leader of Genomics, Genetics
and Epigenetics Research Program and Scientific Co-Director of Center
for Breast Cancer of Yale Cancer Center. "We are constantly searching
for new effective therapeutic strategies to help patients with this
potentially deadly disease." In this study, researchers profiled 13
pairs of primary and metastatic breast tumor samples from patients with
breast cancer. They identified a therapeutic target, a gene called CECR2,
that increased expression in the tumors that have spread to distant
organs. The research team discovered that CECR2 allowed the breast cancer
cells to migrate and invade to adjacent tissues and evade surveillance
by the host immune system. As the result, CECR2 targeting resulted in
the activation of T cells and prevented the tumor from spreading.

Researchers also discovered that small molecule inhibitors of CECR2
can suppress the ability of TNBC cells to spread in cell cultures
and animal models, providing a new avenue of therapeutic strategy to
treat advanced disease. According to researchers, the findings could
translate to increased response to current immunotherapies, which had
modest efficacy on breast cancer as monotherapies.

"We will continue to study these important findings," added Yan. "We
are working on characterizing the mechanisms by which CECR2 modulates
gene expression and tumor microenvironment using multiple cutting-edge technologies.

In addition, we hope to develop small molecule inhibitors of CECR2 for
clinical studies." The study was funded by the Department of Defense
Breast Cancer Research Program, the National Institutes of Health,
a Yale Cancer Center Class of '61 Cancer Research Award and the James
Hudson Brown-Alexander Brown Coxe Postdoctoral Fellowship.

========================================================================== Story Source: Materials provided by Yale_University. Note: Content may
be edited for style and length.


========================================================================== Journal Reference:
1. Meiling Zhang, Zongzhi Z. Liu, Keisuke Aoshima, Wesley L. Cai,
Hongyin
Sun, Tianrui Xu, Yangyi Zhang, Yongyan An, Jocelyn F. Chen, Lok
Hei Chan, Asako Aoshima, Sabine M. Lang, Zhenwei Tang, Xuanlin Che,
Yao Li, Sara J.

Rutter, Veerle Bossuyt, Xiang Chen, Jon S. Morrow, Lajos Pusztai,
David L. Rimm, Mingzhu Yin, Qin Yan. CECR2 drives breast cancer
metastasis by promoting NF-kB signaling and macrophage-mediated
immune suppression.

Science Translational Medicine, 2022; 14 (630) DOI: 10.1126/
scitranslmed.abf5473 ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2022/02/220202165903.htm

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