Hormone Receptor Negative Breast Cancer

We identified unique periods of susceptibility to NO2 and PM2.5 for breast cancer risk by ER status.

P=N/A, N=130, Recruiting, Jewish General Hospital | Trial completion date: Jun 2023 --> Dec 2027 | Trial primary completion date: Jun 2022 --> Dec 2027

Whole-genome sequencing of tumor samples carrying these germline risk variants revealed that they harbored mutational signatures indicative of a deficiency of homologous recombination. These findings suggest that hereditary POLH p.K589T and RAD51 p.M1fs are candidate variants associated with an increased risk of hormone receptor-negative breast cancer.

These findings advance our understanding of genetic susceptibility to different cancers. Future work in larger, more diverse GWAS, coupled with more comprehensive annotation atlases, is essential to expand upon and validate our results.

Subset of AI mice had long-term sustained release tamoxifen placed subscapular on day 8 postpartum...Early metabolic phenotypes in AI and GI glands may be caused by differences in adipocyte repopulation related to estrogen signaling. Long-term metabolic effects of AI lead to similar metabolic effects found in breast cancer.

In conclusion, HER2-ultralow status is not associated with distinct clinicopathologic or genomic characteristics. HER2-IHC 0 (MS-) and ultralow statuses often coexist within the same patient.

Sophia George was funded by the National Institute on Minority Health and Health Disparities (L60MD014321), Chan Zuckerberg Initiative - Ancestry Network DAF2021-240624, Sylvester Comprehensive Cancer COE - IFP. Research reported in this publication was performed in part at the Biostatistics and Bioinformatics Shared Resource of the Sylvester Comprehensive Cancer Center at the University of Miami, RRID: SCR022890, which is supported by the National Cancer Institute of the NIH under award number P30CA240139.

We demonstrated that CDD-1274 induced proteasomal degradation of ERα variants in breast cancer cell lines and caused Y537S ERα degradation more effectively than elacestrant in a palbociclib-resistant cell line. These findings establish that CDD-1274 potently blocks ligand-dependent and ligand-independent ER signaling in endocrine-resistant breast cancer cells and could be further optimized for developing a new class of ERα degraders for endocrine therapy-resistant breast cancer.

Importantly, our results confirm previous data indicating that p.Arg658∗ carriers are at moderate risk of developing ER-neg (OR = 2.08, P = 0.030) and TN (OR = 3.26; P = 0.0034), whereas carriers of p.Gln1701∗ and p.Gly1906Alafs∗12 should not be considered at increased risk. Our data are useful for counseling carriers of FANCM PTVs, but further analyses are warranted to obtain more precise risk estimates.

This highlights a crucial need to explore the underlying mechanisms for these differences to address specific treatment needs and to optimize systemic adjuvant treatment outcomes. Therefore, this narrative review provides an overview of published data regarding the recognized factors and ongoing challenges associated with the risk of relapse in women with HER2+ early breast cancer and proposes potential adjuvant treatment strategies to minimize risk of recurrence in high-risk patients.

Despite lower ORRs in patients with BRCA1 mutations or MYC amplifications, the differences were not statistically significant. This study confirms the clinical efficacy and manageable safety profile of T-DXd in this population, identifying high-risk subgroups and potential resistance biomarkers to inform treatment decisions.

P2, N=27, Active, not recruiting, M.D. Anderson Cancer Center | Recruiting --> Active, not recruiting