ER positive

Despite the initiation of corticosteroids and methotrexate, the patient showed clinical deterioration over four weeks...Following neoadjuvant chemotherapy, surgery, and radiation, the patient achieved complete remission of her myositis, with normalisation of creatine phosphokinase (CPK) levels, resolution of rash, and recovery of muscle strength, confirming the paraneoplastic aetiology. This case underscores the imperative to pursue malignancy screening in DM patients unresponsive to immunosuppressive therapy, regardless of age. It highlights the critical role of thorough physical examination and the superiority of breast imaging in young women with dense breasts.

Pharmacologic inhibition of HMGCR with simvastatin, alone or combined with IL-6 blockade, restored CDK4/6i sensitivity in vitro and in vivo, highlighting a clinically accessible strategy to overcome adipocyte-mediated resistance. Collectively, our findings establish that CAAs confer CDK4/6i resistance in ER+ breast cancer through the IL-6-driven SREBF2 activation axis, sustained by a reciprocal exosomal miR-1246/UCHL1-mediated feedback loop.

Altogether, we uncovered a previously unrecognized triad of ERG-driven processes -dedifferentiation, senescence, and inflammation- that may underpin its oncogenic potential and shape PCa initiation and therapeutic response. Implications: Temporal control of ERG expression in prostate cells enabled accurate mapping of ERG-driven processes, identifying dedifferentiation, senescence, and inflammation as candidate contributors to ERG-dependent tumorigenesis and therapeutic response.

Receptor discordance between primary tumors and nodal metastases is common, with most shifts occurring within the HER2-spectrum. There was a trend toward higher RS and ER or HER2-receptor discordance. HER2 discordance was also associated with larger tumor size and larger size of nodal metastasis. As strategies emerge to target HER2-low cohorts and to include ER-low/HER2-negative disease within treatment regimens for TNBC, it may become important to consider receptor testing of nodal disease in the future.

We further argue that a mechanistic understanding of dormancy requires integrative frameworks that bridge single-cell level regulatory programs - including cell-cycle arrest, translational inhibition, and metabolic reprogramming - with systems-level networks capturing the dynamic, multistage nature of metastasis. Such integration may uncover actionable vulnerabilities within dormant cell populations and guide the development of precision therapies targeting minimal residual disease.

Letrozole-associated panuveitis has not previously been reported. This case highlights the importance of detailed medication history as well as the need for interdisciplinary collaboration when managing drug-induced uveitis. Early recognition and appropriate therapy can result in favorable visual outcomes.

By contrast, identical genetic alterations in mice failed to yield ER+ tumors, underscoring critical species differences in tumorigenesis. Together, this work establishes a versatile platform for the rapid generation of clinically relevant rat tumor models, opening avenues to study tumor biology, therapeutic response, and immune interactions in cancer subtypes previously inaccessible to experimental modeling.

Cell viability was quantified using a tetrazolium-based colorimetric assay and apoptosis was evaluated by the Muse® Annexin V & Dead Cell assay based on Annexin V and 7-amino-actinomycin D staining; the expression levels of JNK, p38, ERK, beclin-1, microtubule-associated protein 1 light chain 3B (LC3B), p62/sequestosome 1 (SQSTM1) and poly (ADP-ribose) polymerase (PARP) were assessed by western blotting. Pharmacological inhibition with SP600125 attenuated JNK phosphorylation, reduced apoptotic responses and diminished autophagy-associated marker accumulation, supporting the notion that JNK signaling contributes, at least in part, to these effects. These findings indicate that RTA-408 exerts nanomolar antiproliferative activity in both hormone receptor-positive and triple-negative BC cells through a JNK-dependent mechanism that simultaneously engages apoptosis and autophagy, supporting further in vivo and translational investigation.

P2, N=110, Recruiting, Dana-Farber Cancer Institute | N=180 --> 110

P2, N=700, Not yet recruiting, UNICANCER

This study highlights PR-negativity in ER+/HER2- ILRR tumors as a poor prognostic factor after ILRR, independent of the PR status of the primary breast cancer, emphasizing the need for tailored treatment strategies.

In summary, these findings suggest that E-NACOS exert relevant anti-migratory and pro-apoptotic effects in breast cancer cell models, potentially through oxidative stress associated mechanisms. Although further mechanistic insights and in vivo validation are required, A. faecalis-derived E-NACOS represent a promising bioactive preparation worthy of continued exploration for prospective applications in breast cancer management.